subject:(Progesterone Receptor Membrane Component 1)

1. L. Terzaghi. ROLE OF PROGESTERONE RECEPTOR MEMBRANE COMPONENT 1 (PGRMC1) IN CONTROLLING GERMINAL AND SOMATIC CELL DIVISION AND FUNCTION.

Degree: 2018, Università degli Studi di Milano

URL: http://hdl.handle.net/2434/550339

► La sub-fertilità rappresenta uno dei principali problemi che l'industria lattiero-casearia si trova ad affrontare attualmente. Si tratta di un problema multifattoriale che dipende da diversi… (more)

▼ La sub-fertilità rappresenta uno dei principali problemi che l'industria lattiero-casearia si trova ad affrontare attualmente. Si tratta di un problema multifattoriale che dipende da diversi aspetti della funzione riproduttiva. La qualità dell'ovocita, determinata durante la follicologenesi, è sicuramente cruciale per ottenere risultati riproduttivi ottimali. Per migliorare la fertilità femminile nel bovino è fondamentale definire i fattori e i meccanismi che determinano la qualità del gamete femminile, in quanto il declino della funzione riproduttiva in questa specie è dovuto principalmente alla scarsa qualità degli ovociti. In particolare, è importante conoscere quali proteine regolano la meiosi, la fecondabilità e lo sviluppo embrionale dell'ovocita. In questo progetto, abbiamo considerato principalmente il ruolo del Progesterone Receptor Membrane Component-1 (PGRMC1) sia nell'ovocita che nel compartimento follicolare, considerato che il dialogo tra compartimento germinale e compartimento somatico è uno dei fattori chiave coinvolti nell'acquisizione della competenza allo sviluppo del gamete femminile. Il PGRMC1 è una proteina multifunzionale ed altamente conservata in specie anche filogeneticamente distanti. Nei mammiferi è espressa in diversi sistemi, compresi gli organi riproduttivi, e localizza in diversi compartimenti subcellulari. Tuttavia, il suo ruolo e il preciso meccanismo d'azione in ogni sistema e/o compartimento subcellulare non sono ancora del tutto conosciuti. La parte più considerevole di questo progetto di dottorato riguarda gli studi effettuati sul ruolo del PGRMC1 nella divisione cellulare, data la sua localizzazione a livello di fuso mitotico e meiotico. Abbiamo dimostrato che la deplezione del PGRMC1 determina difetti nella divisione cellulare e la sua interazione con l'Aurora chinasi B (AURKB) indica che potrebbe svolgere la sua azione durante la citodieresi, l'ultima fase della divisione. Durante la maturazione meiotica, abbiamo valutato anche il suo ruolo nel mediare l'azione del progesterone (P4) confrontando il suo effetto con quello del recettore nucleare del progesterone (nPGR). L'inibizione di entrambi i tipi di recettore determina lo stesso effetto sull'organizzazione della piastra metafasica e sulla competenza allo sviluppo dell'ovocita, ma in fasi differenti. Inoltre, abbiamo testato l'ipotesi che il PGRMC1 possa modulare la funzione del nucleolo. Studi di immunofluorescenza hanno confermato la presenza del PGRMC1 nel nucleolo di cellule della granulosa (bGC) e negli ovociti di bovino, nonchè la colocalizzazione con la nucleolina, la proteina nucleolare più abbondante che svolge importanti funzioni in questo compartimento subcellulare. Inoltre, la down-regolazione del PGRMC1 determina uno spostamento della nucleolina dal nucleolo al nucleoplasma suggerendo un'associazione funzionale tra queste due proteine. Questa interazione è probabilmente mediata dalla presenza di ulteriori molecole in quanto successivi esperimenti di "in-situ proximity ligation" mostrano che le due… Advisors/Committee Members: tutor: V. Lodde, cotutor: A. M. Luciano, coordinatore: F. Gandolfi, LODDE, VALENTINA, GANDOLFI, FULVIO.

Subjects/Keywords: Progesterone Receptor Membrane Component 1; PGRMC1; fertility; reproduction; cell division; meiosis; mitosis; bovine granulosa cells; bovine oocyte; nucleolin; Canine Mammary tumors; progesterone; Settore VET/01 - Anatomia degli Animali Domestici; Settore VET/02 - Fisiologia Veterinaria; Settore BIO/06 - Anatomia Comparata e Citologia; Settore BIO/09 - Fisiologia; Settore BIO/11 - Biologia Molecolare; Settore BIO/17 - Istologia

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Terzaghi, L. (2018). ROLE OF PROGESTERONE RECEPTOR MEMBRANE COMPONENT 1 (PGRMC1) IN CONTROLLING GERMINAL AND SOMATIC CELL DIVISION AND FUNCTION. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/550339

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Terzaghi, L.. “ROLE OF PROGESTERONE RECEPTOR MEMBRANE COMPONENT 1 (PGRMC1) IN CONTROLLING GERMINAL AND SOMATIC CELL DIVISION AND FUNCTION.” 2018. Thesis, Università degli Studi di Milano. Accessed January 26, 2021. http://hdl.handle.net/2434/550339.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Terzaghi, L.. “ROLE OF PROGESTERONE RECEPTOR MEMBRANE COMPONENT 1 (PGRMC1) IN CONTROLLING GERMINAL AND SOMATIC CELL DIVISION AND FUNCTION.” 2018. Web. 26 Jan 2021.

Vancouver:

Terzaghi L. ROLE OF PROGESTERONE RECEPTOR MEMBRANE COMPONENT 1 (PGRMC1) IN CONTROLLING GERMINAL AND SOMATIC CELL DIVISION AND FUNCTION. [Internet] [Thesis]. Università degli Studi di Milano; 2018. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/2434/550339.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Terzaghi L. ROLE OF PROGESTERONE RECEPTOR MEMBRANE COMPONENT 1 (PGRMC1) IN CONTROLLING GERMINAL AND SOMATIC CELL DIVISION AND FUNCTION. [Thesis]. Università degli Studi di Milano; 2018. Available from: http://hdl.handle.net/2434/550339

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

2. Chung, Beryl. Nicotinic Signalling and Neurosteroid Modulation in Principal Neurons of the Hippocampal Formation and Prefrontal Cortex.

Degree: PhD, Department of Biomedical Sciences, 2018, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/12943

► Nicotinic signalling plays an important role in coordinating the response of neuronal networks in many brain regions. During pre- and postnatal circuit formation, neurotransmission mediated… (more)

▼ Nicotinic signalling plays an important role in coordinating the response of neuronal networks in many brain regions. During pre- and postnatal circuit formation, neurotransmission mediated by nicotinic acetylcholine receptors (nAChRs) influences neuronal survival and regulates neuronal excitability, synaptic transmission, and synaptic plasticity. Nicotinic signalling is also necessary for the proper function of the hippocampal formation (HF) and prefrontal cortex (PFC), which are anatomically and functionally connected and facilitate higher-order cognitive functions. The decline or dysfunction in nicotinic signalling and nAChR function has been observed in various neurological disorders, and the disruption or alteration of nicotinic signalling in the HF and/or PFC can impair learning and memory. While the location and functional role of the α4β2* nAChR isoform has been well characterized in the medial portion of the PFC, this is not well-established in the HF. What is the role of α4β2* nAChRs in excitatory principal neurons of the HF during early development? Growing evidence suggests that the progesterone metabolite allopregnanolone (ALLO) plays a role in mediating the proper function of the HF and the PFC, and that it may also inhibit nAChR function. How mightALLO influence α4β2* nAChR function during early development and/or affect neuronal excitation within a living system? This thesis aims to develop a foundation towards understanding the role of α4β2* nAChR-mediated neurotransmission in principal neurons of the HF during development, and the role of ALLO in modulating α4β2* nicotinic receptor function during this period. In this thesis, I demonstrate that functional ⍺4β2* nAChRs are present in principal neurons of the developing mouse HF. The function of these receptors is developmentally regulated, and nicotinic excitation differs between male and female mice. I also demonstrate that ALLO negatively modulates α4β2* nAChR function in living neurons. I show for the first time that crosstalk between the membrane progesterone receptor complex and the nAChR likely facilitates the actions of ALLO to modulate nAChR function. The findings in this thesis present new insights on ⍺4β2* nAChR expression and function, while adding to our understanding of how these receptors may influence neuronal excitability, synaptic transmission, and synaptic plasticity during early development. Advisors/Committee Members: Bailey, Craig (advisor).

Subjects/Keywords: acetylcholine; neurosteroid; hippocampal formation; prefrontal cortex; electrophysiology; allopregnanolone; membrane progesterone receptor; nicotinic receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chung, B. (2018). Nicotinic Signalling and Neurosteroid Modulation in Principal Neurons of the Hippocampal Formation and Prefrontal Cortex. (Doctoral Dissertation). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/12943

Chicago Manual of Style (16^th Edition):

Chung, Beryl. “Nicotinic Signalling and Neurosteroid Modulation in Principal Neurons of the Hippocampal Formation and Prefrontal Cortex.” 2018. Doctoral Dissertation, University of Guelph. Accessed January 26, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/12943.

MLA Handbook (7^th Edition):

Chung, Beryl. “Nicotinic Signalling and Neurosteroid Modulation in Principal Neurons of the Hippocampal Formation and Prefrontal Cortex.” 2018. Web. 26 Jan 2021.

Vancouver:

Chung B. Nicotinic Signalling and Neurosteroid Modulation in Principal Neurons of the Hippocampal Formation and Prefrontal Cortex. [Internet] [Doctoral dissertation]. University of Guelph; 2018. [cited 2021 Jan 26]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/12943.

Council of Science Editors:

Chung B. Nicotinic Signalling and Neurosteroid Modulation in Principal Neurons of the Hippocampal Formation and Prefrontal Cortex. [Doctoral Dissertation]. University of Guelph; 2018. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/12943

University of Southern California

3. Bali, Namrata. Progesterone receptors in the rat brain and their role in steroidal regulation of neurite outgrowth.

Degree: PhD, Molecular Biology, 2012, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/46403/rec/5268

► Estrogen (E2) and progesterone (P4) regulate synaptic plasticity in the adult rat hippocampus during the normal rat estrous cycle and in response to deafferenting lesions.… (more)

▼ Estrogen (E2) and progesterone (P4) regulate synaptic plasticity in the adult rat hippocampus during the normal rat estrous cycle and in response to deafferenting lesions. E2 increases neurite sprouting, whereas P4 antagonizes the E2-induced neurite outgrowth. Moreover, in the in vitro wounding-in-a-dish lesion model with glia-neuron co-cultures, E2 increases neurite outgrowth and P4 antagonizes the E2-induced neurite outgrowth. However, the P4-E2 antagonism of neurite outgrowth was only seen in the presence of microglia. The receptors involved in the P4 responses to neurite outgrowth are not well understood. Two progesterone mediators, Pgrmc1 and Pgr are studied in this thesis. ❧ Both Pgrmc1 and Pgr are expressed in the CA1, CA3 and DG hippocampal neurons, although their expression patterns differ between the neuronal subtypes. Both Pgrmc1 and Pgr are also regulated by E2 and P4 in the hippocampal neurons. Pgrmc1 mRNA is upregulated by both E2 and P4 in CA1, CA3 and DG neurons, while Pgr is hormonally regulated in CA1 neurons only. The differential expression and regulation of Pgrmc1 and Pgr in different hippocampal neurons could be due to possible different functions mediated by each in the different neurons. Pgrmc1 and Pgr are also expressed in glia. While both are expressed in astrocytes, only Pgrmc1 is expressed in microglia. ❧ Using a new microglia add-back protocol, microglia are shown to be required for P4-E2 antagonism of neurite outgrowth. However, physical contact between microglia and neurons is not required for the P4 antagonism, and soluble factors from activated microglia suffice to restore P4-E2 antagonism. Moreover, Pgrmc1 expression in microglia is required for the P4-E2 antagonism of neurite outgrowth. ❧ These findings together provide evidence of a P4 mediator in microglia with novel roles in P4 regulation of neurite outgrowth and in regulation of microglial activation. Understanding the mechanisms involved in P4-E2 regulation of synaptic plasticity is important in optimization of postmenopausal hormone therapy and in the therapeutic use of P4 for traumatic brain injury. Advisors/Committee Members: Finch, Caleb E. (Committee Chair), Tower, John G. (Committee Member), Schauwecker, P. Elyse (Committee Member).

Subjects/Keywords: microglia; Pgrmc1; progesterone; neurite outgrowth; progesterone receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bali, N. (2012). Progesterone receptors in the rat brain and their role in steroidal regulation of neurite outgrowth. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/46403/rec/5268

Chicago Manual of Style (16^th Edition):

Bali, Namrata. “Progesterone receptors in the rat brain and their role in steroidal regulation of neurite outgrowth.” 2012. Doctoral Dissertation, University of Southern California. Accessed January 26, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/46403/rec/5268.

MLA Handbook (7^th Edition):

Bali, Namrata. “Progesterone receptors in the rat brain and their role in steroidal regulation of neurite outgrowth.” 2012. Web. 26 Jan 2021.

Vancouver:

Bali N. Progesterone receptors in the rat brain and their role in steroidal regulation of neurite outgrowth. [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2021 Jan 26]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/46403/rec/5268.

Council of Science Editors:

Bali N. Progesterone receptors in the rat brain and their role in steroidal regulation of neurite outgrowth. [Doctoral Dissertation]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/46403/rec/5268

University of Melbourne

4. Bumbak, Fabian. Characterising the conformational diversity of the neurotensin receptor 1.

Degree: 2016, University of Melbourne

URL: http://hdl.handle.net/11343/124282

► G Protein-Coupled Receptors (GPCRs) deliver approximately 80% of all signals across the cell membrane and are targets for around 26% of all prescription drugs. Conversely,… (more)

▼ G Protein-Coupled Receptors (GPCRs) deliver approximately 80% of all signals across the cell membrane and are targets for around 26% of all prescription drugs. Conversely, over 85% of the GPCR family remain undrugged, often despite clear linkage to disease. Important reasons for this are that high-throughput screening has failed to deliver optimal drug leads and a lack of structural knowledge about how ligands engage GPCRs has hindered compound optimisation. The neurotensin receptor 1 (NTS1) is a GPCR for the tridecapeptide neurotensin (NT). Activation of NTS1 by NT has been implicated in schizophrenia, Parkinson’s disease and hypothermia, as well as cancer progression and drug abuse. Crystal structures of NTS1 bound to fragments of NT, as well as mutagenesis data, have defined intermediate states of NTS1 along with the high affinity binding site for NT. However, little is known about this receptor’s conformational dynamics and conformations that mediate particular signalling responses upon ligand interaction. Furthermore, transient interactions that may underlie NT binding remain uncharted. Like most integral membrane proteins, GPCRs are unstable in isolation, while recombinant expression yields remain poor. To overcome those hurdles, our laboratory used cellular high-throughput encapsulation, solubilisation and screening (CHESS)-based directed evolution to generate thermostable mutants of NTS1 suitable for biophysical studies. This thesis outlines expression of CHESS-derived NTS1 mutants to the E. coli inner membrane, their reconstitution in n-dodecyl β-D-maltopyranoside (DDM) micelles and their purification close to heterogeneity in the absence of stabilising ligands. Using small angle X-ray scattering (SAXS) we could show that our NTS1 mutant is monomeric when reconstituted in DDM micelles while a label free cell signalling assay indicated that it is signalling competent despite being thermostabilised. Dissociation constants (Kd’s) for a number of NT truncates as well as non-peptide ligands could be determined for one of our NTS1 mutants by means of surface plasmon resonance (SPR) spectroscopy. Saturation transfer difference NMR (STD NMR) was applied to detect low affinity peptide interactions to our engineered NTS1 mutants. The high stability of these receptors in detergent allowed us to repeatedly measure the binding of NT fragments over periods of up to 96 h at 25°C without significant loss of STD binding signal. Analysis of STD spectra enabled epitope mapping of the NT10-13/NTS1 interface. Molecular dynamics (MD) simulations of both NT8-13 and NT10-13 in complex with a homology model of our NTS1 mutant supported our solution NMR derived NT binding pose, which is not in complete agreement with available crystal structures. We show that the Y11 sidechain of NT10-13 is likely to populate two distinct conformations while the crystal structures only reveal one conformation. Furthermore, utilising a methionine biosynthesis pathway inhibition strategy we were able to achieve more than 95%…

Subjects/Keywords: membrane proteins; GPCR; peptide receptor; neurotensin receptor 1; ligand binding; conformational dynamics; NMR; MD

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bumbak, F. (2016). Characterising the conformational diversity of the neurotensin receptor 1. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/124282

Chicago Manual of Style (16^th Edition):

Bumbak, Fabian. “Characterising the conformational diversity of the neurotensin receptor 1.” 2016. Doctoral Dissertation, University of Melbourne. Accessed January 26, 2021. http://hdl.handle.net/11343/124282.

MLA Handbook (7^th Edition):

Bumbak, Fabian. “Characterising the conformational diversity of the neurotensin receptor 1.” 2016. Web. 26 Jan 2021.

Vancouver:

Bumbak F. Characterising the conformational diversity of the neurotensin receptor 1. [Internet] [Doctoral dissertation]. University of Melbourne; 2016. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/11343/124282.

Council of Science Editors:

Bumbak F. Characterising the conformational diversity of the neurotensin receptor 1. [Doctoral Dissertation]. University of Melbourne; 2016. Available from: http://hdl.handle.net/11343/124282

University of Cambridge

5. Solt, Andras Sandor. Investigating the molecular signatures of β1-adrenergic receptor activation.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/295594

► In this thesis I have investigated the molecular signatures of receptor activation, using the β1-adrenergic receptor (β1AR) as a prototypical class A G-protein coupled receptor… (more)

▼ In this thesis I have investigated the molecular signatures of receptor activation, using the β1-adrenergic receptor (β1AR) as a prototypical class A G-protein coupled receptor (GPCR). I have used a minimally thermostabilised turkey β1AR and expressed it functionally in insect cells using a baculovirus system. The work described here established the labelling, expression, purification and sample preparation of the receptor in LMNG detergent micelles for use in nuclear magnetic resonance (NMR) spectroscopy. GPCRs are highly dynamic molecular systems, and the use of solution NMR is highly suited to the study of fine structural changes that take place within the receptor as a consequence of receptor activation. To this end the receptor was selectively labelled with 13C at the methyl position of methionine residues. The labelling was carried out during insect cell expression, by supplementing methionine deficient media with the labelled amino acid. In this way the methionines throughout the receptor served as reporters. The radio frequency signals emitted by the nuclei of these labelled residues were monitored. NMR experiments were recorded on the receptor in the presence of ligands of various efficacies together with and without G-protein mimetic nanobodies, and changes in the signal were recorded. This allowed for a pattern of molecular signatures to be established, reporting on the effect ligands and G-protein mimetics have on the receptor. This identified two conformational equilibria, between an inactive and a ligand bound-pre-activated state and between a more and a less active ternary state when bound to a G-protein mimetic. Furthermore, it was also observed that ligand binding to the G-protein mimetic saturated basal active state elicits further changes on the receptor cytoplasmic side, demonstrating that ligand efficacy modulates the nature of receptor interaction with G-proteins, which may underpin partial agonism. It was also observed that ligand binding affects the dynamics and rigidity of the receptor, with a full agonist bound receptor exhibiting extensive µs to ms timescale dynamics, compared to a more rigid nanobody bound state. The increased dynamics suggest that full agonist binding primes the receptor for interaction with various downstream signalling partners. Once this coupling takes place, ligand efficacy determines the quality of interaction in this rigidified system. In addition to activation by ligands, certain proteins, such as antibodies can cause receptor agonism in the absence of a small molecule agonist. An example of this takes place in chronic Chagas’ heart disease, where anti-Trypanosoma cruzi antibodies inappropriately cross-react to β1AR, leading to chronic cardiac overstimulation and heart failure. In this thesis, the production of a published monoclonal antibody fragment was explored, in order to generate a tool for the study of this activation mechanism.

Subjects/Keywords: Beta-1 adrenergic receptor; GPCR; NMR; Membrane proteins; Adrenergic receptors

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Solt, A. S. (2019). Investigating the molecular signatures of β1-adrenergic receptor activation. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/295594

Chicago Manual of Style (16^th Edition):

Solt, Andras Sandor. “Investigating the molecular signatures of β1-adrenergic receptor activation.” 2019. Doctoral Dissertation, University of Cambridge. Accessed January 26, 2021. https://www.repository.cam.ac.uk/handle/1810/295594.

MLA Handbook (7^th Edition):

Solt, Andras Sandor. “Investigating the molecular signatures of β1-adrenergic receptor activation.” 2019. Web. 26 Jan 2021.

Vancouver:

Solt AS. Investigating the molecular signatures of β1-adrenergic receptor activation. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 26]. Available from: https://www.repository.cam.ac.uk/handle/1810/295594.

Council of Science Editors:

Solt AS. Investigating the molecular signatures of β1-adrenergic receptor activation. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/295594

University of Cambridge

6. Solt, Andras Sandor. Investigating the molecular signatures of β1-adrenergic receptor activation.

Degree: PhD, 2019, University of Cambridge

URL: https://doi.org/10.17863/CAM.42643 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782999

► In this thesis I have investigated the molecular signatures of receptor activation, using the β1-adrenergic receptor (β1AR) as a prototypical class A G-protein coupled receptor… (more)

▼ In this thesis I have investigated the molecular signatures of receptor activation, using the β1-adrenergic receptor (β1AR) as a prototypical class A G-protein coupled receptor (GPCR). I have used a minimally thermostabilised turkey β1AR and expressed it functionally in insect cells using a baculovirus system. The work described here established the labelling, expression, purification and sample preparation of the receptor in LMNG detergent micelles for use in nuclear magnetic resonance (NMR) spectroscopy. GPCRs are highly dynamic molecular systems, and the use of solution NMR is highly suited to the study of fine structural changes that take place within the receptor as a consequence of receptor activation. To this end the receptor was selectively labelled with 13C at the methyl position of methionine residues. The labelling was carried out during insect cell expression, by supplementing methionine deficient media with the labelled amino acid. In this way the methionines throughout the receptor served as reporters. The radio frequency signals emitted by the nuclei of these labelled residues were monitored. NMR experiments were recorded on the receptor in the presence of ligands of various efficacies together with and without G-protein mimetic nanobodies, and changes in the signal were recorded. This allowed for a pattern of molecular signatures to be established, reporting on the effect ligands and G-protein mimetics have on the receptor. This identified two conformational equilibria, between an inactive and a ligand bound-pre-activated state and between a more and a less active ternary state when bound to a G-protein mimetic. Furthermore, it was also observed that ligand binding to the G-protein mimetic saturated basal active state elicits further changes on the receptor cytoplasmic side, demonstrating that ligand efficacy modulates the nature of receptor interaction with G-proteins, which may underpin partial agonism. It was also observed that ligand binding affects the dynamics and rigidity of the receptor, with a full agonist bound receptor exhibiting extensive µs to ms timescale dynamics, compared to a more rigid nanobody bound state. The increased dynamics suggest that full agonist binding primes the receptor for interaction with various downstream signalling partners. Once this coupling takes place, ligand efficacy determines the quality of interaction in this rigidified system. In addition to activation by ligands, certain proteins, such as antibodies can cause receptor agonism in the absence of a small molecule agonist. An example of this takes place in chronic Chagas' heart disease, where anti-Trypanosoma cruzi antibodies inappropriately cross-react to β1AR, leading to chronic cardiac overstimulation and heart failure. In this thesis, the production of a published monoclonal antibody fragment was explored, in order to generate a tool for the study of this activation mechanism.

Subjects/Keywords: Beta-1 adrenergic receptor; GPCR; NMR; Membrane proteins; Adrenergic receptors

Record Details Similar Records Cite « Share

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Solt, A. S. (2019). Investigating the molecular signatures of β1-adrenergic receptor activation. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.42643 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782999

Chicago Manual of Style (16^th Edition):

Solt, Andras Sandor. “Investigating the molecular signatures of β1-adrenergic receptor activation.” 2019. Doctoral Dissertation, University of Cambridge. Accessed January 26, 2021. https://doi.org/10.17863/CAM.42643 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782999.

MLA Handbook (7^th Edition):

Solt, Andras Sandor. “Investigating the molecular signatures of β1-adrenergic receptor activation.” 2019. Web. 26 Jan 2021.

Vancouver:

Solt AS. Investigating the molecular signatures of β1-adrenergic receptor activation. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 26]. Available from: https://doi.org/10.17863/CAM.42643 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782999.

Council of Science Editors:

Solt AS. Investigating the molecular signatures of β1-adrenergic receptor activation. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://doi.org/10.17863/CAM.42643 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782999

7. M. Giunta. RUOLO PREDITTIVO DELL'ESPRESSIONE DEL RECETTORE SCAVENGER CD36 NELLA MALATTIA DI ALZHEIMER.

Degree: 2011, Università degli Studi di Milano

URL: http://hdl.handle.net/2434/150259

► Among pathologies of the old people, dementia represent one of the main sanitary problems. Approximately 70% of the dementia cases it is represented by the… (more)

▼ Among pathologies of the old people, dementia represent one of the main sanitary problems. Approximately 70% of the dementia cases it is represented by the Alzheimer’s Disease, a neurodegenerative cerebral pathology, whose prevalence is supposed to be increased in the next years. One pathological hallmark is represented by amyloid-beta (Aβ) plaques, which represent the key element to oxidative and pro-inflammatory mechanisms by the activated microglia. The interaction, in fact, between activated microglia and plaques of Aβ induces the release of pro-inflammatory citokynes, like interleukin-6 (IL-6), or neurotoxic factors, like the tumor necrosis factor-α, and stimulates the expression by the microglia of some scavengers receptors, deputies to remove the Aβ plaques: among them the multifunctional protein of class B type I (SRBI) CD36. Currently an effective diagnosis of AD is possible only post mortem: for this reason during the last few years has been intensified the search for biological and hormonal markers that could be useful in the early diagnosis of AD. These markers are expressed also from the peripheral leucocytes, cells easily obtainable, which express virtually all hormones and hormone receptors, which are under the same regulatory mechanisms that control their expression in the brain. So the leucocytes may be profitably used as tools to investigated the changes occurring in brain areas reportedly inaccessible in humans. In particular, it has been recently demonstrated that the leukocyte expression of CD36 is significantly reduced in patients with AD and in patients with mild cognitive impairment (MCI), a prodromic phase of AD. CD36 could represent an earlier marker of increased neurodegenerative risk. Epidemiologic studies have shown a greater incidence of AD in the individuals of female sex. A possible cause of this is represented by the modifications of the endocrine functions, that occur during the menopausal transition and that develop an unfavorable hormonal milieu predisposing to the neurodegeneration. It is demonstrated that estrogens have a neuroprotective and neurotrophic role by the binding to specific receptors, present in two isoformes (ER-α and ER-β), and that in course of AD they prevent the formation of the Aβ-fibrils, inhibit the inflammatory reaction due to the plaque deposition, and protect the cells from their cytotoxic action. The diminished estrogen secretion in postmenopausal age, in fact, is correlated inversely with the “cerebral health” and directly with the entity of the cognitive deterioration. An other female sexual hormone, the progesterone, seems to carry out multiple functions centers different from the riproduction function: the regulation of the cognitive processes, the mitochondrial function of the neuronal cell, the neurogenesis and the repair of the damaged nervous tissue. The neuronal response regulated from the progesterone are mediated by the receptors PR-A and PR-B, included some forms derived from alternative splicing. At the level of the central nervous system them… Advisors/Committee Members: tutor: Silvano Gabriele Cella, coordinatore: Alberto Panerai, CELLA, SILVANO GABRIELE, PANERAI, ALBERTO EMILIO.

Subjects/Keywords: Alzheimer's Disease; CD36; menopausal transition; estrogen receptors; progesterone receptor; IGF-1; IL-6; topi APP23; Settore BIO/14 - Farmacologia

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Giunta, M. (2011). RUOLO PREDITTIVO DELL'ESPRESSIONE DEL RECETTORE SCAVENGER CD36 NELLA MALATTIA DI ALZHEIMER. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/150259

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Giunta, M.. “RUOLO PREDITTIVO DELL'ESPRESSIONE DEL RECETTORE SCAVENGER CD36 NELLA MALATTIA DI ALZHEIMER.” 2011. Thesis, Università degli Studi di Milano. Accessed January 26, 2021. http://hdl.handle.net/2434/150259.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Giunta, M.. “RUOLO PREDITTIVO DELL'ESPRESSIONE DEL RECETTORE SCAVENGER CD36 NELLA MALATTIA DI ALZHEIMER.” 2011. Web. 26 Jan 2021.

Vancouver:

Giunta M. RUOLO PREDITTIVO DELL'ESPRESSIONE DEL RECETTORE SCAVENGER CD36 NELLA MALATTIA DI ALZHEIMER. [Internet] [Thesis]. Università degli Studi di Milano; 2011. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/2434/150259.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Giunta M. RUOLO PREDITTIVO DELL'ESPRESSIONE DEL RECETTORE SCAVENGER CD36 NELLA MALATTIA DI ALZHEIMER. [Thesis]. Università degli Studi di Milano; 2011. Available from: http://hdl.handle.net/2434/150259

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Houston

8. Mehta, Fabiola Melissa 1985-. Suppression of Cervical Cancer by the Progesterone Receptor Signaling.

Degree: PhD, Biology, 2016, University of Houston

URL: http://hdl.handle.net/10657/3271

► Cervical cancer is the fourth-most common cancer in woman and fourth leading cause of cancer death worldwide. The majority of cervical cancer is associated with… (more)

▼ Cervical cancer is the fourth-most common cancer in woman and fourth leading cause of cancer death worldwide. The majority of cervical cancer is associated with high-risk human papillomaviruses (HPVs). Their tumorigenic potential stems mainly from viral oncoproteins E6 and E7, which are best known to inactivate p53 and pRb tumor suppressor, respectively. Epidemiological evidence suggests that, in addition to persistent HPV infections, other cofactors are required for cervical cancer. Multiple pregnancies and oral contraceptive use increases the risk for cervical cancer in HPV-infected women, implicating a role of estrogen and progesterone in cervical cancer. Prior studies utilizing an HPV transgenic mouse model expressing E6 and E7 (K14E6/K14E7) have demonstrated the requirement of estrogen receptor alpha (ERα) and estradiol (E2) for cervical carcinogenesis. Accumulating evidence suggests that ERα may be important for human cervical cancer. The role of progesterone and progesterone receptor (PR) in cervical cancer remains elusive. Our laboratory has demonstrated that PR agonist medroxyprogesterone acetate (MPA) promotes regression of cervical cancer and cervical intraepithelial neoplasia (CIN) in the K14E6/K14E7 mice. Goals of my dissertation project were to determine whether cervical cancer recurs after MPA therapy and whether epithelial PR is required for therapeutic effect of MPA. Using the K14E6/K14E7 mice, I found that cervical cancer recurred even if MPA treatment was continued, and recurring cervical cancer expressed PR but was refractory to MPA. In addition to PR, MPA interacts with other nuclear receptors including glucocorticoid receptor. Using the Cre/LoxP recombination system, I found that epithelial PR promoted apoptosis and inhibited proliferation in the cervical epithelium. I also determined that epithelial PR was required for MPA-mediated regression of cervical cancer, which was inhibited by E2. My results strongly support the hypothesis that epithelial PR is ligand-dependent tumor suppressor in cervical cancer. Approximately 33% of cervical cancer expresses PR. My results suggest that PR expression may not be sufficient to benefit from MPA therapy. My results also warrants further study to determine mechanism of recurrence and therapy resistance, which will facilitate the development of a better therapy for the disease. Advisors/Committee Members: Chung, Sang-Hyuk (advisor), Bawa-Khalfe, Tasneem (committee member), Frigo, Daniel E. (committee member), Weigel, Nancy L. (committee member).

Subjects/Keywords: Progesterone receptor; Cervical cancer; Female reproductive tract

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mehta, F. M. 1. (2016). Suppression of Cervical Cancer by the Progesterone Receptor Signaling. (Doctoral Dissertation). University of Houston. Retrieved from http://hdl.handle.net/10657/3271

Chicago Manual of Style (16^th Edition):

Mehta, Fabiola Melissa 1985-. “Suppression of Cervical Cancer by the Progesterone Receptor Signaling.” 2016. Doctoral Dissertation, University of Houston. Accessed January 26, 2021. http://hdl.handle.net/10657/3271.

MLA Handbook (7^th Edition):

Mehta, Fabiola Melissa 1985-. “Suppression of Cervical Cancer by the Progesterone Receptor Signaling.” 2016. Web. 26 Jan 2021.

Vancouver:

Mehta FM1. Suppression of Cervical Cancer by the Progesterone Receptor Signaling. [Internet] [Doctoral dissertation]. University of Houston; 2016. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10657/3271.

Council of Science Editors:

Mehta FM1. Suppression of Cervical Cancer by the Progesterone Receptor Signaling. [Doctoral Dissertation]. University of Houston; 2016. Available from: http://hdl.handle.net/10657/3271

University of California – San Francisco

9. Yang, Cindy. Molecular and neural control of female sexual behavior.

Degree: Neuroscience, 2012, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/76b4f2k6

► In many animals, the display of female sexual receptivity relies on internal states such as the hormonal status of the animal. Female mice, for example,… (more)

Subjects/Keywords: Neurosciences; female behavior; genetics; hypothalamus; progesterone receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Yang, C. (2012). Molecular and neural control of female sexual behavior. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/76b4f2k6

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Yang, Cindy. “Molecular and neural control of female sexual behavior.” 2012. Thesis, University of California – San Francisco. Accessed January 26, 2021. http://www.escholarship.org/uc/item/76b4f2k6.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Yang, Cindy. “Molecular and neural control of female sexual behavior.” 2012. Web. 26 Jan 2021.

Vancouver:

Yang C. Molecular and neural control of female sexual behavior. [Internet] [Thesis]. University of California – San Francisco; 2012. [cited 2021 Jan 26]. Available from: http://www.escholarship.org/uc/item/76b4f2k6.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Yang C. Molecular and neural control of female sexual behavior. [Thesis]. University of California – San Francisco; 2012. Available from: http://www.escholarship.org/uc/item/76b4f2k6

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universitat de Barcelona

10. Gris Ormo, Georgia. Selective blockade of the sigma-1 receptor for the treatment of pain of different aetiology: Preclinical studies.

Degree: 2015, Universitat de Barcelona

URL: http://hdl.handle.net/10803/361398

► La presente Tesis Doctoral se centra en el estudio del receptor sigma-1 (σ1) en el campo del dolor. Esta investigación ha sido parte de un… (more)

Subjects/Keywords: Dolor; Pain; Proteïnes de membrana; Proteínas de membranas; Membrane proteins; Receptor Sigma-1; Sigma-1 receptor; Algesia; Algèsia; Medicina del dolor; Pain medicine; Ciències de la Salut; 615

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gris Ormo, G. (2015). Selective blockade of the sigma-1 receptor for the treatment of pain of different aetiology: Preclinical studies. (Thesis). Universitat de Barcelona. Retrieved from http://hdl.handle.net/10803/361398

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Gris Ormo, Georgia. “Selective blockade of the sigma-1 receptor for the treatment of pain of different aetiology: Preclinical studies.” 2015. Thesis, Universitat de Barcelona. Accessed January 26, 2021. http://hdl.handle.net/10803/361398.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Gris Ormo, Georgia. “Selective blockade of the sigma-1 receptor for the treatment of pain of different aetiology: Preclinical studies.” 2015. Web. 26 Jan 2021.

Vancouver:

Gris Ormo G. Selective blockade of the sigma-1 receptor for the treatment of pain of different aetiology: Preclinical studies. [Internet] [Thesis]. Universitat de Barcelona; 2015. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10803/361398.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Gris Ormo G. Selective blockade of the sigma-1 receptor for the treatment of pain of different aetiology: Preclinical studies. [Thesis]. Universitat de Barcelona; 2015. Available from: http://hdl.handle.net/10803/361398

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Virginia Commonwealth University

11. Solotskaya, Anna. NEUTROPHIL PRODUCTS CONTROL THE EXPRESSION OF PROGESTERONE RECEPTORS AND MATRIX METALLOPROTEINASE-1 IN THE DECIDUAL AND MYOMETRIUM AND ARE POSSIBLE REGULATORS OF PREMATURE LABOR.

Degree: MS, Physiology, 2010, Virginia Commonwealth University

URL: https://doi.org/10.25772/KT5M-5P11 ; https://scholarscompass.vcu.edu/etd/2112

► Neutrophils infiltrate myometrium and decidual tissue prior to parturition. Activated neutrophils release reactive oxygen species (ROS) and tumor necrosis factor α (TNFα), which might increase… (more)

Subjects/Keywords: Preterm Labor; MMP-1; Progesterone Receptor; Neutrophils; Myometrium; Decidua; Life Sciences; Physiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Solotskaya, A. (2010). NEUTROPHIL PRODUCTS CONTROL THE EXPRESSION OF PROGESTERONE RECEPTORS AND MATRIX METALLOPROTEINASE-1 IN THE DECIDUAL AND MYOMETRIUM AND ARE POSSIBLE REGULATORS OF PREMATURE LABOR. (Thesis). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/KT5M-5P11 ; https://scholarscompass.vcu.edu/etd/2112

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Solotskaya, Anna. “NEUTROPHIL PRODUCTS CONTROL THE EXPRESSION OF PROGESTERONE RECEPTORS AND MATRIX METALLOPROTEINASE-1 IN THE DECIDUAL AND MYOMETRIUM AND ARE POSSIBLE REGULATORS OF PREMATURE LABOR.” 2010. Thesis, Virginia Commonwealth University. Accessed January 26, 2021. https://doi.org/10.25772/KT5M-5P11 ; https://scholarscompass.vcu.edu/etd/2112.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Solotskaya, Anna. “NEUTROPHIL PRODUCTS CONTROL THE EXPRESSION OF PROGESTERONE RECEPTORS AND MATRIX METALLOPROTEINASE-1 IN THE DECIDUAL AND MYOMETRIUM AND ARE POSSIBLE REGULATORS OF PREMATURE LABOR.” 2010. Web. 26 Jan 2021.

Vancouver:

Solotskaya A. NEUTROPHIL PRODUCTS CONTROL THE EXPRESSION OF PROGESTERONE RECEPTORS AND MATRIX METALLOPROTEINASE-1 IN THE DECIDUAL AND MYOMETRIUM AND ARE POSSIBLE REGULATORS OF PREMATURE LABOR. [Internet] [Thesis]. Virginia Commonwealth University; 2010. [cited 2021 Jan 26]. Available from: https://doi.org/10.25772/KT5M-5P11 ; https://scholarscompass.vcu.edu/etd/2112.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Solotskaya A. NEUTROPHIL PRODUCTS CONTROL THE EXPRESSION OF PROGESTERONE RECEPTORS AND MATRIX METALLOPROTEINASE-1 IN THE DECIDUAL AND MYOMETRIUM AND ARE POSSIBLE REGULATORS OF PREMATURE LABOR. [Thesis]. Virginia Commonwealth University; 2010. Available from: https://doi.org/10.25772/KT5M-5P11 ; https://scholarscompass.vcu.edu/etd/2112

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universitat Politècnica de València

12. Rodríguez Solovey, Leisa Natacha. IDENTIFICATION OF TARGETS AND AUXILIARY PROTEINS OF PYR/PYL/RCAR ABA RECEPTORS: PROTEIN PHOSPHATASES TYPE 2C (PP2Cs) AND C2-DOMAIN ABA-RELATED PROTEINS (CARs).

Degree: 2015, Universitat Politècnica de València

URL: http://hdl.handle.net/10251/58862

► [EN] ABSTRACT Abscisic acid (ABA) signaling plays a critical role in regulating root growth and root system architecture. ABA-mediated growth promotion and root tropic response… (more)

▼ [EN] ABSTRACT Abscisic acid (ABA) signaling plays a critical role in regulating root growth and root system architecture. ABA-mediated growth promotion and root tropic response under water stress are key responses for plant survival under limiting water conditions. In this work, we have explored the role of Arabidopsis (Arabidopsis thaliana) PYR/PYL/RCAR receptors (PYRABACTIN RESISTANCE1 (PYR1)/PYR1 LIKE (PYL)/REGULATORY COMPONENTS OF ABA RECEPTORS) for root ABA signaling. As a result, we discovered that PYL8 plays a nonredundant role for the regulation of root ABA sensitivity. Unexpectedly, given the multigenic nature and partial functional redundancy observed in the PYR/PYL family, the single pyl8 mutant showed reduced sensitivity to ABA-mediated root growth inhibition. This effect was due to the lack of PYL8-mediated inhibition of several clade A phosphatases type 2C (PP2Cs), since PYL8 interacted in vivo with at least five PP2Cs, namely HYPERSENSITIVE TO ABA1 (HAB1), HAB2, ABAINSENSITIVE1 (ABI1), ABI2, and PP2CA/ABA-HYPERSENSITIVE GERMINATION3 as revealed by tandem affinity purification and mass spectrometry proteomic approaches. Membrane-delimited abscisic acid (ABA) signal transduction plays a critical role in early ABA signaling, but the molecular mechanisms linking core signaling components to the plasma membrane are unclear. We show that transient calciumdependent interactions of PYR/PYL/RCAR ABA receptors with membranes are mediated through a 10-member family of C2-domain ABA-related (CAR) proteins in Arabidopsis thaliana. Specifically, we found that PYL4 interacted in an ABA-independent manner with CAR1 in both the plasma membrane and nucleus of plant cells. CAR1 belongs to a plant-specific gene family encoding CAR1 to CAR10 proteins, and bimolecular fluorescence complementation and coimmunoprecipitation assays showed that PYL4-CAR1 as well as other PYR/PYL-CAR pairs interacted in plant cells. The crystal structure of CAR4 was solved, which revealed that, in addition to a classical calcium-dependent lipid binding C2 domain, a specific CAR signature is likely responsible for the interaction with PYR/PYL/RCAR receptors and their recruitment to phospholipid vesicles. This interaction is relevant for PYR/PYL/RCAR function and ABA signaling, since different car triple mutants affected in CAR1, CAR4, CAR5, and CAR9 genes showed reduced sensitivity to ABA in seedling establishment and root growth assays. In summary, we identified PYR/PYL/RCAR-interacting partners that mediate a transient Ca2+-dependent interaction with phospholipid vesicles, which affects PYR/PYL/RCAR subcellular localization and positively regulates ABA signaling.; [ES] RESUMEN La señalización por la hormona vegetal ácido abscísico (ABA) desempeña un papel crítico en la regulación del crecimiento de la raíz y en la arquitectura del sistema radical. La promoción de crecimiento de la raíz en condiciones de estrés hídrico mediada por ABA es clave para la supervivencia de las plantas bajo condiciones limitantes de agua. En este trabajo, hemos… Advisors/Committee Members: González Guzmán, Miguel (advisor), Rodríguez Egea, Pedro Luís (advisor).

Subjects/Keywords: Abscisic acid (ABA); Arabidopsis thaliana, Abiotic Stress; PYRABACTIN RESISTANCE/PYRABACTIN RESISTANCE 1-LIKE/REGULATORY COMPONENT OF ABA RECEPTOR (PYR/PYL/RCAR) ABA receptors; C2-DOMAIN ABA-RELATED PROTEINS (CARs); CLADE A PROTEIN PHOSPHATASE 2C (PP2C); SUCROSE NON-FERMENTING-1 (SNF1)-RELATED PROTEIN KINASE 2 (SNRK2); Protein Binding Targets; Ca2+-Dependent Lipid-Binding Domain; Subcellular Localization; Plasma-membrane binding; Signal transduction; Root ABA Response; Yeast Two-Hybrid; Tandem Affinity Purification (TAP); Crystal Structure; Bimolecular Fluorescence Complementation (BiFC).

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rodríguez Solovey, L. N. (2015). IDENTIFICATION OF TARGETS AND AUXILIARY PROTEINS OF PYR/PYL/RCAR ABA RECEPTORS: PROTEIN PHOSPHATASES TYPE 2C (PP2Cs) AND C2-DOMAIN ABA-RELATED PROTEINS (CARs). (Doctoral Dissertation). Universitat Politècnica de València. Retrieved from http://hdl.handle.net/10251/58862

Chicago Manual of Style (16^th Edition):

Rodríguez Solovey, Leisa Natacha. “IDENTIFICATION OF TARGETS AND AUXILIARY PROTEINS OF PYR/PYL/RCAR ABA RECEPTORS: PROTEIN PHOSPHATASES TYPE 2C (PP2Cs) AND C2-DOMAIN ABA-RELATED PROTEINS (CARs). ” 2015. Doctoral Dissertation, Universitat Politècnica de València. Accessed January 26, 2021. http://hdl.handle.net/10251/58862.

MLA Handbook (7^th Edition):

Rodríguez Solovey, Leisa Natacha. “IDENTIFICATION OF TARGETS AND AUXILIARY PROTEINS OF PYR/PYL/RCAR ABA RECEPTORS: PROTEIN PHOSPHATASES TYPE 2C (PP2Cs) AND C2-DOMAIN ABA-RELATED PROTEINS (CARs). ” 2015. Web. 26 Jan 2021.

Vancouver:

Rodríguez Solovey LN. IDENTIFICATION OF TARGETS AND AUXILIARY PROTEINS OF PYR/PYL/RCAR ABA RECEPTORS: PROTEIN PHOSPHATASES TYPE 2C (PP2Cs) AND C2-DOMAIN ABA-RELATED PROTEINS (CARs). [Internet] [Doctoral dissertation]. Universitat Politècnica de València; 2015. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10251/58862.

Council of Science Editors:

Rodríguez Solovey LN. IDENTIFICATION OF TARGETS AND AUXILIARY PROTEINS OF PYR/PYL/RCAR ABA RECEPTORS: PROTEIN PHOSPHATASES TYPE 2C (PP2Cs) AND C2-DOMAIN ABA-RELATED PROTEINS (CARs). [Doctoral Dissertation]. Universitat Politècnica de València; 2015. Available from: http://hdl.handle.net/10251/58862

13. Gu, Hongbo. Mass Spectrometry Analysis of Potential Biomarker Proteins.

Degree: PhD, Chemistry, 2012, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:297583/

► Towards the full understanding the physiology of human Sigma-1 receptor (Sig-1R), we developed a novel ligand-based enrichment strategy and mass spectrometry analysis of the receptor.… (more)

▼ Towards the full understanding the physiology of human Sigma-1 receptor (Sig-1R), we developed a novel ligand-based enrichment strategy and mass spectrometry analysis of the receptor. Reduced Haloperidol (RHAL) bead was generated by coupling ligand to the silica bead bearing epoxide groups and applied to pull down the endogenous Sig-1R and its interacting partners from human cancer cell. Our results showed that RHAL bead specifically and quantitatively pulled down the receptor and the peptides obtained by in-gel digestion of the eluted protein using covered over 90% of the primary sequence of the receptor. Besides, oxidation of tryptophan at W81, 89 and 136 with different oxidation stages and two methylation sites at the residues of Q80 and E163. By quantitative comparison using spectral counting and statistical analysis, novel interacting partners of Sig-1R were identified including 80S ribosome, Calnexin, and 26S proteasome. These interactions revealed the involvement of Sig-1R in the regulation of nascent polypeptide load in ER, protein folding as well as ER-associated degradation, which provided possible explanation for the protective role of Sig-1R for cells against ER-stress induced apoptosis. To identify a universal biomarker to indicate immune-response, a unique immunoglobulin G (IgG) species was identified in mouse and rabbit sera immediately after immunogen exposure which was characterized based on its lectin AAL binding property, early production, early detectable and unique kinetics. Serum samples from animals inoculated with various immunogens were used in a lectin antibody microarray using F(ab’)2 anti-IgG as a capture reagent, and a recombinant biotinylated AAL as a detection reagent. Using this immunogen unrelated assay, we identified an IgG species distinct from the majority of circulating core-fucosylated intact IgG molecules. Mass spectrometry analysis of IgGs from serial samples of immunized rabbit revealed a similar kinetics from IgG N-glycosylation subtypes possessing core-fucosylated agalatosyl, bisecting agalactosyl or sialyl-mono-galactosyl structures, suggesting the AAL reactivity are from one or all these glycosylation subtypes. This unique IgG species appears to be a common marker for immune response to various antigens in different animal species. Advisors/Committee Members: Bazemore-Walker, Carthene (Director), Bowen, Wayne (Reader), Basu, Amit (Reader).

Subjects/Keywords: Sigma-1 receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gu, H. (2012). Mass Spectrometry Analysis of Potential Biomarker Proteins. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:297583/

Chicago Manual of Style (16^th Edition):

Gu, Hongbo. “Mass Spectrometry Analysis of Potential Biomarker Proteins.” 2012. Doctoral Dissertation, Brown University. Accessed January 26, 2021. https://repository.library.brown.edu/studio/item/bdr:297583/.

MLA Handbook (7^th Edition):

Gu, Hongbo. “Mass Spectrometry Analysis of Potential Biomarker Proteins.” 2012. Web. 26 Jan 2021.

Vancouver:

Gu H. Mass Spectrometry Analysis of Potential Biomarker Proteins. [Internet] [Doctoral dissertation]. Brown University; 2012. [cited 2021 Jan 26]. Available from: https://repository.library.brown.edu/studio/item/bdr:297583/.

Council of Science Editors:

Gu H. Mass Spectrometry Analysis of Potential Biomarker Proteins. [Doctoral Dissertation]. Brown University; 2012. Available from: https://repository.library.brown.edu/studio/item/bdr:297583/

Univerzitet u Beogradu

14. Robajac, Dragana B., 1985-. N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima.

Degree: Hemijski fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get

►

Biohemija - Biohemija proteina / Biochemistry - Biochemistry of proteins

Funkcije membranskih proteina su brojne: međućelijska komunikacija, adhezija, signalna transdukcija. Većina membranskih proteina je glikozilovana… (more)

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Biohemija - Biohemija proteina / Biochemistry - Biochemistry of proteins

Funkcije membranskih proteina su brojne: međućelijska komunikacija, adhezija, signalna transdukcija. Većina membranskih proteina je glikozilovana i N-glikani imaju važnu ulogu u formiranju trodimenzionalne strukture membranskih proteina, kao i u ispoljavanju njihove funkcije. Receptori za insulin (IR) i faktor rasta sličan insulinu tip 1 (IGF1R) su transmembranske tirozin-kinaze sa visokim stepenom homologije (u nekim domenima čak i 80%). Familija IGF receptora, pored IR i IGF1R, uključuje i receptor za faktore rasta slične insulinu tip 2 (IGF2R). Sva tri receptora (IR, IGF1R i IGF2R) su glikozilovani i obilno prisutni u placenti, gde imaju važne uloge u njenom razvoju i funkcionisanju. Placenta raste i razvija se da bi ispunila različite potrebe fetusa, pa se struktura i funkcija placente menjaju tokom gestacije. Znajući da su proteini odgovorni za biološke funkcije placente pretpostavljeno je da tokom gestacije može doći i do promene u sadržaju različitih tipova N-glikana prisutnih na membranskim proteinima. U ovoj tezi analizirani su tipovi N-glikana koji se mogu naći u sastavu membranskih glikoproteina, odnosno membranski N-glikom proteina humane placente. Ispitana je podložnost membranskog N-glikoma individualnim varijacijama i uticaju starosti majke/trudnice, kao i uticaj gestacije na membranski N-glikom. Znajući da je izmenjena glikozilacija često povezana sa izmenjenom funkcijom, kao i da izmenjena funkcija jednog ili više proteina može biti uzrok bolesti, ispitane su potencijalne promene membranskog N-glikoma u patološkim trudnoćama (kod preeklampsije) i trudnoćama komplikovanim patologijom majki (dijabetes). Uporedo je ispitan i uticaj starosti, gestacije i patologije na tip i zastupljenost različitih N-glikana koji ulaze u sastav receptora IGF sistema. Cilj je bio da se ispita da li promene na ukupnim membranskim proteinima (na N-glikomu) prate promene N-glikana prisutnih na pojedinačnim membranskim glikoproteinima važnim za rast i funkcionisanje placente...

Advisors/Committee Members: Mandić, Ljuba, 1953-.

Subjects/Keywords: membrane proteins; N-glycans; N-glycome; insulin receptor; insulin-like growth factor receptors type 1 and 2; gestational changes; aging; placenta

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Robajac, Dragana B., 1. (2016). N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Robajac, Dragana B., 1985-. “N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima.” 2016. Thesis, Univerzitet u Beogradu. Accessed January 26, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Robajac, Dragana B., 1985-. “N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima.” 2016. Web. 26 Jan 2021.

Vancouver:

Robajac, Dragana B. 1. N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Jan 26]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Robajac, Dragana B. 1. N-glikom membranskih proteina i receptora za insulin i faktore rasta slične insulinu, izolovanih iz humane placente u različitim (pato)fiziološkim stanjima. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:12455/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Illinois – Urbana-Champaign

15. Kaya, Hatice. Identification of molecular signaling pathways underlying human endometrial stromal cell differentiation.

Degree: PhD, 0325, 2014, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/46949

► Decidualization, the differentiation of endometrial stromal cells, is essential for a successful pregnancy. Although the steroid hormones estrogen (E) and progesterone (P) are known to… (more)

▼ Decidualization, the differentiation of endometrial stromal cells, is essential for a successful pregnancy. Although the steroid hormones estrogen (E) and progesterone (P) are known to control decidualization, the precise mechanisms via which these hormones act to control this differentiation process are poorly understood. We used primary cultures of human endometrial stromal cells (HESC) to analyze the role of estrogen receptor alpha (ESR1) and progesterone receptor isoforms (PRA and PRB) in human decidualization. Previous studies established that HESC, when treated with the differentiation cocktail containing E, P, and a cyclic adenosine monophosphate (cAMP) analog, cease proliferation and undergo differentiation. In the present study, when ESR1 expression was silenced, the HESC continued to proliferate in the presence of the differentiation cocktail and their differentiation was severely inhibited. Gene expression profiling revealed that, in the absence of ESR1, the expression levels of several cell cycle regulatory factors were increased and those of specific cell cycle inhibitors were decreased. Our study also revealed that ESR1 promoted the expression of key regulators of HESC differentiation (PGR, FOXO1 and WNT4). Expression of these targets was dependent on the addition of cAMP, suggested a functional link between cAMP and ESR1 signaling. Using a proteomic approach, we identified MED1 as a target of cAMP-activated protein kinase (PKA) during HESC differentiation. The PKA-dependent phosphorylation of MED1 enhanced its ability to interact efficiently with ESR1. Furthermore, loss of MED1 expression inhibited HESC differentiation with parallel impairment in the expression of a subset of ESR1 target genes. Addition of cAMP increased recruitment of MED1 to the ESR1 binding regions of a target gene (WNT4). Collectively, these results indicated that, during decidualization, ESR1 suppresses HESC proliferation and promotes their differentiation via interactions with MED1, which is activated in response to cAMP signaling. Progesterone, acting through its receptors, is essential for the precise regulation of the endometrial processes required for a successful pregnancy, including decidualization. However, the specific roles of the progesterone receptor isoforms, PRA and PRB, during endometrial differentiation in the human have remained unknown. A major focus of my project was to shed light on the roles of the receptor isoforms by identifying their cistromes and correlated gene expression profiles during differentiation of human stromal cells. We expressed PRA and PRB individually after silencing endogenous progesterone receptors so that the roles of the isoforms could be analyzed independently as well as jointly. Identification of the cistromes of PRA and PRB using chromatin immunoprecipitation (ChIP) followed by high throughput sequencing (ChIP-seq), revealed that PRB cistrome was larger, covering that of PRA, at an early time point of in vitro differentiation of human endometrial stromal cells. Our de novo motif… Advisors/Committee Members: Bagchi, Milan K. (advisor), Bagchi, Milan K. (Committee Chair), Bagchi, Indrani C. (committee member), Katzenellenbogen, Benita S. (committee member), Kemper, Jongsook K. (committee member), Raetzman, Lori T. (committee member).

Subjects/Keywords: Human endometrial stromal cell differentiation; estrogen receptor alpha; progesterone receptor isoforms

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kaya, H. (2014). Identification of molecular signaling pathways underlying human endometrial stromal cell differentiation. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/46949

Chicago Manual of Style (16^th Edition):

Kaya, Hatice. “Identification of molecular signaling pathways underlying human endometrial stromal cell differentiation.” 2014. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed January 26, 2021. http://hdl.handle.net/2142/46949.

MLA Handbook (7^th Edition):

Kaya, Hatice. “Identification of molecular signaling pathways underlying human endometrial stromal cell differentiation.” 2014. Web. 26 Jan 2021.

Vancouver:

Kaya H. Identification of molecular signaling pathways underlying human endometrial stromal cell differentiation. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2014. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/2142/46949.

Council of Science Editors:

Kaya H. Identification of molecular signaling pathways underlying human endometrial stromal cell differentiation. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2014. Available from: http://hdl.handle.net/2142/46949

Univerzitet u Beogradu

16. Božović, Ana M., 1977-. Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke.

Degree: Biološki fakultet, 2014, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get

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Biologija - Molekularna genetika kancera / Biology - Molecular genetics of cancer

Invazivni karcinom dojke je najčešći kancer kod žena. Pored genetičkih i epigenetički faktori… (more)

Subjects/Keywords: Breast cancer; estrogen receptor alpha; estrogen receptor beta; progesterone receptor; methylation; quantitative PCR

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Božović, Ana M., 1. (2014). Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Božović, Ana M., 1977-. “Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke.” 2014. Thesis, Univerzitet u Beogradu. Accessed January 26, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Božović, Ana M., 1977-. “Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke.” 2014. Web. 26 Jan 2021.

Vancouver:

Božović, Ana M. 1. Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke. [Internet] [Thesis]. Univerzitet u Beogradu; 2014. [cited 2021 Jan 26]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Božović, Ana M. 1. Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke. [Thesis]. Univerzitet u Beogradu; 2014. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Université Paris-Sud – Paris XI

17. Khan, Junaid Ali. Progesterone Receptor Isoforms : functional Selectivity and Pharmacological Targeting : Isoformes du récepteur de la progestérone : sélectivité fonctionnelle et ciblage pharmacologique.

Degree: Docteur es, Endocrinologie moléculaire et cellulaire, 2011, Université Paris-Sud – Paris XI

URL: http://www.theses.fr/2011PA11T055

► Le récepteur de la progestérone (PR) est un cible pharmacologique majeure pour la contraception, et pour le traitement de certaines pertubations endocriniennes ainsi que des… (more)

▼ Le récepteur de la progestérone (PR) est un cible pharmacologique majeure pour la contraception, et pour le traitement de certaines pertubations endocriniennes ainsi que des cancers hormono-dépendants de l’utérus et du sein. Chez la femme, PR est exprimé sous deux isoformes majeures PRA et PRB qui sont des facteurs de transcription fonctionnellement distincts. L’expression de PRA vs PRB est souvent altérée dans certaines situations pathologiques selon des mécanismes encore mal identifiés. Dans cette thèse, nous démontrons que des phosphorylations clés regulées par des MAPK distincts contrôlent la stabilité de PRB et PRA. PRA est sélectivement stabilisée par la p38 MAPK tandis que PRB est préférentiellement stabilisé par la p42/44 MAPK. Ces mécanismes différentiels régulent donc le rapport d’expression PRA/PRB de façon ligand-dépendente et mettent les fonctions progestatives sous le contrôle de l’activité des facteurs de croissance et des cytokines pro-inflammatoires. Or, dans les cellules cancéreuses, la suractivité de certains stimuli extracellulaires provenant de telles signalisations et activant préférentiellement p42/44 et/ou p38 MAPK, pourrait être à l’origine des pertubations du rapport PRA/PRB observées dans les tumeurs du sein. Afin d’explorer la contribution différentielle des isoformes du PR dans la signalisation cellulaire, nous avons élaboré un modèle cellulaire original permettant de contrôler l’expression de PRA et/ou PRB de façon conditionnelle, réversible et dose-dépendante. Par une approche transcriptomique, nous avons identifiés les gènes régulés de façon différentielle par PRA et/ou PRB en absence ou présence de l’hormone. Nous montrons que plusieurs aspects de la signalisation de PR comme la sélectivité de la régulation transcriptionnelle, la dialogue-croisée avec des facteurs de croissance ainsi que l’efficacité antiproliférative des antiprogestatifs dépendent de l’expression differentielle des isoformes du PR. Une nouvelle approche thérapeutique ou préventive possible dans les cancers hormono-dépendants pourrait consister à administrer des antagonistes du PR. Cependant, la plupart des antiprogestatifs disponibles comme la mifépristone présentent des effets agonistes partiels et ne sont pas sélectifs du PR, produisant ainsi des effets indésirables majeurs. Dans un projet collaboratif, et sur la base d’études cristallographiques de PR, nous avons synthétisé et caractérisé plusieurs dizaines de molécules antagonistes du PR, nommés APRn. L’étude des relations structure-fonctions de ces APRn a permis d’identifier les substitutions introduites dans la structure stéroïdienne qui sont responsables des propriétés agonistes/antagonistes de ces molécules. Plusieurs APRn sélectionnés sont dépourvus d’effets agonistes partiels, sont spécifiques du PR et inhibent son activité transcriptionnelle par un nouveau mécanisme d’action dit « passif », en raison de leur capacité particulière à inhiber le recrutement des corégulateurs transcriptionnels. Ces antagonistes sélectifs de PR offrent des perspectives… Advisors/Committee Members: Loosfelt, Hugues (thesis director).

Subjects/Keywords: Progesterone; Isoformes du récepteur de la progestérone; Rapport PRA/PRB; Antiprogestatifs; Transcription; Progesterone; Progesterone receptor isoforms; PRA/PRB ratio; Antiprogestins; Transcription

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Khan, J. A. (2011). Progesterone Receptor Isoforms : functional Selectivity and Pharmacological Targeting : Isoformes du récepteur de la progestérone : sélectivité fonctionnelle et ciblage pharmacologique. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2011PA11T055

Chicago Manual of Style (16^th Edition):

Khan, Junaid Ali. “Progesterone Receptor Isoforms : functional Selectivity and Pharmacological Targeting : Isoformes du récepteur de la progestérone : sélectivité fonctionnelle et ciblage pharmacologique.” 2011. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed January 26, 2021. http://www.theses.fr/2011PA11T055.

MLA Handbook (7^th Edition):

Khan, Junaid Ali. “Progesterone Receptor Isoforms : functional Selectivity and Pharmacological Targeting : Isoformes du récepteur de la progestérone : sélectivité fonctionnelle et ciblage pharmacologique.” 2011. Web. 26 Jan 2021.

Vancouver:

Khan JA. Progesterone Receptor Isoforms : functional Selectivity and Pharmacological Targeting : Isoformes du récepteur de la progestérone : sélectivité fonctionnelle et ciblage pharmacologique. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2011. [cited 2021 Jan 26]. Available from: http://www.theses.fr/2011PA11T055.

Council of Science Editors:

Khan JA. Progesterone Receptor Isoforms : functional Selectivity and Pharmacological Targeting : Isoformes du récepteur de la progestérone : sélectivité fonctionnelle et ciblage pharmacologique. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2011. Available from: http://www.theses.fr/2011PA11T055

18. Iasmim Ribeiro da Costa. ANÁLISE DO POLIMORFISMO DO GENE RECEPTOR DE PROGESTERONA (PROGINS) EM MULHERES COM ENDOMETRIOSE.

Degree: 2010, Universidade Católica de Goiás

URL: http://tede.biblioteca.ucg.br/tde_busca/arquivo.php?codArquivo=789

► A endometriose é definida como aparecimento de focos de tecido endometrial com características glandulares e/ou estromais idênticos aos da cavidade uterina em outras localizações, que… (more)

▼ A endometriose é definida como aparecimento de focos de tecido endometrial com características glandulares e/ou estromais idênticos aos da cavidade uterina em outras localizações, que não o endométrio, apresentando um forte componente genético. Incide principalmente em mulheres em idade reprodutiva, podendo estar relacionada com infertilidade em 30% a 40% dos casos. É uma patologia de diagnóstico histológico, devendo o mesmo, confirmar as suspeitas clínicas e os achados macroscópicos encontrados em cirurgias. Pode afetar vários órgãos, sendo por isso mesmo denominada atualmente de multi-sistêmica. A expressão exagerada de receptores de estrogênio e defeitos no receptor de progesterona são consequências da anormalidade do efeito progestacional sobre o endométrio tópico e ectópico. Alterações da sua função podem, portanto, facilitar o aparecimento da moléstia porque, no sentido amplo, deixa de antagonizar os efeitos proliferativos dos estrogênios. Recentemente, vários polimorfismos do receptor de progesterona têm sido descritos. Dentre eles destaca-se o polimorfismo PROGINS que consiste em uma inserção Alu de 306 pb no íntron G entre o exon 7 e 8 do gene do receptor de progesterona humano. Este estudo tem como objetivo verificar a possível correlação entre a endometriose e o Polimorfismo do Gene do Receptor de Progesterona (PROGINS). O grupo endometriose foi composto por 54 pacientes de um centro de referência em videolaparoscopia e infertilidade de Goiânia (FÉRTILE). O grupo controle incluiu 45 mulheres sem diagnóstico de endometriose por anamnese. Os genótipos para o polimorfismo PROGINS (A1/A1, A1/A2 e A2/A2) foram determinados por PCR. A frequência dos genótipos polimórficos (A1/A2 e A2/A2) é duas vezes maior nas pacientes com endometriose (33,3%) do que no grupo controle (15,5%). Houve significância estatística que indicasse a associação entre o polimorfismo PROGINS e a patologia endometriose (P = 0,0426). Advisors/Committee Members: Waldemar Naves do Amaral, Katia Karina Verolli de Oliveira Moura, Flávia Melo Rodrigues.

Subjects/Keywords: PCR; PROGINS; PCR; receptor de progesterona; PROGINS; endometriose; GENETICA; progesterone receptor; endometriosis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Costa, I. R. d. (2010). ANÁLISE DO POLIMORFISMO DO GENE RECEPTOR DE PROGESTERONA (PROGINS) EM MULHERES COM ENDOMETRIOSE. (Thesis). Universidade Católica de Goiás. Retrieved from http://tede.biblioteca.ucg.br/tde_busca/arquivo.php?codArquivo=789

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Costa, Iasmim Ribeiro da. “ANÁLISE DO POLIMORFISMO DO GENE RECEPTOR DE PROGESTERONA (PROGINS) EM MULHERES COM ENDOMETRIOSE.” 2010. Thesis, Universidade Católica de Goiás. Accessed January 26, 2021. http://tede.biblioteca.ucg.br/tde_busca/arquivo.php?codArquivo=789.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Costa, Iasmim Ribeiro da. “ANÁLISE DO POLIMORFISMO DO GENE RECEPTOR DE PROGESTERONA (PROGINS) EM MULHERES COM ENDOMETRIOSE.” 2010. Web. 26 Jan 2021.

Vancouver:

Costa IRd. ANÁLISE DO POLIMORFISMO DO GENE RECEPTOR DE PROGESTERONA (PROGINS) EM MULHERES COM ENDOMETRIOSE. [Internet] [Thesis]. Universidade Católica de Goiás; 2010. [cited 2021 Jan 26]. Available from: http://tede.biblioteca.ucg.br/tde_busca/arquivo.php?codArquivo=789.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Costa IRd. ANÁLISE DO POLIMORFISMO DO GENE RECEPTOR DE PROGESTERONA (PROGINS) EM MULHERES COM ENDOMETRIOSE. [Thesis]. Universidade Católica de Goiás; 2010. Available from: http://tede.biblioteca.ucg.br/tde_busca/arquivo.php?codArquivo=789

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universitat Pompeu Fabra

19. Wierer, Michael, 1982-. Role of PLK1 in steroid hormone signaling in breast cancer cells.

Degree: Departament de Ciències Experimentals i de la Salut, 2013, Universitat Pompeu Fabra

URL: http://hdl.handle.net/10803/283474

► Steroid receptors (SRs) are hormone-induced transcription factors that regulate gene expression by their concerted actions with coregulatory proteins. Performing a quantitative mass spectrometry-based interaction screen… (more)

Subjects/Keywords: PLK1; Estrogen Receptor; Progesterone Receptor; Breast cancer; Phosphorylation; Gene transcription; MLL2; Phosphoproteomics; Interactomics; SILAC; 616

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wierer, Michael, 1. (2013). Role of PLK1 in steroid hormone signaling in breast cancer cells. (Thesis). Universitat Pompeu Fabra. Retrieved from http://hdl.handle.net/10803/283474

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wierer, Michael, 1982-. “Role of PLK1 in steroid hormone signaling in breast cancer cells.” 2013. Thesis, Universitat Pompeu Fabra. Accessed January 26, 2021. http://hdl.handle.net/10803/283474.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wierer, Michael, 1982-. “Role of PLK1 in steroid hormone signaling in breast cancer cells.” 2013. Web. 26 Jan 2021.

Vancouver:

Wierer, Michael 1. Role of PLK1 in steroid hormone signaling in breast cancer cells. [Internet] [Thesis]. Universitat Pompeu Fabra; 2013. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10803/283474.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wierer, Michael 1. Role of PLK1 in steroid hormone signaling in breast cancer cells. [Thesis]. Universitat Pompeu Fabra; 2013. Available from: http://hdl.handle.net/10803/283474

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Bridgeport

20. Callis, Chanté Maria. Are Natural Therapies Effective in the Prevention/Treatment of ER+/PR+ Breast Cancer? .

Degree: 2013, University of Bridgeport

URL: https://scholarworks.bridgeport.edu/xmlui/handle/123456789/1390

► Breast cancer is now the second leading cause of cancer death in women. Researchers continue to study the etiology of breast cancer so that more… (more)

Subjects/Keywords: Naturopathy; Cancer; Breast cancer; Estrogen receptor positive (ER+); Progesterone receptor positive (PR+)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Callis, C. M. (2013). Are Natural Therapies Effective in the Prevention/Treatment of ER+/PR+ Breast Cancer? . (Thesis). University of Bridgeport. Retrieved from https://scholarworks.bridgeport.edu/xmlui/handle/123456789/1390

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Callis, Chanté Maria. “Are Natural Therapies Effective in the Prevention/Treatment of ER+/PR+ Breast Cancer? .” 2013. Thesis, University of Bridgeport. Accessed January 26, 2021. https://scholarworks.bridgeport.edu/xmlui/handle/123456789/1390.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Callis, Chanté Maria. “Are Natural Therapies Effective in the Prevention/Treatment of ER+/PR+ Breast Cancer? .” 2013. Web. 26 Jan 2021.

Vancouver:

Callis CM. Are Natural Therapies Effective in the Prevention/Treatment of ER+/PR+ Breast Cancer? . [Internet] [Thesis]. University of Bridgeport; 2013. [cited 2021 Jan 26]. Available from: https://scholarworks.bridgeport.edu/xmlui/handle/123456789/1390.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Callis CM. Are Natural Therapies Effective in the Prevention/Treatment of ER+/PR+ Breast Cancer? . [Thesis]. University of Bridgeport; 2013. Available from: https://scholarworks.bridgeport.edu/xmlui/handle/123456789/1390

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Wake Forest University

21. Alzayadneh, Ebaa M. A ROLE FOR ANGIOTENSIN-(1-7) TO ATTENUATE ADVANCED GLYCATION END PRODUCT -INDUCED MYOFIBROBLAST TRANSITION IN THE NRK-52E RENAL PROXIMAL TUBULE CELL LINE.

Degree: 2014, Wake Forest University

URL: http://hdl.handle.net/10339/39401

► There is compelling evidence for a role of intracellular renin-angiotensin system (RAS) in cell signaling, function and cardiovascular pathologies. Diabetic nephropathy is a very common… (more)

▼ There is compelling evidence for a role of intracellular renin-angiotensin system (RAS) in cell signaling, function and cardiovascular pathologies. Diabetic nephropathy is a very common complication in which tubulointerstitial fibrosis may arise from epithelial to mesenchymal transition (EMT) of the proximal tubules cells. Advanced glycated end product (AGEs) including methylglyoxal-modified albumin (MGA) may contribute to the development and progression of diabetic nephropathy via activation of the receptors for AGE (RAGE) and the RAS. The RAS is functionally partitioned into the angiotensin II (Ang II)-angiotensin type 1 receptor (AT1R) and the Ang-(1-7)-AT7-MasR pathways that generally oppose the actions of one another. Although AGE-RAGE activation may stimulate the Ang II-AT1R axis, the role of Ang-(1-7) in AGE-induced EMT in the kidney is not known. The present study characterized the intracellular expression of the RAS in renal proximal tubules utilizing NRK-52E tubular epithelial cell line. Furthermore, we examined the influence of AGE on Ang-(1-7)-AT7-MasR axis in MGA-exposed in NRK-52E cells. The RAS precursor protein angiotensinogen (AGT), and its processing enzyme renin were visualized by immunofluorescent (IMF) staining in the cell nuclei; we confirmed the protein expression in isolated nuclei by immunoblots. Renin activity (AGT to Ang I conversion) was demonstrated in the nuclei of NRK-52E cells and trypsin activation studies on the pro-form of renin revealed a prorenin to renin ratio of 3:1. Peptide IMF staining localized Ang II and Ang-(1-7) to the nucleus and immunoreactive peptide content averaged 59 ± 2 and 57 ± 22 fmol per mg protein (n=4), respectively. Peptide metabolism studies in isolated nuclei revealed a pathway for the direct processing of Ang I to Ang-(1-7) by the enzyme thimet oligopeptidase. We then assessed the impact of AGE on the intracellular RAS of NRK-52E cells. MGA exposure for 48 hours significantly reduced the intracellular levels of Ang-(1-7) by 50%; however, expression of Ang I or Ang II was not altered. The reduced cellular content of Ang-(1-7) by MGA was associated with increased metabolism of the peptide to the inactive metabolite Ang-(1-4) with no change in the conversion of Ang I to Ang-(1-7). Exogenous addition of Ang-(1-7) reversed the cellular effects of MGA on cellular hypertrophy and myofibroblast transition; Ang-(1-7) reduced immunostaining and protein expression of á-smooth muscle actin by 60% (á-SMA) [n=3, p<0.05]. Moreover, Ang-(1-7) abolished AGE-induced activation of the MAP kinase ERK1/2 to a similar extent as the TGF-â receptor kinase inhibitor SB58059. The inhibitory actions Ang-(1-7) were apparently mediated by the MasR as the antagonist D-Ala7-Ang-(1-7) (A779) abrogated these effects. Collectively, we conclude that NRK-52E cells express RAS components that may contribute to the intracellular expression of the bioactive peptides Ang II and Ang-(1-7). Moreover, Ang-(1-7) may provide a novel therapeutic approach in addition to the conventional RAS…

Subjects/Keywords: Ang-(1-7)-Mas receptor

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APA (6^th Edition):

Alzayadneh, E. M. (2014). A ROLE FOR ANGIOTENSIN-(1-7) TO ATTENUATE ADVANCED GLYCATION END PRODUCT -INDUCED MYOFIBROBLAST TRANSITION IN THE NRK-52E RENAL PROXIMAL TUBULE CELL LINE. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/39401

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Alzayadneh, Ebaa M. “A ROLE FOR ANGIOTENSIN-(1-7) TO ATTENUATE ADVANCED GLYCATION END PRODUCT -INDUCED MYOFIBROBLAST TRANSITION IN THE NRK-52E RENAL PROXIMAL TUBULE CELL LINE.” 2014. Thesis, Wake Forest University. Accessed January 26, 2021. http://hdl.handle.net/10339/39401.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Alzayadneh, Ebaa M. “A ROLE FOR ANGIOTENSIN-(1-7) TO ATTENUATE ADVANCED GLYCATION END PRODUCT -INDUCED MYOFIBROBLAST TRANSITION IN THE NRK-52E RENAL PROXIMAL TUBULE CELL LINE.” 2014. Web. 26 Jan 2021.

Vancouver:

Alzayadneh EM. A ROLE FOR ANGIOTENSIN-(1-7) TO ATTENUATE ADVANCED GLYCATION END PRODUCT -INDUCED MYOFIBROBLAST TRANSITION IN THE NRK-52E RENAL PROXIMAL TUBULE CELL LINE. [Internet] [Thesis]. Wake Forest University; 2014. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10339/39401.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Alzayadneh EM. A ROLE FOR ANGIOTENSIN-(1-7) TO ATTENUATE ADVANCED GLYCATION END PRODUCT -INDUCED MYOFIBROBLAST TRANSITION IN THE NRK-52E RENAL PROXIMAL TUBULE CELL LINE. [Thesis]. Wake Forest University; 2014. Available from: http://hdl.handle.net/10339/39401

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

22. Robinson, Ryan Everitt. RING finger protein PLR-1 blocks Wnt signaling by altering trafficking of Wnt receptors.

Degree: 2013, University of Nevada – Reno

URL: http://hdl.handle.net/11714/3046

► Secreted Wnt proteins control a wide range of essential developmental processes, including axon guidance and establishment of anteroposterior neuronal polarity. We identified a transmembrane RING… (more)

Subjects/Keywords: Frizzled; PLR-1; Wnt receptor

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APA (6^th Edition):

Robinson, R. E. (2013). RING finger protein PLR-1 blocks Wnt signaling by altering trafficking of Wnt receptors. (Thesis). University of Nevada – Reno. Retrieved from http://hdl.handle.net/11714/3046

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Robinson, Ryan Everitt. “RING finger protein PLR-1 blocks Wnt signaling by altering trafficking of Wnt receptors.” 2013. Thesis, University of Nevada – Reno. Accessed January 26, 2021. http://hdl.handle.net/11714/3046.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Robinson, Ryan Everitt. “RING finger protein PLR-1 blocks Wnt signaling by altering trafficking of Wnt receptors.” 2013. Web. 26 Jan 2021.

Vancouver:

Robinson RE. RING finger protein PLR-1 blocks Wnt signaling by altering trafficking of Wnt receptors. [Internet] [Thesis]. University of Nevada – Reno; 2013. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/11714/3046.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Robinson RE. RING finger protein PLR-1 blocks Wnt signaling by altering trafficking of Wnt receptors. [Thesis]. University of Nevada – Reno; 2013. Available from: http://hdl.handle.net/11714/3046

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Stellenbosch University

23. Cabral, Angelique Aida. Crosstalk between the androgen receptor and progesterone receptor isoforms in breast and prostate cancer.

Degree: MSc, Biochemistry, 2018, Stellenbosch University

URL: http://hdl.handle.net/10019.1/103887

► ENGLISH ABSTRACT: Breast and prostate cancer growth and survival are dependent on signalling via the estrogen receptor (ER) and androgen receptor (AR), respectively. However, other… (more)

▼ ENGLISH ABSTRACT: Breast and prostate cancer growth and survival are dependent on signalling via the estrogen receptor (ER) and androgen receptor (AR), respectively. However, other steroid receptors such as the progesterone receptor (PR), are also implicated in both cancers, and emerging evidence suggests considerable crosstalk between these steroid receptors in breast cancer. Investigations into similar crosstalk mechanisms are lacking in prostate cancer. As the AR and PR are likely co-expressed in a subset of breast and prostate cancers, it is surprising that no studies have investigated crosstalk between the AR and PR in these cancers. Both these receptors can activate transcription by binding to DNA on a classical response element, termed either the progesterone response element (PRE) when the PR is bound, or the classical androgen response element (ARE) when the AR is bound. However, the AR can also bind to an AR-selective ARE as well as to the ER binding site, termed the estrogen response element (ERE). Whether the PR isoforms, PRA and PRB, can similarly activate the AR-selective ARE and ERE is not known. In this study, we investigated whether the PR isoforms, in the absence and presence of known PR agonists (synthetic promegestone (R5020), natural progesterone (P4), and synthetic progestin medroxyprogesterone acetate (MPA)), could modulate the transactivation function of the AR via the above-mentioned response elements in the MDA-MB-231 breast cancer and PC3 prostate cancer cell lines. The cells were transiently transfected with the expression vectors for the AR and/or PR isoforms, together with the applicable promoter-reporter constructs. The general trend observed was that both the unliganded and liganded PR isoforms augmented AR activity in a cell line-, ligand- and/or promoter-specific manner. Specifically, we showed that PRB, both in the absence and presence of PR ligands, generally upregulated AR transactivation on the various response elements in the breast and prostate cancer cells. While AR transactivation function was also increased by PRA on the selective ARE and ERE, PRA decreased AR-mediated transactivation on the classical ARE. We also provide novel evidence that both PR isoforms mimic AR activity on the selective ARE and the ERE in both cell lines, which may provide a mechanism through which the PR mediates oncogenic effects in both cancers. We did not observe cell proliferation in the presence of 5α-dihydrotestosterone (DHT) in either cell line transfected with the AR under the experimental conditions used in this study. In summary, even though the results from this study are preliminary, we are the first to show that the transactivation function of the AR is generally enhanced in the presence of the PR isoforms in both breast and prostate cancer. These findings support a potential crosstalk mechanism between the AR and PR isoforms in these cancers. Although the precise physiological implications of these results require further investigation, our findings contribute to the understanding of… Advisors/Committee Members: Africander, Donita, Storbeck, Karl-Heinz, Stellenbosch University. Faculty of Science. Dept. of Biochemistry..

Subjects/Keywords: Breast cancer; Prostate cancer; Androgens – Receptor; Glucocorticoids – Receptors; Progesterone; UCTD

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cabral, A. A. (2018). Crosstalk between the androgen receptor and progesterone receptor isoforms in breast and prostate cancer. (Masters Thesis). Stellenbosch University. Retrieved from http://hdl.handle.net/10019.1/103887

Chicago Manual of Style (16^th Edition):

Cabral, Angelique Aida. “Crosstalk between the androgen receptor and progesterone receptor isoforms in breast and prostate cancer.” 2018. Masters Thesis, Stellenbosch University. Accessed January 26, 2021. http://hdl.handle.net/10019.1/103887.

MLA Handbook (7^th Edition):

Cabral, Angelique Aida. “Crosstalk between the androgen receptor and progesterone receptor isoforms in breast and prostate cancer.” 2018. Web. 26 Jan 2021.

Vancouver:

Cabral AA. Crosstalk between the androgen receptor and progesterone receptor isoforms in breast and prostate cancer. [Internet] [Masters thesis]. Stellenbosch University; 2018. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10019.1/103887.

Council of Science Editors:

Cabral AA. Crosstalk between the androgen receptor and progesterone receptor isoforms in breast and prostate cancer. [Masters Thesis]. Stellenbosch University; 2018. Available from: http://hdl.handle.net/10019.1/103887

24. Van der Meer, Yolandi. Investigating progesterone and estrogen receptor crosstalk in breast cancer.

Degree: MSc, Biochemistry, 2017, Stellenbosch University

URL: http://hdl.handle.net/10019.1/101432

► ENGLISH ABSTRACT: Progestins are synthetic compounds designed to mimic the natural hormone progesterone (Prog), and are widely used in hormone replacement therapy (HRT) and contraception.… (more)

▼ ENGLISH ABSTRACT: Progestins are synthetic compounds designed to mimic the natural hormone progesterone (Prog), and are widely used in hormone replacement therapy (HRT) and contraception. These compounds can be divided into four generations, with newer generations increasing in progesterone receptor (PR) specificity. Although progestins have many therapeutic benefits, a number of undesirable side-effects, such as increased risk of breast cancer, have been reported. As a result, many postmenopausal women have sought alternatives for HRT, such as compounded bio-identical hormones like bio-identical Prog (bProg), claimed not to increase breast cancer risk. Progestins, Prog and bProg (collectively referred to as progestogens) elicit their biological effects primarily by binding to the PR, which exists as two predominant isoforms, PR-A and PR-B, with PR-B being the more transcriptionally active and proliferative isoform in breast cancer. Emerging evidence suggest that the PR plays an important role in breast cancer development and progression, and that there is crosstalk between the PR and estrogen receptor (ER)-α, a major etiological factor in breast cancer biology. Moreover, it has been shown that ER-α is required for PR-B-mediated effects of medroxyprogesterone acetate (MPA) on activation of gene expression and breast cancer cell proliferation. The latter raised the questions of whether ER-α is needed for PR-B-mediated effects of other progestins, and whether the ERβ subtype would also be required. Given that PR-B has both transactivation and transrepression functions, this study used transactivation and transrepression transcriptional assays to investigate the PR-B-mediated agonist efficacies and potencies of Prog, bProg and select progestins from different generations (MPA, norethisterone acetate (NET-A), levonorgestrel (LNG), gestodene (GES) and drospirenone (DRSP)), and whether these were modulated by ERα and/or ERβ. Furthermore, the effects of the progestogens on breast cancer cell proliferation were evaluated in the absence and presence of ERα- and ERβ-specific antagonists. Results showed that progestins mostly displayed similar agonist efficacies and potencies for transactivation and transrepression via PR-B. The exception was first generation MPA that was less efficacious for transactivation and least potent for transrepression, and third generation GES that was more potent for transactivation. This study is the first to show that ERα and ERβ differentially decreased PR-B-mediated agonist efficacies of progestogens for transactivation and transrepression. However, the ERα-specific antagonist had no effect on progestogen-induced expression of the endogenous PR-B regulated c-myc gene or repression of the interleukin (IL)-8 gene in the T47D breast cancer cell line, while the ERβ-specific antagonist had no effect on progestogen-induced c-myc gene expression, and appeared to abolish repression of the IL-8 gene. Additionally, we showed that all progestogens, except NET-A and DRSP, displayed similar proliferative… Advisors/Committee Members: Africander, Donita, Louw-du Toit, Renate, Stellenbosch University. Faculty of Science. Dept. of Biochemistry..

Subjects/Keywords: Progesterone receptor; Estrogen recepter; Breast cancer; Hormone replacement therapy; UCTD

13 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Van der Meer, Y. (2017). Investigating progesterone and estrogen receptor crosstalk in breast cancer. (Masters Thesis). Stellenbosch University. Retrieved from http://hdl.handle.net/10019.1/101432

Chicago Manual of Style (16^th Edition):

Van der Meer, Yolandi. “Investigating progesterone and estrogen receptor crosstalk in breast cancer.” 2017. Masters Thesis, Stellenbosch University. Accessed January 26, 2021. http://hdl.handle.net/10019.1/101432.

MLA Handbook (7^th Edition):

Van der Meer, Yolandi. “Investigating progesterone and estrogen receptor crosstalk in breast cancer.” 2017. Web. 26 Jan 2021.

Vancouver:

Van der Meer Y. Investigating progesterone and estrogen receptor crosstalk in breast cancer. [Internet] [Masters thesis]. Stellenbosch University; 2017. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10019.1/101432.

Council of Science Editors:

Van der Meer Y. Investigating progesterone and estrogen receptor crosstalk in breast cancer. [Masters Thesis]. Stellenbosch University; 2017. Available from: http://hdl.handle.net/10019.1/101432

University of Illinois – Chicago

25. Toh, May Fern. Identification and Biological Characterization of Progestins from Botanicals In Vitro and In Vivo.

Degree: 2014, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/18868

► Extensive studies have been conducted on botanicals for the presence of estrogenic molecules, unfortunately, very little has ever been done to identify plant-based progestins. This… (more)

▼ Extensive studies have been conducted on botanicals for the presence of estrogenic molecules, unfortunately, very little has ever been done to identify plant-based progestins. This underexplored area is troubling especially since there is a body of scientific evidence supporting the presence of progesterone receptor (PR) modulators in plant material that may affect endocrine function. The goal of this dissertation was to identify and characterize natural progesterone (P4)-like compounds from botanical extracts for the improvement of women’s health. Red clover, hops, angelica, black cohosh, kudzu, dogwood, and chaste-tree berry were investigated for their ability to interact with purified PR, to activate PRE-luciferase transcription in human breast cancer cells, and for tissue specific regulation of P4 inducible genes. Kaempferol was identified as having P4-like activity and may function in a cell-specific manner. In vivo studies revealed that kaempferol exhibited P4-like effects in ovariectomized Sprague-Dawley rat model. Since genistein is a phytoestrogen that previously demonstrated to increase uterine weight and proliferation, the ability of kaempferol to block genistein action in the uterus was investigated. Analyses of proliferation, steroid receptor expression, and induction of well-established PR-regulated targets Areg and Hand2 were completed. In addition, kaempferol in silico binding analysis was completed for PR, as was the activation of ER and AR signaling in vitro in order to determine receptor specificity. The data from this dissertation suggest that kaempferol interacts with PR, activates the receptor without stimulating its degradation, induces known PR target genes in vitro and in vivo and blocked genistein-induced proliferation in the luminal epithelial cells in Sprague-Dawley rat uteri. The toxicity of hops extracts in cell-based assays precluded further investigation in vitro, but an initial bioassay screen suggested that natural progestins can be identified from hops extracts. Further chemical and biological analyses are warranted to identify and characterize progestins from hops. The comprehensive framework outlined in this thesis will provide a promising avenue for the identification of potentially better and safer compounds capable of activating PR signaling from botanical extracts used for women's health. Advisors/Committee Members: Burdette, Joanna E. (advisor), Murphy, Brian T. (committee member), Moore, Terry W. (committee member), Thomas, Douglas D. (committee member), Stocco, Carlos D. (committee member).

Subjects/Keywords: Kaempferol; Progestin; Hormone replacement therapy; Genistein; Red clover; Progesterone receptor

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APA (6^th Edition):

Toh, M. F. (2014). Identification and Biological Characterization of Progestins from Botanicals In Vitro and In Vivo. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/18868

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Toh, May Fern. “Identification and Biological Characterization of Progestins from Botanicals In Vitro and In Vivo.” 2014. Thesis, University of Illinois – Chicago. Accessed January 26, 2021. http://hdl.handle.net/10027/18868.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Toh, May Fern. “Identification and Biological Characterization of Progestins from Botanicals In Vitro and In Vivo.” 2014. Web. 26 Jan 2021.

Vancouver:

Toh MF. Identification and Biological Characterization of Progestins from Botanicals In Vitro and In Vivo. [Internet] [Thesis]. University of Illinois – Chicago; 2014. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10027/18868.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Toh MF. Identification and Biological Characterization of Progestins from Botanicals In Vitro and In Vivo. [Thesis]. University of Illinois – Chicago; 2014. Available from: http://hdl.handle.net/10027/18868

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

26. Askin, Nesime. Metabolic Regulation of Fast- and Slow-twitch Skeletal Muscles by Estradiol and Progesterone in Females and their Impact during Ischemia.

Degree: PhD, 2014, University of Toronto

URL: http://hdl.handle.net/1807/68380

► The roles of estradiol and progesterone were investigated to determine the effect of these hormones on metabolism in skeletal muscle composed of different fiber types… (more)

Subjects/Keywords: estradiol; estrogen receptor; fiber types; ischemia; progesterone; skeletal muscle; 0719

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APA (6^th Edition):

Askin, N. (2014). Metabolic Regulation of Fast- and Slow-twitch Skeletal Muscles by Estradiol and Progesterone in Females and their Impact during Ischemia. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/68380

Chicago Manual of Style (16^th Edition):

Askin, Nesime. “Metabolic Regulation of Fast- and Slow-twitch Skeletal Muscles by Estradiol and Progesterone in Females and their Impact during Ischemia.” 2014. Doctoral Dissertation, University of Toronto. Accessed January 26, 2021. http://hdl.handle.net/1807/68380.

MLA Handbook (7^th Edition):

Askin, Nesime. “Metabolic Regulation of Fast- and Slow-twitch Skeletal Muscles by Estradiol and Progesterone in Females and their Impact during Ischemia.” 2014. Web. 26 Jan 2021.

Vancouver:

Askin N. Metabolic Regulation of Fast- and Slow-twitch Skeletal Muscles by Estradiol and Progesterone in Females and their Impact during Ischemia. [Internet] [Doctoral dissertation]. University of Toronto; 2014. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/1807/68380.

Council of Science Editors:

Askin N. Metabolic Regulation of Fast- and Slow-twitch Skeletal Muscles by Estradiol and Progesterone in Females and their Impact during Ischemia. [Doctoral Dissertation]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/68380

University of Southern California

27. Taylor, DeShawn. Characterization of breast tissue in early pregnancy to help define the effect of induced abortion on breast cancer risk.

Degree: MS, Preventive Medicine (Health Behavior), 2007, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/527360/rec/1297

► Prospective studies show that pregnancies interrupted by induced abortion may provide as much as 70% of the breast cancer protection provided by a term pregnancy.… (more)

Subjects/Keywords: induced abortion; progesterone receptor; breast

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APA (6^th Edition):

Taylor, D. (2007). Characterization of breast tissue in early pregnancy to help define the effect of induced abortion on breast cancer risk. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/527360/rec/1297

Chicago Manual of Style (16^th Edition):

Taylor, DeShawn. “Characterization of breast tissue in early pregnancy to help define the effect of induced abortion on breast cancer risk.” 2007. Masters Thesis, University of Southern California. Accessed January 26, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/527360/rec/1297.

MLA Handbook (7^th Edition):

Taylor, DeShawn. “Characterization of breast tissue in early pregnancy to help define the effect of induced abortion on breast cancer risk.” 2007. Web. 26 Jan 2021.

Vancouver:

Taylor D. Characterization of breast tissue in early pregnancy to help define the effect of induced abortion on breast cancer risk. [Internet] [Masters thesis]. University of Southern California; 2007. [cited 2021 Jan 26]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/527360/rec/1297.

Council of Science Editors:

Taylor D. Characterization of breast tissue in early pregnancy to help define the effect of induced abortion on breast cancer risk. [Masters Thesis]. University of Southern California; 2007. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/527360/rec/1297

28. Zanatta, Alysson. Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide.

Degree: PhD, Obstetrícia e Ginecologia, 2013, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-06112013-085759/ ;

► INTRODUÇÃO: Apesar de a endometriose profunda (EPF) ser a forma da doença de maior repercussão clínica, os estudos sobre a doença costumam ser baseados em… (more)

▼ INTRODUÇÃO: Apesar de a endometriose profunda (EPF) ser a forma da doença de maior repercussão clínica, os estudos sobre a doença costumam ser baseados em lesões de endometriose ovariana (EOV) e peritoneal (EPT). A patogênese da EPF ainda é objeto de amplo debate, pois há poucos estudos feitos exclusivamente com lesões de EPF. O fator de transcrição codificado pelo gene homeobox A10 (HOXA10) regula a conferência de identidade tecidual de útero ao ducto paramesonéfrico indiferenciado durante o período embrionário. O gene mantém um padrão de expressão temporal e espacial bem definido e, durante a fase adulta, continua expresso no miométrio e endométrio. Sugere-se que HOXA10 esteja implicado na patogênese da endometriose, pois é expresso em EOV, EPT, endometriose pulmonar e endometriose retovaginal, um tipo de EPF. Possivelmente, o gene HOXA10 seja necessário para conferir identidade de endometriose a um tecido indiferenciado. O estradiol e a progesterona ativam a transcrição do gene HOXA10 e regulam diretamente sua ação. Esses hormônios estão envolvidos na patogênese da EPF, e suas atividades podem ser inferidas pelo estudo da expressão tecidual de seus receptores. A endometriose de reto-sigmoide (ERS) é um modelo representativo para o estudo da EPF. Neste estudo, avaliamos a expressão proteica do fator de transcrição HOXA10, das isoformas ? (ER-alfa) e beta (ER-beta) dos receptores de estrogênio, e do receptor de progesterona AB (PR-AB) e sua isoforma B (PR-B) na lesão (LES) e no tecido muscular liso perilesional (TMLP) de ERS de pacientes inférteis, durante as fases proliferativa e secretora do ciclo menstrual. MÉTODOS: amostras de LES e TMLP de ERS de 18 pacientes (9 operadas em cada fase do ciclo menstrual) foram agrupadas em blocos de microarranjos de tecidos (tissue microarray). As amostras foram coradas com anticorpos específicos para análise imunoistoquímica de cada uma das proteínas. Foram então avaliadas por microscopia ótica (MO) e pela análise das imagens digitalizadas das lâminas com por um software específico, a análise morfométrica (AM). RESULTADOS: HOXA10 foi expresso no estroma de LES de ERS durante a fase secretora, de acordo com a MO. ER-alfa e ER-betaforam expressos em glândulas e estroma de LES e TMLP de ERS durante ambas as fases do ciclo, de acordo com a MO e a AM. PR-AB e PR-B foram expressos em glândulas e estroma de LES de ERS durante ambas as fases do ciclo, de acordo com a MO. PR-B foi mais expresso durante a fase secretora, independentemente do local de expressão, segundo a AM. A expressão de HOXA10 correlacionou-se diretamente com PR-AB e PR-B na ERS, segundo a AM. Não houve correlação entre ER-alfa e ER-beta com HOXA10, PR-AB ou PR-B em nenhuma fase do ciclo ou local de expressão de ERS. CONCLUSÕES: HOXA10 é expresso em ERS, um local fora do seu eixo espacial de expressão. A presença de HOXA10 pode ser necessária para conferir a identidade \"de novon̈a EPF, incluindo ERS. A progesterona pode ativar o gene HOXA10 e regular esta ação, possivelmente mediada por PR-B. O estradiol exerce sua… Advisors/Committee Members: Serafini, Paulo Cesar.

Subjects/Keywords: Deep endometriosis; Endometriose de retosigmoide; Endometriose profunda; Estrogen receptor-alfa; Estrogen receptor-beta; Gene HOXA10; HOXA gene; Progesterone receptor-B; Progesterone receptor; Receptor de estrogênio alfa; Receptor de estrogênio beta; Receptor de progesterona; Receptor de progesterona B; Rectosigmoid endometriosis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zanatta, A. (2013). Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5139/tde-06112013-085759/ ;

Chicago Manual of Style (16^th Edition):

Zanatta, Alysson. “Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide.” 2013. Doctoral Dissertation, University of São Paulo. Accessed January 26, 2021. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-06112013-085759/ ;.

MLA Handbook (7^th Edition):

Zanatta, Alysson. “Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide.” 2013. Web. 26 Jan 2021.

Vancouver:

Zanatta A. Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide. [Internet] [Doctoral dissertation]. University of São Paulo; 2013. [cited 2021 Jan 26]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-06112013-085759/ ;.

Council of Science Editors:

Zanatta A. Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide. [Doctoral Dissertation]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-06112013-085759/ ;

29. Božović Ana. Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers.

Degree: PhD, Biology, 2013, University of Belgrade

URL: http://dx.doi.org/10.2298/BG20130703BOZOVIC ; http://eteze.bg.ac.rs/application/showtheses?thesesId=799 ; https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=44646927

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Breast cancer is the most common invasive cancer in women. Beside genetic, epigenetic factors influence its initiation and progression. The purpose of this study was… (more)

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Breast cancer is the most common invasive cancer in women. Beside genetic, epigenetic factors influence its initiation and progression. The purpose of this study was to test whether methylation of the promoter ON of the gene for ERβ protein (ESR2) influences its expression (on mRNA and protein level) and to correlate the methylation index of the ON promoter, ERβ1-mRNA and ERβ1 protein levels with clinicopathological parameters. In this study, 131 archival samples of breast cancer tissue were used. Custom designed two step PCR method, was done for amplification and relative quantification of the specific region of the ON promoter of the ESR2 gene. Measuring of ERβ1-mRNA was done by quantitative real time RT-PCR, and relative quantification of ERβ1 protein isoform was done by Western blot. Statistical analysis was performed and results for methylation index of ON promoter, mRNA and ERβ1 protein levels were correlated with clinicopathological parameters. The methylation index of ERβ-ON promoter was significantly higher in a group of patients with positive axillary lymph node status, than in a group with negative one. A significant positive correlation between methylation index of ON promoter and ERα protein levels was obtained. It can be concluded that methylation index of the ERβ-ON promoter could be more confident parameter for prediction and/or prognosis of breast cancer, than measuring of ERβ1-mRNA or ERβ1 protein levels.

Invazivni karcinom dojke je najčešći kancer kod žena. Pored genetičkih i epigenetički faktori imaju važnu ulogu u njegovoj inicijaciji i progresiji. Cilj ove studije bio je ispitati da li metilacija promotora ON, gena za ERβ protein (ESR2) utiče na njegovu ekspresiju (na nivou iRNK i proteina) i utvrditi povezanost metilacionog indeksa promotora ON sa nivoima ERβ1-iRNK i ERβ1 proteina, kao i sa kliničkim i patohistološkim parametrima. U ovoj studiji analiziran je 131 arhivski uzorak kancera dojke. Pomoću posebno dizajniranog PCR testa iz dva koraka, amplifikovan je i kvantifikovan specifični region promotora ON ESR2 gena. Za kvantifikaciju ERβ1-iRNK korišćena je metoda kvantitativnog RT-PCR u realnom vremenu. Metoda „Western Blot“ je korišćena za relativnu kvantifikaciju ERβ1 proteinske izoforme. Dobijeni podaci, metilacioni indeks promotora ON, nivoi iRNK i ERβ1 proteina, analizirani su i korelisani sa kliničkopatološkim parametrima neparametrijskim statističkim testovima. Nađeno je da je metilacioni indeks promotora ON ERβ gena značajno veći u grupi pacijentkinja sa pozitivnim, u odnosu na grupu sa negativnim statusom aksilarnih limfnih čvorova. Takođe, pronađena je značajna pozitivna korelacija metilacionog indeksa promotora ON ERβ gena sa nivoom estrogenskog receptora α. Na osnovu dobijenih rezultata pokazano je da metilacioni indeks promotora ON, ERβ gena može biti pouzdaniji marker prognoze kancera dojke nego ekspresija ERβ1-iRNK ili proteina ERβ1.

Subjects/Keywords: Breast cancer; estrogen receptor alpha; estrogen receptor beta; progesterone receptor; methylation; quantitative PCR; Kancer dojke; estrogenski receptor alfa; estrogenski receptor beta; progesteronski receptor; metilacija; kvantitativni PCR

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ana, B. (2013). Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers. (Doctoral Dissertation). University of Belgrade. Retrieved from http://dx.doi.org/10.2298/BG20130703BOZOVIC ; http://eteze.bg.ac.rs/application/showtheses?thesesId=799 ; https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=44646927

Chicago Manual of Style (16^th Edition):

Ana, Božović. “Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers.” 2013. Doctoral Dissertation, University of Belgrade. Accessed January 26, 2021. http://dx.doi.org/10.2298/BG20130703BOZOVIC ; http://eteze.bg.ac.rs/application/showtheses?thesesId=799 ; https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=44646927.

MLA Handbook (7^th Edition):

Ana, Božović. “Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers.” 2013. Web. 26 Jan 2021.

Vancouver:

Ana B. Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers. [Internet] [Doctoral dissertation]. University of Belgrade; 2013. [cited 2021 Jan 26]. Available from: http://dx.doi.org/10.2298/BG20130703BOZOVIC ; http://eteze.bg.ac.rs/application/showtheses?thesesId=799 ; https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=44646927.

Council of Science Editors:

Ana B. Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers. [Doctoral Dissertation]. University of Belgrade; 2013. Available from: http://dx.doi.org/10.2298/BG20130703BOZOVIC ; http://eteze.bg.ac.rs/application/showtheses?thesesId=799 ; https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=44646927

Université Paris-Sud – Paris XI

30. Desreumaux Communal, Laudine. Influence des hormones stéroïdes et potentiel préventif d'un antiprogestatif, l'ulpristal acétate, dans la tumorigenèse liée à la mutation du gène BRCA1 : Steroid hormones involvement and ulipristal acetate ability to prevent BRCA1 mutated breast tumorigenesis.

Degree: Docteur es, Cancérologie - Biochimie, Biologie cellulaire et moléculaire, 2011, Université Paris-Sud – Paris XI

URL: http://www.theses.fr/2011PA11T102

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Les hormones ovariennes sont impliquées dans le développement du cancer du sein des femmes porteuses de mutations du gène BRCA1. L’étude du tissu mammaire normal… (more)

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Les hormones ovariennes sont impliquées dans le développement du cancer du sein des femmes porteuses de mutations du gène BRCA1. L’étude du tissu mammaire normal de femmes mutées et non mutées nous a permis de montrer des altérations de la signalisation de l’estradiol et la progestérone dans un modèle de greffes chez la souris. Ces dérégulations concernent l’activité proliférative et l’expression des récepteurs hormonaux, et sont hétérogènes d’une patiente mutée à l’autre. De plus, une diminution de l’expression de la forme phosphorylée en sérine 211 du récepteur des glucocorticoïdes a été mise en évidence dans le tissu muté BRCA1. Ces observations posent la question de la place d’unantiprogestatif/anti-glucocorticoïde tel que l’ulipristal acétate (UPA) dans le traitement préventif des femmes mutées pour BRCA1. Les effets de l’UPA ont été caractérisés in vitro dans les cellules mammaires normales pour préciser les conséquences de son utilisation sur le sein. Son action a ensuite été examinée sur les xénogreffes de sein de patientes mutées et non mutées. Nous montrons que l’UPA est capable d’inhiber la prolifération du tissu muté lorsqu’elle est induite par la progestérone. Ce résultat encourage son utilisation dans la prévention tumorale mais indique une spécificité d’action en fonction des dérégulations hormonales associées au tissu muté.

Ovarian hormones, estradiol and progesterone, are known to promote breast carcinogenesis in BRCA1 mutated women. Using normal mammary gland xenografted in mice, we found that hormonal responses were deregulated in a heterogeneous fashion within BRCA1 mutation carriers. These observations raise the question of a potential use ofantiprogestin treatment as ulipristal acetate (UPA) to prevent breast tumorigenesis in BRCA1mutated women. Studies with this experimental model and epithelial normal breast cells in vitro, revealed that UPA alone had no proliferative activity on breast tissue but was efficient to inhibit proliferative activity when induced by progesterone treatment in mutated tissue. UPAcould be a promising treatment to prevent breast tumorigenesis for some mutated women. In addition, we observed a severe decrease of the phosphorylated Serine 211 glucocorticoid receptor isoform in BRCA1 carriers compared to non mutated tissue. This observation suggests that the glucocorticoid receptor expression and activation should be taken intoaccount in BRCA1 carriers.

Advisors/Committee Members: Gompel, Anne (thesis director).

Subjects/Keywords: Récepteur de l’estradiol; Récepteur de la progestérone; Récepteur des glucocorticoïdes; P-S211GR; Estradiol receptor; Progesterone receptor; Glucocorticoid receptor; P-S211GR

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Desreumaux Communal, L. (2011). Influence des hormones stéroïdes et potentiel préventif d'un antiprogestatif, l'ulpristal acétate, dans la tumorigenèse liée à la mutation du gène BRCA1 : Steroid hormones involvement and ulipristal acetate ability to prevent BRCA1 mutated breast tumorigenesis. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2011PA11T102

Chicago Manual of Style (16^th Edition):

Desreumaux Communal, Laudine. “Influence des hormones stéroïdes et potentiel préventif d'un antiprogestatif, l'ulpristal acétate, dans la tumorigenèse liée à la mutation du gène BRCA1 : Steroid hormones involvement and ulipristal acetate ability to prevent BRCA1 mutated breast tumorigenesis.” 2011. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed January 26, 2021. http://www.theses.fr/2011PA11T102.

MLA Handbook (7^th Edition):

Desreumaux Communal, Laudine. “Influence des hormones stéroïdes et potentiel préventif d'un antiprogestatif, l'ulpristal acétate, dans la tumorigenèse liée à la mutation du gène BRCA1 : Steroid hormones involvement and ulipristal acetate ability to prevent BRCA1 mutated breast tumorigenesis.” 2011. Web. 26 Jan 2021.

Vancouver:

Desreumaux Communal L. Influence des hormones stéroïdes et potentiel préventif d'un antiprogestatif, l'ulpristal acétate, dans la tumorigenèse liée à la mutation du gène BRCA1 : Steroid hormones involvement and ulipristal acetate ability to prevent BRCA1 mutated breast tumorigenesis. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2011. [cited 2021 Jan 26]. Available from: http://www.theses.fr/2011PA11T102.

Council of Science Editors:

Desreumaux Communal L. Influence des hormones stéroïdes et potentiel préventif d'un antiprogestatif, l'ulpristal acétate, dans la tumorigenèse liée à la mutation du gène BRCA1 : Steroid hormones involvement and ulipristal acetate ability to prevent BRCA1 mutated breast tumorigenesis. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2011. Available from: http://www.theses.fr/2011PA11T102

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