subject:(receptor)

1. Allen, Stacy-ann A. Characterization of BKPyV Interaction with Disialylated Gangliosides and PKC Regulated Viral Entry.

Degree: PhD, Pathobiology, 2013, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:320592/

► The human polyomavirus BK is a clinically relevant virus that causes the diseases Polyomavirus Induced Nephropathy and Hemorrhagic Cystitis in immune suppressed kidney and bone… (more)

▼ The human polyomavirus BK is a clinically relevant virus that causes the diseases Polyomavirus Induced Nephropathy and Hemorrhagic Cystitis in immune suppressed kidney and bone marrow transplant patients. BKPyV attachment to receptors on host cells has implications for virus spread, tissue and species tropism. As such, the interaction between BKPyV and host cellular receptors and the signaling events that facilitate entry are significant areas of interest in the field. Gangliosides GD1b and GT1b are receptors for BKV. A common shared feature is the presence of a disialic acid moiety. Using viral infection assays we show that in addition to GD1b and GT1b, the disialylated gangliosides GD3 and GD2 can serve as receptors for BKPyV. NMR spectroscopy identifies the α2,8-disialic acid motif as the primary binding epitope for BKPyV. The crystal structure of the BKPyV capsid protein VP1 in complex with GD3 reveals contacts with both sialic acid moieties, providing a basis for the observed specificity. A structure-based model of the GD1b interaction suggests additional, affinity-enhancing contacts, which when evaluated, subtly influence BKPyV infection. Comparison of the receptor binding surfaces of BKPyV and SV40 reveals an amino acid at position 68 in BKPyV VP1 as the major determinant of specificity. Mutation of this amino acid from lysine in BKPyV to serine in SV40 switches the specificity of BKPyV to recognize GM1 versus GD3. Following interaction with its receptors, entry of BKPyV is mediated by caveolae endocytosis which is regulated by Protein Kinase C (PKC). We investigate the role of PKC in BKPyV infection using the PKC inhibitor Bisindolylmaleimide I. Transient inhibition of PKC, which exploits the reversibility of the inhibitor, results in virus susceptibility to BKPyV antibody neutralization and an increase in membrane localization of PKC. Removal of inhibition increases infection. Additionally, exogenous addition of the BKPyV ganglioside receptor GT1b stimulates increased endocytosis of BKPyV and in combination with PKC inhibition, causes a synergistic increase in infection. The data demonstrates that the disialylated gangliosides GD3, GD2, GD1b and GT1b are important for BKPyV infection and that glycosphingolipid mediated caveolae uptake of BKPyV is regulated by PKC. Advisors/Committee Members: Atwood, Walter (Director), Reichner, Johnathan (Reader), Page, Rebecca (Reader), Shank, Peter (Reader), DiMaio, Daniel (Reader).

Subjects/Keywords: receptor

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APA (6^th Edition):

Allen, S. A. (2013). Characterization of BKPyV Interaction with Disialylated Gangliosides and PKC Regulated Viral Entry. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:320592/

Chicago Manual of Style (16^th Edition):

Allen, Stacy-ann A. “Characterization of BKPyV Interaction with Disialylated Gangliosides and PKC Regulated Viral Entry.” 2013. Doctoral Dissertation, Brown University. Accessed April 11, 2021. https://repository.library.brown.edu/studio/item/bdr:320592/.

MLA Handbook (7^th Edition):

Allen, Stacy-ann A. “Characterization of BKPyV Interaction with Disialylated Gangliosides and PKC Regulated Viral Entry.” 2013. Web. 11 Apr 2021.

Vancouver:

Allen SA. Characterization of BKPyV Interaction with Disialylated Gangliosides and PKC Regulated Viral Entry. [Internet] [Doctoral dissertation]. Brown University; 2013. [cited 2021 Apr 11]. Available from: https://repository.library.brown.edu/studio/item/bdr:320592/.

Council of Science Editors:

Allen SA. Characterization of BKPyV Interaction with Disialylated Gangliosides and PKC Regulated Viral Entry. [Doctoral Dissertation]. Brown University; 2013. Available from: https://repository.library.brown.edu/studio/item/bdr:320592/

Universidad de Cantabria

2. Ortiz de Zárate Bautista, Marta. Estudio básico del receptor de cavidad de una central termosolar de torre: Basic study of receptor in solar tower power plant.

Degree: Máster en Ingeniería Industrial, 2016, Universidad de Cantabria

URL: http://hdl.handle.net/10902/10056

► El presente proyecto es la continuación del que se realizó al finalizar la titulación de Grado en Ingeniería en Tecnologías Industriales, a continuación se presenta… (more)

▼ El presente proyecto es la continuación del que se realizó al finalizar la titulación de Grado en Ingeniería en Tecnologías Industriales, a continuación se presenta un resumen del mismo con el fin de recordar los datos de partida y los resultados y conclusiones obtenidas. En primer lugar se describieron los diferentes tipos de centrales termosolares que existen para posteriormente poder seleccionar la más adecuada para este proyecto; estas se diferencian en la posición relativa de la torre donde se aloja el receptor respecto al campo de heliostatos. Finalmente, teniendo en cuenta las localizaciones que se barajaban, todas ellas en el sur de la península ibérica, se seleccionó una central de tipo campo norte, esta decisión se basa en la posición relativa de la localización de la central respecto al ecuador; el recorrido del Sol se observará inclinado hacia el sur, con lo que para optimizar el área de los espejos, estos se situarán todos al norte de la torre. En el anterior proyecto, titulado “Diseño de una central termosolar de torre de 10 MW”, se desarrolló un software con la ayuda del programa de cálculo MatLab, con el fin de calcular el tamaño del campo de heliostatos y la altura de la torre y analizar el comportamiento del conjunto. Todas las características de diseño podían ser especificadas por el usuario; a partir de ellas el programa calculaba el comportamiento del sistema para todos los momentos del año, a partir de estos resultados era posible elegir aquel con un rendimiento óptimo respecto a la inversión necesaria y adaptado a la potencia final deseada para la central. Seguidamente, estimando de forma razonada los rendimientos de cada una de las partes de la central, conociendo la potencia nominal deseada y las limitaciones del campo, se puede hallar el valor de potencia que es necesario concentrar en el receptor situado en lo alto de la torre. En dicho proyecto se analizó la eficacia del campo de heliostatos en sus diferentes zonas, y su evolución en el tiempo. El tamaño de campo seleccionado cuenta finalmente con 72 anillos en los que se distribuyen 4596 heliostatos, por otro lado la altura de torre se fijó en 125 m. Advisors/Committee Members: Silió Salcines, Delfín (advisor), Universidad de Cantabria (other).

Subjects/Keywords: Receptor

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

APA (6^th Edition):

Ortiz de Zárate Bautista, M. (2016). Estudio básico del receptor de cavidad de una central termosolar de torre: Basic study of receptor in solar tower power plant. (Masters Thesis). Universidad de Cantabria. Retrieved from http://hdl.handle.net/10902/10056

Chicago Manual of Style (16^th Edition):

Ortiz de Zárate Bautista, Marta. “Estudio básico del receptor de cavidad de una central termosolar de torre: Basic study of receptor in solar tower power plant.” 2016. Masters Thesis, Universidad de Cantabria. Accessed April 11, 2021. http://hdl.handle.net/10902/10056.

MLA Handbook (7^th Edition):

Ortiz de Zárate Bautista, Marta. “Estudio básico del receptor de cavidad de una central termosolar de torre: Basic study of receptor in solar tower power plant.” 2016. Web. 11 Apr 2021.

Vancouver:

Ortiz de Zárate Bautista M. Estudio básico del receptor de cavidad de una central termosolar de torre: Basic study of receptor in solar tower power plant. [Internet] [Masters thesis]. Universidad de Cantabria; 2016. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/10902/10056.

Council of Science Editors:

Ortiz de Zárate Bautista M. Estudio básico del receptor de cavidad de una central termosolar de torre: Basic study of receptor in solar tower power plant. [Masters Thesis]. Universidad de Cantabria; 2016. Available from: http://hdl.handle.net/10902/10056

University of Illinois – Urbana-Champaign

3. Parent, Alexander A. Second-site inhibitors of the estrogen and androgen hormone receptors.

Degree: PhD, 0335, 2012, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/29523

► The estrogen and androgen receptors are members of the nuclear hormone receptor protein superfamily and play an important role in the development of primary and… (more)

▼ The estrogen and androgen receptors are members of the nuclear hormone receptor protein superfamily and play an important role in the development of primary and secondary female and male sexual characteristics. Although necessary for proper development, in certain contexts activation of these receptors contributes to the formation and progression of hyperplastic diseases, namely breast and prostate cancers. Current treatment for metastatic hormone responsive breast and prostate tumors involves either chemical ‘castration’ techniques which target the synthesis of the endogenous estrogen and androgen agonists, or the administration of hormone antagonists which displace endogenous agonist from the ligand binding domain of the receptor causing a conformational change such that the transcriptional activity of the protein is inhibited. While efficacious for a duration ranging from a few months to years, breast and prostate tumors eventually cease to respond to these treatments, entering a hormone-refractory state for which there is no adequate treatment. Multiple new approaches to estrogen and androgen receptor inhibition have been reported in recent years. Among these are efforts to directly disrupt the nuclear receptor/coactivator and the nuclear receptor/DNA interactions, and to increase degradation of receptor through binding of small-molecules at non-traditional binding sites. Due to the essential nature of these interactions for estrogen and androgen receptor signaling, it has been proposed that such second-site inhibition may be less susceptible to the mutations and receptor and coregulator overexpression that are currently exhibited in hormone-refractory breast and prostate cancers. As described herein, we have investigated a number of chemical systems for their ability to disrupt the estrogen and androgen receptor/steroid receptor coactivator interaction. In chapters 2 and 3 we describe the structure-based design of pyrimidine-core small-molecules that mimic the three interacting leucine/phenylalanine residues of the estrogen and androgen receptor coactivators. Members of this library bind to both nuclear receptors and disrupt the nuclear receptor/coactivator complex with Ki’s in the low micromolar range. In our screening against the two subtypes of the estrogen receptor, we discovered a only few compounds that exhibited binding to the estrogen receptor beta, and the vast majority show strong preference for estrogen receptor alpha inhibition. Based on its ability to accommodate larger aromatic residues at the coactivator binding site, we anticipated that pyrimidine-core molecules with bulky aromatic substituents would selectively bind to the androgen receptor. Indeed, this approach produced multiple coactivator binding inhibitors that displayed potent and selective inhibition of the androgen receptor, without concomitant disruption of the estrogen receptor/coactivator complex. During the synthesis of the pyrimidine-core coactivator binding inhibitors, a tetra-aryl cyclobutane compound that showed potent… Advisors/Committee Members: Katzenellenbogen, John A. (advisor), Katzenellenbogen, John A. (Committee Chair), van der Donk, Wilfred A. (committee member), Hergenrother, Paul J. (committee member), Gennis, Robert B. (committee member).

Subjects/Keywords: estrogen receptor; androgen receptor; inhibitor; nuclear receptor

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

APA (6^th Edition):

Parent, A. A. (2012). Second-site inhibitors of the estrogen and androgen hormone receptors. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/29523

Chicago Manual of Style (16^th Edition):

Parent, Alexander A. “Second-site inhibitors of the estrogen and androgen hormone receptors.” 2012. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed April 11, 2021. http://hdl.handle.net/2142/29523.

MLA Handbook (7^th Edition):

Parent, Alexander A. “Second-site inhibitors of the estrogen and androgen hormone receptors.” 2012. Web. 11 Apr 2021.

Vancouver:

Parent AA. Second-site inhibitors of the estrogen and androgen hormone receptors. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2012. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2142/29523.

Council of Science Editors:

Parent AA. Second-site inhibitors of the estrogen and androgen hormone receptors. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2012. Available from: http://hdl.handle.net/2142/29523

Universidad Andrés Bello

4. Bravo Tello, Karina. Rol de los receptores Cxcr2 y Gcsfr en la migración de neutrófilos desde el tejido caudal hematopoyético a los vasos sanguíneos en pez cebra .

Degree: 2018, Universidad Andrés Bello

URL: http://repositorio.unab.cl/xmlui/handle/ria/6047

► En mamíferos, la migración de neutrófilos durante un proceso de inflamación está regulada por la vía de señalización GCSF-GCSFR. Esta citoquina y su receptor permiten… (more)

▼ En mamíferos, la migración de neutrófilos durante un proceso de inflamación está regulada por la vía de señalización GCSF-GCSFR. Esta citoquina y su receptor permiten la salida de los neutrófilos desde los tejidos hematopoyéticos después de un daño estéril. En pez cebra, Gcsf-Chr19 controla el proceso mencionado anteriormente, pero se desconoce si esta citoquina se une a Gcsfr para ello. Además, el receptor Cxcr2 también participa en este proceso regulando la entrada de neutrófilos a los vasos sanguíneos, pero en presencia de patógenos. Debido a las posibles diferencias en las vías de señalización que regulan la inflamación por daños estériles y aquellas provocadas por patógenos, además de la posible diferencia entre mamíferos y peces, determinamos la función de Cxcr2 y Gscfr en la migración de neutrófilos a través de los vasos sanguíneos después de un daño estéril. Para ello realizamos dos tipos de daños estériles (severo y leve) en larvas de pez cebra Tg(Bacmpx:GFP)i114. Donde desarrollamos análisis de falta función ya sea por la microinyección de un morfolino contra Gcsfr o por la incubación con SB225002 (inhibidor químico de Cxcr2) y monitoreamos la migración de neutrófilos a distintas regiones de interés durante 3 horas. Nuestros resultados indicaron que Cxcr2 favorece la entrada de los neutrófilos a los vasos sanguíneos, así como también la llegada de estos al área inflamada en el caso de un daño estéril. Con respecto a Gcsfr nuestros resultados indican que este receptor no participa en la entrada de los neutrófilos a los vasos sanguíneos al desencadenarse un daño estéril, pero si está involucrado indirectamente en la direccionalidad de éstos al área dañada.; In mammals, the migration of neutrophils during an inflammation process is regulated by the GCSF-GCSFR signaling pathway. This cytokine and its receptor allow the exit of neutrophils from hematopoietic tissues after sterile damage. In zebrafish, Gcsf-Chr19 controls the process mentioned above, but it is unknown if this cytokine binds to Gcsfr for it. In addition, the Cxcr2 receptor also participates in this process by regulating the entry of neutrophils into the blood vessels, but in the presence of pathogens. Due to the possible differences in the signaling pathways that regulate inflammation due to sterile damage and those caused by pathogens, in addition to the possible difference between mammals and fish, we determine the function of Cxcr2 and Gscfr in the migration of neutrophils through the blood vessels after sterile damage. To achieve this goal, we performed two types of sterile damage (severe and mild) in larvae of zebrafish Tg (Bacmpx: GFP) i114. Where we developed lack function analysis either by the microinjection of a morpholino against Gcsfr or by incubation with SB225002 (chemical inhibitor of Cxcr2) and we monitored the migration of neutrophils to different regions of interest for 3 hours. Our results indicated that Cxcr2 favors the entry of neutrophils into the blood vessels, as well as the arrival of… Advisors/Committee Members: Feijóo García, Carmen Gloria (advisor).

Subjects/Keywords: Neutrófilos; Receptor CXCR2; Receptor GCSFR

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APA (6^th Edition):

Bravo Tello, K. (2018). Rol de los receptores Cxcr2 y Gcsfr en la migración de neutrófilos desde el tejido caudal hematopoyético a los vasos sanguíneos en pez cebra . (Thesis). Universidad Andrés Bello. Retrieved from http://repositorio.unab.cl/xmlui/handle/ria/6047

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):

Bravo Tello, Karina. “Rol de los receptores Cxcr2 y Gcsfr en la migración de neutrófilos desde el tejido caudal hematopoyético a los vasos sanguíneos en pez cebra .” 2018. Thesis, Universidad Andrés Bello. Accessed April 11, 2021. http://repositorio.unab.cl/xmlui/handle/ria/6047.

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

MLA Handbook (7^th Edition):

Bravo Tello, Karina. “Rol de los receptores Cxcr2 y Gcsfr en la migración de neutrófilos desde el tejido caudal hematopoyético a los vasos sanguíneos en pez cebra .” 2018. Web. 11 Apr 2021.

Vancouver:

Bravo Tello K. Rol de los receptores Cxcr2 y Gcsfr en la migración de neutrófilos desde el tejido caudal hematopoyético a los vasos sanguíneos en pez cebra . [Internet] [Thesis]. Universidad Andrés Bello; 2018. [cited 2021 Apr 11]. Available from: http://repositorio.unab.cl/xmlui/handle/ria/6047.

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

Council of Science Editors:

Bravo Tello K. Rol de los receptores Cxcr2 y Gcsfr en la migración de neutrófilos desde el tejido caudal hematopoyético a los vasos sanguíneos en pez cebra . [Thesis]. Universidad Andrés Bello; 2018. Available from: http://repositorio.unab.cl/xmlui/handle/ria/6047

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

Georgia Tech

5. Walker, Christopher L. Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application.

Degree: PhD, Chemistry and Biochemistry, 2019, Georgia Tech

URL: http://hdl.handle.net/1853/61211

► Nuclear receptors are ligand activated transcription factors that are widely distributed throughout the mammalians. There are 48 known human nuclear receptors within the body located… (more)

▼ Nuclear receptors are ligand activated transcription factors that are widely distributed throughout the mammalians. There are 48 known human nuclear receptors within the body located in various systems. While some nuclear receptors can be located wholly within certain regions and tissues the clear majority are widely distributed, overlapping expression in the same locations. The role of nuclear receptors as transcription factors has caused them to be implicated in a vast number of diseases including metabolic, cardiovascular and neurological. The role of nuclear receptors in diseases and the potential to promote ligand activated transcription makes nuclear receptors of pharmaceutical significance. Currently it is estimated that 33% of nuclear receptors are targeted by the pharmaceutical industry resulting in ~20% of pharmaceutical development worldwide. The potential to control physiological responses via introduction of a ligand to nuclear receptors has continued the interest in development of new ligands to further the understanding of nuclear receptor behavior. The challenge nuclear receptors present is to develop ligands that are selective in targeting within families and among different classes of nuclear receptors. At the core, ligand activated nuclear receptor modulation is chiefly centered around the relationship between the ligand binding pocket of the receptor and the ligand. Composed primarily of non-polar amino acid residues the ligand binding pocket is the cavity by which small hydrophobic molecules bind. Demonstrating large variance across classes of nuclear receptor and little divergence within families the ligand binding pocket serves as the focal point for targeting selectivity. Successful binding and thus receptor response is contingent upon the ligand meeting criteria established by the ligand binding pocket such as satisfactory size/volume of the ligand and key ligand-receptor amino acid residue interaction. Research conducted by Katzenellenbogen was paramount in understanding the relationship between the estrogen receptors and its ligands. His established pharmacophore unraveled features for potential ligands that are exchangeable from those that are indispensable. The commercial success of estrogen receptor ligands has fueled the interest in not only understanding ligand-receptor binding interactions but its subcellular movement. The Green Fluorescent Protein completely revolutionized the way in which cellular probing is conducted. The chromophore internally synthesized by the protein through a series of folding of amino acid residues afforded the opportunity to monitor cellular movements with the aid of fluorescence. Commonly utilized in visualization as a fusion protein, the GFP chromophore provided the ideal tool for understanding protein cellular movement and interaction. Simply put due to the chromophore that resides at the center, GFP provides the perfect technique for cellular probing. Here in we report the use of GFP-chromophore inspired ligands for utility as estrogen receptor agonist.… Advisors/Committee Members: Williams, Loren (advisor), Liotta, Charles (committee member), Snell, Terry (committee member), Oyelere, Adegboyega (committee member), Azizi, Bahareh (committee member).

Subjects/Keywords: Estrogen receptor

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

APA (6^th Edition):

Walker, C. L. (2019). Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/61211

Chicago Manual of Style (16^th Edition):

Walker, Christopher L. “Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application.” 2019. Doctoral Dissertation, Georgia Tech. Accessed April 11, 2021. http://hdl.handle.net/1853/61211.

MLA Handbook (7^th Edition):

Walker, Christopher L. “Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application.” 2019. Web. 11 Apr 2021.

Vancouver:

Walker CL. Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application. [Internet] [Doctoral dissertation]. Georgia Tech; 2019. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1853/61211.

Council of Science Editors:

Walker CL. Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application. [Doctoral Dissertation]. Georgia Tech; 2019. Available from: http://hdl.handle.net/1853/61211

University of Debrecen

6. Hegedűs, Krisztina. CB2 receptorok megoszlása gerincvelő hátsó szarvában .

Degree: DE – TEK – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, 2011, University of Debrecen

URL: http://hdl.handle.net/2437/105934

► Az endocannabinoid rendszer működése és aktivitása a szervezet legtöbb szövetében és szervében igazolt, szerepet játszik számos fiziológiai és patológiai folyamatban. A CB2 elsősorban az immunrendszer… (more)

▼ Az endocannabinoid rendszer működése és aktivitása a szervezet legtöbb szövetében és szervében igazolt, szerepet játszik számos fiziológiai és patológiai folyamatban. A CB2 elsősorban az immunrendszer sejtjeiben, valamint a hemopoetikus rendszerben expresszálódik. Sikerült kimutatni a központi idegrendszerben, agyi és gerincvelői szinten egyaránt, viszont pontos megoszlását és működésének mechanizmusát nem ismerjük. A CB2 receptor gerincvelői szinten betöltött szerepének és működésének megismerése érdekében célul tűztük ki a CB2 receptor megoszlásának vizsgálatát a gerincvelő hátsó szarvában. A kereskedelmi forgalomban kapható CB2 antitestek közül ki akartuk választani azt, amelyik specifikusan képes kimutatni a CB2 receptorokat az általunk használt kísérleti állatok, patkányok és egerek gerincvelőjének hátsó szarvában. A specifikusnak talált antitesttel vizsgálni akartuk a CB2 receptor megoszlását a lumbalis gerincvelői szürkeállomány hátsó szarvában. A rendelkezésünkre álló antitestekkel DAB és fluoreszcens alapú immunhisztokémiai reakciót végeztünk a CB2 receptor kimutatására vad típusú (Black 6), illetve CB2 K.O. egerek lumbalis gerincvelői szakaszaiból származó metszeteken. Az immunhisztokémiai reakciókkal párhuzamosan Western blot vizsgálatokat is végeztünk annak érdekében, hogy kiválaszthassuk a legspecifikusabb antitestet további vizsgálataink céljára. Az immunhisztokémiai és a Western blot vizsgálatok alapján az Abcam anti-CB2 AB 45942 antitest tűnt a legmegfelelőbbnek a teszteltek közül. További kísérleteinket az Abcam anti-CB2 AB 45942 antitestjével végeztük. A kiválasztott Abcam ab45942 antitesttel a továbbiakban patkány gerincvelő lumbalis szegmentumának metszetein fluoreszcens alapú immunhisztokémiai kettős jelöléses reakciókkal mikroglia (CD11b) és astrocita (GFAP) markerekkel kívántuk meghatározni azt, hogy a CB2 receptor gliasejteken, vagy neuronokon lokalizálódik-e a gerincvelő hátsó szarvában. A CB2 jelölés pont, illetve foltszerű festődést mutat. A mikroglia sejtek esetén a CB2 receptor főként a sejttestben helyezkedik el, megjelenése a nyúlványokon nem jellemző. Az astrocita sejteket tekintve a CB2 receptort a nyúlványokon figyelhetünk meg. A co-lokalizáció mértéke ebben az esetben szemmel láthatóan kisebb, mint a mikroglia sejtek esetén. Eredményeink az irodalmi adatokkal egybehangzóan azt mutatják, hogy a CB2 receptor a gerincvelő hátsó szarvában mikroglia és astrocita sejteken egyaránt megtalálható. A CB2 receptor gerincvelő hátsó szarvában való megoszlásának pontosabb meghatározásához további vizsgálatokra van szükség. Elektronmikroszkópos, illetve további fluoreszcens alapú immunhisztokémiai vizsgálatok és a reakciókról készült konfokális felvételek kvantitatív elemzésének eredményei eddigi eredményeinkkel együttesen nézve pontosabb képet kaphatnánk a CB2 receptor megoszlásáról a gerincvelő hátsó szarvában. Advisors/Committee Members: Antal, Miklós (advisor).

Subjects/Keywords: CB2 receptor

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

APA (6^th Edition):

Hegedűs, K. (2011). CB2 receptorok megoszlása gerincvelő hátsó szarvában . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/105934

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):

Hegedűs, Krisztina. “CB2 receptorok megoszlása gerincvelő hátsó szarvában .” 2011. Thesis, University of Debrecen. Accessed April 11, 2021. http://hdl.handle.net/2437/105934.

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

MLA Handbook (7^th Edition):

Hegedűs, Krisztina. “CB2 receptorok megoszlása gerincvelő hátsó szarvában .” 2011. Web. 11 Apr 2021.

Vancouver:

Hegedűs K. CB2 receptorok megoszlása gerincvelő hátsó szarvában . [Internet] [Thesis]. University of Debrecen; 2011. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2437/105934.

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

Council of Science Editors:

Hegedűs K. CB2 receptorok megoszlása gerincvelő hátsó szarvában . [Thesis]. University of Debrecen; 2011. Available from: http://hdl.handle.net/2437/105934

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

University of Debrecen

7. Garlati, Betina Sabrina. A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtek túlélését és migrációját glioblasztóma sejtvonalon .

Degree: DE – TEK – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, 2011, University of Debrecen

URL: http://hdl.handle.net/2437/106050

► A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtek túlélését és migrációját glioblasztóma sejtvonalon. Napjainkban számos kutatócsoport foglalkozik a molekulárisan célzott carcinogenesis… (more)

Subjects/Keywords: PDGF receptor

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APA (6^th Edition):

Garlati, B. S. (2011). A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtek túlélését és migrációját glioblasztóma sejtvonalon . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/106050

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):

Garlati, Betina Sabrina. “A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtek túlélését és migrációját glioblasztóma sejtvonalon .” 2011. Thesis, University of Debrecen. Accessed April 11, 2021. http://hdl.handle.net/2437/106050.

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

MLA Handbook (7^th Edition):

Garlati, Betina Sabrina. “A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtek túlélését és migrációját glioblasztóma sejtvonalon .” 2011. Web. 11 Apr 2021.

Vancouver:

Garlati BS. A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtek túlélését és migrációját glioblasztóma sejtvonalon . [Internet] [Thesis]. University of Debrecen; 2011. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2437/106050.

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

Council of Science Editors:

Garlati BS. A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtek túlélését és migrációját glioblasztóma sejtvonalon . [Thesis]. University of Debrecen; 2011. Available from: http://hdl.handle.net/2437/106050

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

University of Debrecen

8. Kassakürti, Zsanett. A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtproliferációt glioblasztóma sejtvonalon .

Degree: DE – TEK – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, 2011, University of Debrecen

URL: http://hdl.handle.net/2437/106152

A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtproliferációt glioblasztóma sejtvonalon. Tumoros idegsejtek növekedési faktorainak vizsgálata szignáltranszdukciós útvonalakon keresztül. Advisors/Committee Members: Szöőr, Árpád (advisor).

Subjects/Keywords: PDGF receptor

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APA (6^th Edition):

Kassakürti, Z. (2011). A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtproliferációt glioblasztóma sejtvonalon . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/106152

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):

Kassakürti, Zsanett. “A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtproliferációt glioblasztóma sejtvonalon .” 2011. Thesis, University of Debrecen. Accessed April 11, 2021. http://hdl.handle.net/2437/106152.

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

MLA Handbook (7^th Edition):

Kassakürti, Zsanett. “A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtproliferációt glioblasztóma sejtvonalon .” 2011. Web. 11 Apr 2021.

Vancouver:

Kassakürti Z. A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtproliferációt glioblasztóma sejtvonalon . [Internet] [Thesis]. University of Debrecen; 2011. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2437/106152.

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

Council of Science Editors:

Kassakürti Z. A PDGF receptorok konfluencia és lipid raft függő módon szabályozzák a sejtproliferációt glioblasztóma sejtvonalon . [Thesis]. University of Debrecen; 2011. Available from: http://hdl.handle.net/2437/106152

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

Cornell University

9. Poon, Kinning. Understanding The Single Channel Behavior Of Glua3 Receptors.

Degree: PhD, Pharmacology, 2011, Cornell University

URL: http://hdl.handle.net/1813/33563

► A tremendous amount of research has been dedicated to elucidating the functional mechanism of glutamate receptors. AMPA receptors in particular were the first in which… (more)

▼ A tremendous amount of research has been dedicated to elucidating the functional mechanism of glutamate receptors. AMPA receptors in particular were the first in which structure was correlated to function; specifically, the structures of the isolated ligand binding domain (LBD) bound to different agonists, partial agonists, and antagonists, were compared to whole cell electrophysiological recordings. A correlation between the degree of lobe closure and maximal currents was discovered; that is, the greater the degree of LBD closure, the larger the measured currents. However, as more information relating LBD closure to channel activation began to surface, it became clear the relationship was not as direct as previously thought. The studies in this dissertation look at the single channel behavior of GluA3 receptors and supply new evidence that both full and partial agonists induce a similar mechanism of activation on AMPA receptors. These studies examine how subtle changes in the LBD can affect single channel properties. GluA3 channels have three conductance levels and the probability of opening to any of these levels is dependent on the agonist; that is, full agonists are more likely to open the channel to the largest conductance level than partial agonists. GluA3 channels also display modal behaviors that are determined by the open probability and vary from very low to very high. A never before seen fast channel blocking effect is also reported. These modal behaviors are present at low agonist concentrations and observed for all the agonists tested (glutamate, FW, ClW and NO2W). The agonists tested were all able to induce full LBD closures. The stability of the closures differed in the D655/S656 peptide conformation and the M712 orientation. D655/S656 flipped conformation allows H-bonding across the lobes to occur, stabilizing LBD closures. Bulkier substituents in the 5 position of the willardiine compounds reorients M712, which could alter the M4 transmembrane helix, thereby affecting channel gating. Based on these studies, although the mechanism of activation is similar for the agonists tested, it seems that subtle dynamic conformations of amino acids in the LBD caused by agonist binding can affect the agonist induced activation. Advisors/Committee Members: Oswald, Robert Edward (chair), Lin, David M. (committee member), Weiland, Gregory Arthur (committee member), Nowak, Linda M (committee member).

Subjects/Keywords: Single Channel Recordings; AMPA Receptor; Glutamate Receptor

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APA (6^th Edition):

Poon, K. (2011). Understanding The Single Channel Behavior Of Glua3 Receptors. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/33563

Chicago Manual of Style (16^th Edition):

Poon, Kinning. “Understanding The Single Channel Behavior Of Glua3 Receptors.” 2011. Doctoral Dissertation, Cornell University. Accessed April 11, 2021. http://hdl.handle.net/1813/33563.

MLA Handbook (7^th Edition):

Poon, Kinning. “Understanding The Single Channel Behavior Of Glua3 Receptors.” 2011. Web. 11 Apr 2021.

Vancouver:

Poon K. Understanding The Single Channel Behavior Of Glua3 Receptors. [Internet] [Doctoral dissertation]. Cornell University; 2011. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1813/33563.

Council of Science Editors:

Poon K. Understanding The Single Channel Behavior Of Glua3 Receptors. [Doctoral Dissertation]. Cornell University; 2011. Available from: http://hdl.handle.net/1813/33563

University of Toronto

10. Kanawaty, Ashlin. The Role of EphB2 Receptors in the Development of Morphine Tolerance.

Degree: 2012, University of Toronto

URL: http://hdl.handle.net/1807/42889

►

Recently we have begun to investigate a novel role of EphB receptors in opiate-dependant analgesia. EphB2-β-galactosidase knockins demonstrate that EphB2 is persistently expressed within a… (more)

Subjects/Keywords: Eph receptor; Morphine; Mu opioid receptor; 0317

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APA (6^th Edition):

Kanawaty, A. (2012). The Role of EphB2 Receptors in the Development of Morphine Tolerance. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/42889

Chicago Manual of Style (16^th Edition):

Kanawaty, Ashlin. “The Role of EphB2 Receptors in the Development of Morphine Tolerance.” 2012. Masters Thesis, University of Toronto. Accessed April 11, 2021. http://hdl.handle.net/1807/42889.

MLA Handbook (7^th Edition):

Kanawaty, Ashlin. “The Role of EphB2 Receptors in the Development of Morphine Tolerance.” 2012. Web. 11 Apr 2021.

Vancouver:

Kanawaty A. The Role of EphB2 Receptors in the Development of Morphine Tolerance. [Internet] [Masters thesis]. University of Toronto; 2012. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1807/42889.

Council of Science Editors:

Kanawaty A. The Role of EphB2 Receptors in the Development of Morphine Tolerance. [Masters Thesis]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/42889

University of Manitoba

11. Chooniedass, Shilpa. The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer.

Degree: Biochemistry and Medical Genetics, 2011, University of Manitoba

URL: http://hdl.handle.net/1993/4421

► In 1999, the discovery of the Steroid Receptor RNA Activator (SRA) was unprecedented in the field of steroid receptor co-regulator research. It was the first… (more)

▼ In 1999, the discovery of the Steroid Receptor RNA Activator (SRA) was unprecedented in the field of steroid receptor co-regulator research. It was the first time that an RNA molecule was demonstrated to function similarly to its protein counterpart and modulate the activity of steroid receptors. This peculiar steroid receptor co-activator thus attracted the attention of numerous research groups. Over the years, studies were reported deciphering SRA mechanisms of action, its role in co-regulating nuclear receptors and its possible implication in human diseases. While SRA was originally thought to exist solely as a non-coding RNA, our laboratory has identified longer SRA RNA isoforms with the theoretical capacity to encode for a protein. This discovery impelled us to investigate the existence of a Steroid Receptor RNA Activator Protein or SRAP. In this thesis, we first demonstrated the existence and function of endogenous evolutionary conserved SRA proteins. Based on these results we further explored SRAP expression in breast tumors. Interestingly, Western blot analysis of a small cohort of estrogen positive breast tumors suggested that SRAP expression correlates with a better overall survival in patients treated with tamoxifen. This observation prompted us to explore the biological role of SRAP. We found that MCF-7 cells stably expressing coding SRA isoforms had lower ligand dependent estrogen receptor alpha transcriptional activity. In order to dissect the function of the protein independently of its RNA counterpart, we separated the functions of the protein by introducing extensive silent mutations into the RNA sequence. Using this model, we established that SRAP, independent of its RNA counterpart, enhances estrogen receptor alpha activity in a ligand and response-element dependent manner. Furthermore, we showed for the first time that SRAP physically interacts with multiple transcription factors and is recruited to specific promoter regions. Moreover, by artificially recruiting SRAP to the promoter of a luciferase reporter gene under the control of the strong transcriptional activator VP16, we observed a decrease in transcription. These latter results suggest that SRA could function as a repressor through direct association with promoters. Overall, we believe that SRA is a very peculiar example of a bi-faceted system consisting of a functional RNA and its corresponding protein. Altogether our data suggest that SRAP, similarly to its RNA counterpart, is involved in many critical pathways that directly participate in gene expression regulation. Advisors/Committee Members: Leygue, Etienne (Biochemistry and Medical Genetics) (supervisor), Murphy, Leigh (Biochemistry and Medical Genetics) Davie, Jim (Biochemistry and Medical Genetics) Xie, Juiyong (Physiology) (examiningcommittee).

Subjects/Keywords: steoid receptor RNA activator; estrogen receptor

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APA (6^th Edition):

Chooniedass, S. (2011). The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/4421

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):

Chooniedass, Shilpa. “The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer.” 2011. Thesis, University of Manitoba. Accessed April 11, 2021. http://hdl.handle.net/1993/4421.

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

MLA Handbook (7^th Edition):

Chooniedass, Shilpa. “The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer.” 2011. Web. 11 Apr 2021.

Vancouver:

Chooniedass S. The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer. [Internet] [Thesis]. University of Manitoba; 2011. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1993/4421.

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

Council of Science Editors:

Chooniedass S. The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer. [Thesis]. University of Manitoba; 2011. Available from: http://hdl.handle.net/1993/4421

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

George Mason University

12. Blanchard, Charles J. Vacuous Chewing Movements and Variability in Neuropeptide and Dopamine Receptor Expression in the Direct and Indirect Striatal Efferent Pathways .

Degree: 2012, George Mason University

URL: http://hdl.handle.net/1920/7518

► Tardive dyskinesia is a serious and limiting side effect in long-term neuroleptic treatment that is still poorly understood. This study examined the expression of enkephalin… (more)

Subjects/Keywords: D1 Receptor; Dynorphin; D2 Receptor; Enkephalin

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APA (6^th Edition):

Blanchard, C. J. (2012). Vacuous Chewing Movements and Variability in Neuropeptide and Dopamine Receptor Expression in the Direct and Indirect Striatal Efferent Pathways . (Thesis). George Mason University. Retrieved from http://hdl.handle.net/1920/7518

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):

Blanchard, Charles J. “Vacuous Chewing Movements and Variability in Neuropeptide and Dopamine Receptor Expression in the Direct and Indirect Striatal Efferent Pathways .” 2012. Thesis, George Mason University. Accessed April 11, 2021. http://hdl.handle.net/1920/7518.

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

MLA Handbook (7^th Edition):

Blanchard, Charles J. “Vacuous Chewing Movements and Variability in Neuropeptide and Dopamine Receptor Expression in the Direct and Indirect Striatal Efferent Pathways .” 2012. Web. 11 Apr 2021.

Vancouver:

Blanchard CJ. Vacuous Chewing Movements and Variability in Neuropeptide and Dopamine Receptor Expression in the Direct and Indirect Striatal Efferent Pathways . [Internet] [Thesis]. George Mason University; 2012. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1920/7518.

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

Council of Science Editors:

Blanchard CJ. Vacuous Chewing Movements and Variability in Neuropeptide and Dopamine Receptor Expression in the Direct and Indirect Striatal Efferent Pathways . [Thesis]. George Mason University; 2012. Available from: http://hdl.handle.net/1920/7518

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

University of Illinois – Urbana-Champaign

13. Nieves, Evelyn. Dissection of receptor functions through the generation of a tcu-PA cleavage resistant u-PAR: a u-PA independent active u-PAR.

Degree: PhD, 0318, 2013, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/42459

► The regulation of protease activity is essential for physiological events, such as angiogenesis, inflammation, wound healing, and tumor invasion. Urokinase plasminogen activator receptor (u-PAR) has… (more)

▼ The regulation of protease activity is essential for physiological events, such as angiogenesis, inflammation, wound healing, and tumor invasion. Urokinase plasminogen activator receptor (u-PAR) has been widely studied in both systemic and cellular processes. Systemic roles for u-PAR include angiogenesis, inflammation and cancer while cellular roles include cell proliferation, survival, adhesion, migration, and localizing activation of plasminogen (Pg) (Blasi, Behrendt et al. 1990; Ellis, Behrendt et al. 1991; Nguyen, Hussaini et al. 1998; Chapman, Wei et al. 1999). u-PAR exerts its effects through both proteolytic and non-proteolytic mechanisms that are inter-related. Both functions are directly affected by the activation of u-PAR through the binding of its cognate ligand, urokinase plasminogen activator (u-PA). u-PAR is a glycosidylphosphatidylinsotol (GPI)-anchored receptor that has the ability to activate Pg through localization of u-PA to the cell surface. In malignant cells, the increased glycosylation of u-PAR confers resistance to cleavage by two-chain urokinase plasminogen activator (tcu-PA) (Montuori, Rossi et al. 1999). Interestingly, the presence of highly glycosylated receptor prevents the tcu-PA from cleaving domain 1 (D1) by decreasing u-PA’s affinity for u-PAR. The central hypothesis of the work described here involves the sensitive balance that is created by the binding of u-PA to u-PAR for both the activation and functional regulation of these proteins. u-PAR has the ability to localize u-PA to the cell surface to initiate Pg activation. tcu-PA also has the ability to cleave D1 of u-PAR from the rest of the protein, which prevents localization of u-PA on the cell-surface. To explore and characterize this relationship, we engineered a mutant u-PAR that prevents cleavage of D1, and studied the effects on the activation of Pg, u-PAR dependent cellular migration and proliferation. Mutation of residues Arg 83 and Arg 89 in u-PAR leads to conformational changes that resemble the active conformation of u-PAR previously observed in crystal structures (Llinas, Le Du et al. 2005; Barinka, Parry et al. 2006; Huai, Mazar et al. 2006). Although our studies indicate that the initiation of the Pg activation cascade of our u-PAR mutants is essentially indistinguishable from wild type wt u-PAR, we also show an acceleration of the rate at which u-PA-PAI-1 complexes are cleared by 2-macroglobulin receptor/ low-density lipoprotein receptor-related protein (LRP) through u-PAR binding. In addition, we observe an increase in cell proliferation, cell migration and changes in cell morphology that correlates with an increase in ERK signaling. The u-PAR:LRP interaction we identified was remarkably novel, although one publication related u-PAR to LRP via binding the u-PA-PAI-1 complex, with u-PAR with minimal interaction via domain 3 of u-PAR (Czekay, Kuemmel et al. 2001). The u-PAR:LRP interaction we observed was supported by an increase in u-PAR detection when the mutant receptor was co-immunoprecipitated… Advisors/Committee Members: Schwartz, Bradford S. (advisor), Schwartz, Bradford S. (Committee Chair), Morrissey, James H. (committee member), Ordal, George W. (committee member), Fratti, Rutilio A. (committee member).

Subjects/Keywords: receptor; internalization; fibrinolysis; plasminogen activation; urokinase receptor

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

APA (6^th Edition):

Nieves, E. (2013). Dissection of receptor functions through the generation of a tcu-PA cleavage resistant u-PAR: a u-PA independent active u-PAR. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/42459

Chicago Manual of Style (16^th Edition):

Nieves, Evelyn. “Dissection of receptor functions through the generation of a tcu-PA cleavage resistant u-PAR: a u-PA independent active u-PAR.” 2013. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed April 11, 2021. http://hdl.handle.net/2142/42459.

MLA Handbook (7^th Edition):

Nieves, Evelyn. “Dissection of receptor functions through the generation of a tcu-PA cleavage resistant u-PAR: a u-PA independent active u-PAR.” 2013. Web. 11 Apr 2021.

Vancouver:

Nieves E. Dissection of receptor functions through the generation of a tcu-PA cleavage resistant u-PAR: a u-PA independent active u-PAR. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2013. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2142/42459.

Council of Science Editors:

Nieves E. Dissection of receptor functions through the generation of a tcu-PA cleavage resistant u-PAR: a u-PA independent active u-PAR. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2013. Available from: http://hdl.handle.net/2142/42459

University of Southern California

14. Wang, Yihui. Ultra-sensitive ethanol receptors as novel tools for alcohol and brain research: optimizing loop 2 mutations in α2 glycine receptors, γ2 and α1 γ-aminobutyric acid type A receptors.

Degree: MS, Molecular Pharmacology and Toxicology, 2015, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/553142/rec/7654

► The lack of specific knowledge on where and how ethanol acts in the CNS and the resultant neurochemical cascades leading to behavioral change limited the… (more)

Subjects/Keywords: AUD; ethanol; glycine receptor; GABA receptor

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APA (6^th Edition):

Wang, Y. (2015). Ultra-sensitive ethanol receptors as novel tools for alcohol and brain research: optimizing loop 2 mutations in α2 glycine receptors, γ2 and α1 γ-aminobutyric acid type A receptors. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/553142/rec/7654

Chicago Manual of Style (16^th Edition):

Wang, Yihui. “Ultra-sensitive ethanol receptors as novel tools for alcohol and brain research: optimizing loop 2 mutations in α2 glycine receptors, γ2 and α1 γ-aminobutyric acid type A receptors.” 2015. Masters Thesis, University of Southern California. Accessed April 11, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/553142/rec/7654.

MLA Handbook (7^th Edition):

Wang, Yihui. “Ultra-sensitive ethanol receptors as novel tools for alcohol and brain research: optimizing loop 2 mutations in α2 glycine receptors, γ2 and α1 γ-aminobutyric acid type A receptors.” 2015. Web. 11 Apr 2021.

Vancouver:

Wang Y. Ultra-sensitive ethanol receptors as novel tools for alcohol and brain research: optimizing loop 2 mutations in α2 glycine receptors, γ2 and α1 γ-aminobutyric acid type A receptors. [Internet] [Masters thesis]. University of Southern California; 2015. [cited 2021 Apr 11]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/553142/rec/7654.

Council of Science Editors:

Wang Y. Ultra-sensitive ethanol receptors as novel tools for alcohol and brain research: optimizing loop 2 mutations in α2 glycine receptors, γ2 and α1 γ-aminobutyric acid type A receptors. [Masters Thesis]. University of Southern California; 2015. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/553142/rec/7654

Vanderbilt University

15. Austin, David C. The Role of Nuclear Factor Kappa B in Benign Prostatic Hyperplasia.

Degree: PhD, Cancer Biology, 2016, Vanderbilt University

URL: http://hdl.handle.net/1803/10843

► Benign prostatic hyperplasia (BPH) is a common, progressive chronic disease. Inflammation is associated with prostatic enlargement and resistance to 5?-reductase inhibitor (5ARI) therapy. Activation of… (more)

▼ Benign prostatic hyperplasia (BPH) is a common, progressive chronic disease. Inflammation is associated with prostatic enlargement and resistance to 5?-reductase inhibitor (5ARI) therapy. Activation of the nuclear factor-kappa B (NF-?B) pathway is linked to both inflammation and ligand-independent prostate cancer progression. Most patients initially respond to 5ARI therapy; however, failure is common. To address why patients fail therapy we used transition zone tissue samples from patients with a wide range of American Urological Association symptom score (AUASS) from incidental BPH in patients treated for low grade, localized peripheral zone prostate cancer to advanced disease requiring surgical intervention. NF-?B activation and androgen receptor variant (AR-V) expression were quantified. To further investigate these pathways, human prostatic stromal and epithelial cell lines were transduced with constitutively active or kinase dead forms of IKK2 to regulate canonical NF-?B activity, AR-FL, and AR-variant 7 (AR-V7). We determined that canonical NF-?B signaling was found to be upregulated in late versus early stage BPH. Elevated expression of AR-V7 was found in advanced BPH samples. Expression of AR-V7 significantly correlated with the patient AUASS. Forced activation of canonical NF-?B in human prostatic epithelial and stromal cells resulted in elevated expression of both AR-FL and AR-V7, with concomitant ligand-independent activation of AR reporters. Activation of NF-?B and over expression of AR-V7 in human prostatic epithelial cells maintained cell viability in the face of 5ARI treatment. To understand why NF-?B and AR-V7 maintained viability within 5ARI treatment we examined the levels of 5?-reductase enzymes (SRD5A1, SRD5A2, SRD5A3). We determined that SRD5A2 is upregulated in more advanced BPH. SRD5A2 was significantly associated with AUASS and patients on a 5ARI. AR-FL and AR-V7 expression increased SRD5A2 expression whereas forced NF-?B activation increased all SRD5A isoforms. In summary, activation of NF-?B and AR-V7 in the prostate is associated with increased disease severity. Increased BPH severity in patients correlates with SRD5A2 expression. De novo synthesis of androgens and AR-V7 expression is inducible in human prostate cells by forced activation of NF-?B. NF-?B and AR-V7 upregulate SRD5A2 resulting in resistance to 5ARI treatment, suggesting a potential mechanism by which patients may become resistant to 5ARI therapy. Advisors/Committee Members: Deborah Lannigan (committee member), Simon Hayward (committee member), Dineo Khabele (committee member), Ann Richmond (committee member), Fiona Yull (Committee Chair).

Subjects/Keywords: Androgen Receptor Variant 7; Inflammation; Androgen Receptor

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

APA (6^th Edition):

Austin, D. C. (2016). The Role of Nuclear Factor Kappa B in Benign Prostatic Hyperplasia. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10843

Chicago Manual of Style (16^th Edition):

Austin, David C. “The Role of Nuclear Factor Kappa B in Benign Prostatic Hyperplasia.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed April 11, 2021. http://hdl.handle.net/1803/10843.

MLA Handbook (7^th Edition):

Austin, David C. “The Role of Nuclear Factor Kappa B in Benign Prostatic Hyperplasia.” 2016. Web. 11 Apr 2021.

Vancouver:

Austin DC. The Role of Nuclear Factor Kappa B in Benign Prostatic Hyperplasia. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1803/10843.

Council of Science Editors:

Austin DC. The Role of Nuclear Factor Kappa B in Benign Prostatic Hyperplasia. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://hdl.handle.net/1803/10843

University of Sydney

16. Woollett, Kim. Interactions between the Calcium-sensing Receptor and Type 1 Taste receptors .

Degree: 2017, University of Sydney

URL: http://hdl.handle.net/2123/17152

► The extracellular calcium sensing receptor (CaSR) heterodimerizes with other members of GPCR class C. These combinations of subunits result in the formation of novel receptors… (more)

Subjects/Keywords: Calcium-Sensing Receptor; Taste Receptor; Heterodimerization

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APA (6^th Edition):

Woollett, K. (2017). Interactions between the Calcium-sensing Receptor and Type 1 Taste receptors . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/17152

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):

Woollett, Kim. “Interactions between the Calcium-sensing Receptor and Type 1 Taste receptors .” 2017. Thesis, University of Sydney. Accessed April 11, 2021. http://hdl.handle.net/2123/17152.

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

MLA Handbook (7^th Edition):

Woollett, Kim. “Interactions between the Calcium-sensing Receptor and Type 1 Taste receptors .” 2017. Web. 11 Apr 2021.

Vancouver:

Woollett K. Interactions between the Calcium-sensing Receptor and Type 1 Taste receptors . [Internet] [Thesis]. University of Sydney; 2017. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2123/17152.

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

Council of Science Editors:

Woollett K. Interactions between the Calcium-sensing Receptor and Type 1 Taste receptors . [Thesis]. University of Sydney; 2017. Available from: http://hdl.handle.net/2123/17152

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

17. Garcia, Dioscaris R. Sigma-2 Receptor-mediated Cytotoxicity And Calcium Signaling: Evidence for Bifurcating Pathways.

Degree: PhD, Molecular Pharmacology, Physiology, and Biotechnology, 2012, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:297557/

► Sigma receptors are a unique pharmacologically defined class of drug-binding proteins comprised of the sigma-1 and sigma-2 subtypes. These subtypes are differentiated by their pharmacological… (more)

▼ Sigma receptors are a unique pharmacologically defined class of drug-binding proteins comprised of the sigma-1 and sigma-2 subtypes. These subtypes are differentiated by their pharmacological profile, functionality and size (25kDa and 21.5kDa respectively). To date, sigma receptors have been found in the CNS and peripheral organs such as liver, kidneys and pancreas and are highly expressed in tumor cells. Sigma receptors have been implicated neuronal processes such as synaptic plasticity, schizophrenia and drug abuse as well as cellular processes ranging from modulation of calcium release and neurotransmitters, growth and apoptosis and regulation of movement and posture. The sigma-2 selective ligand CB-64D has shown the ability to produce a biphasic calcium signal consisting of a rapid, transient rise followed by a delayed, prolonged calcium signal. In cytotoxicity studies, CB-64D has a dose-dependent cytotoxic effect with an EC50 of 6+/-2M under normal conditions in the SK-N-SH neuroblastoma cell line. In addition, the ability of the CB-64D analog CB-184 to induce a dose-dependent formation of Sphingosylphosphorylcholine (SPC) and ceramide, has provided additional insight on the possible second messengers responsible for modulating the apoptotic and non-cytotoxic signals. Focusing on the non-cytotoxic signal, we characterized Sphingosylphosphorylcholine in parallel with CB-64D, testing their ability to induce cell survival, proliferation and DNA-synthesis. While CB-64D showed no induction of the aforementioned effects, SPC appeared to induce cell proliferation in conditions favoring cell death. Due to the absence of an endogenous ligand or cloning of the receptor, we’ve employed the use of synthetic ligands as our primary tool for elucidating the signaling pathway of the sigma-2 receptor. Characterizing the signal transduction of the sigma-2 receptor has led to a bifurcating pathway leading to both apoptosis and non-cytotoxic signals in the neuronal SK-N-SH cell line. This bifurcation has allowed for the proposal of a sigma-2 receptor pathway model based on the signals observed from characterization of the various synthetic ligands tested to date. Advisors/Committee Members: Bowen, Wayne (Director), Marshall, John (Reader), Zimmerman, Anita (Reader), Zhitkovich, Anatoly (Reader), Matsumoto, Rae (Reader).

Subjects/Keywords: Sigma-2 Receptor

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APA (6^th Edition):

Garcia, D. R. (2012). Sigma-2 Receptor-mediated Cytotoxicity And Calcium Signaling: Evidence for Bifurcating Pathways. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:297557/

Chicago Manual of Style (16^th Edition):

Garcia, Dioscaris R. “Sigma-2 Receptor-mediated Cytotoxicity And Calcium Signaling: Evidence for Bifurcating Pathways.” 2012. Doctoral Dissertation, Brown University. Accessed April 11, 2021. https://repository.library.brown.edu/studio/item/bdr:297557/.

MLA Handbook (7^th Edition):

Garcia, Dioscaris R. “Sigma-2 Receptor-mediated Cytotoxicity And Calcium Signaling: Evidence for Bifurcating Pathways.” 2012. Web. 11 Apr 2021.

Vancouver:

Garcia DR. Sigma-2 Receptor-mediated Cytotoxicity And Calcium Signaling: Evidence for Bifurcating Pathways. [Internet] [Doctoral dissertation]. Brown University; 2012. [cited 2021 Apr 11]. Available from: https://repository.library.brown.edu/studio/item/bdr:297557/.

Council of Science Editors:

Garcia DR. Sigma-2 Receptor-mediated Cytotoxicity And Calcium Signaling: Evidence for Bifurcating Pathways. [Doctoral Dissertation]. Brown University; 2012. Available from: https://repository.library.brown.edu/studio/item/bdr:297557/

18. Thaxton, Jessica E. Toll-Like Receptor-Mediated Adverse Pregnancy Outcomes: Immune Dysregulation at the Maternal-Fetal Interface.

Degree: PhD, Division of Biology and Medicine. Pathobiology, 2009, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:134/

► Early and late term pregnancy maladies may correlate with infection and inflammation at the maternal-fetal interface. Infectious agents may manifest systemically or through intrauterine routes,… (more)

▼ Early and late term pregnancy maladies may correlate with infection and inflammation at the maternal-fetal interface. Infectious agents may manifest systemically or through intrauterine routes, and are often present at sub-clinical levels. Consequently, their ability to initiate adverse pregnancy outcomes and the mechanisms that facilitate resultant pregnancy disorders remain largely unknown. A juxtaposition exists at the maternal-fetal interface composed of a delicately regulated pro- and anti-inflammatory milieu that simultaneously allows placental growth and protection of the conceptus. Interleuikin-10 (IL-10) and Toll-like receptors (TLRs) are key components that contribute to the maintenance of equilibrium throughout pregnancy. IL-10 is a regulatory cytokine produced by the majority of cells at the maternal-fetal interface. TLRs, ubiquitous at the maternal-fetal interface, are innate immune sentinel receptors evolved to recognize pathogen associated molecular patterns (PAMPs). The central hypothesis of this work is that IL-10 deficiency coupled with an inflammatory insult may lead to adverse pregnancy outcomes mediated by dysregulation of uterine immunity through pathogenic activation of TLRs. This work explores dysregulation of the uterine immunity in response to various TLR agonists. IL-10 null and wild type (WT) mice are utilized in a pregnancy model to delineate the role of pathogenic TLR activation. We show that, in IL-10 null mice, TLR-9 activation induces an immune cascade marked by production of mKC, neutrophil and macrophage placental influx, and adverse pregnancy outcomes mediated by a TNF-a-macrophage axis. In contrast, we demonstrate that TLR-3-mediated immune dysregulation is not dependent on the availability of IL-10. Rather, in response to TLR-3 activation, IL-10 deficiency leads to an alternative program of cellular response as fetal resorption in WT mice is mediated by a uNK-TNF-a-axis, while IL-10 null mice experience fetal demise as a result of a T-cell-TNF-a axis. Finally, we show that intrauterine administration of TLR-4 agonist causes detrimental effects to the injected horn only marked by uNK cell-mediated placental pathology. Altogether, these findings elucidate novel cellular mechanisms at the maternal-fetal interface that induce adverse pregnancy outcomes in response to bacterial and viral mimics. Advisors/Committee Members: Sharma, Surendra (director), Fast, Loren (reader), Padbury, James (reader), Salazar-Mather, Thais (reader), Kwak-Kim, Joanne (reader).

Subjects/Keywords: Toll-Like Receptor

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APA (6^th Edition):

Thaxton, J. E. (2009). Toll-Like Receptor-Mediated Adverse Pregnancy Outcomes: Immune Dysregulation at the Maternal-Fetal Interface. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:134/

Chicago Manual of Style (16^th Edition):

Thaxton, Jessica E. “Toll-Like Receptor-Mediated Adverse Pregnancy Outcomes: Immune Dysregulation at the Maternal-Fetal Interface.” 2009. Doctoral Dissertation, Brown University. Accessed April 11, 2021. https://repository.library.brown.edu/studio/item/bdr:134/.

MLA Handbook (7^th Edition):

Thaxton, Jessica E. “Toll-Like Receptor-Mediated Adverse Pregnancy Outcomes: Immune Dysregulation at the Maternal-Fetal Interface.” 2009. Web. 11 Apr 2021.

Vancouver:

Thaxton JE. Toll-Like Receptor-Mediated Adverse Pregnancy Outcomes: Immune Dysregulation at the Maternal-Fetal Interface. [Internet] [Doctoral dissertation]. Brown University; 2009. [cited 2021 Apr 11]. Available from: https://repository.library.brown.edu/studio/item/bdr:134/.

Council of Science Editors:

Thaxton JE. Toll-Like Receptor-Mediated Adverse Pregnancy Outcomes: Immune Dysregulation at the Maternal-Fetal Interface. [Doctoral Dissertation]. Brown University; 2009. Available from: https://repository.library.brown.edu/studio/item/bdr:134/

19. 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 (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 April 11, 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. 11 Apr 2021.

Vancouver:

Gu H. Mass Spectrometry Analysis of Potential Biomarker Proteins. [Internet] [Doctoral dissertation]. Brown University; 2012. [cited 2021 Apr 11]. 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/

20. Johnson, Courtney Michele. Molecular Mechanisms Underlying The Human Neutrophil Response To Fungal Beta-Glucan In The Context Of The Extracellular Matrix Protein Fibronectin.

Degree: PhD, Pathobiology, 2015, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:419450/

► Complement Receptor 3 (CR3), a β2 integrin found on neutrophils, plays an important role in fungal recognition and immune response. Co-ligation of CR3 with fibronectin… (more)

▼ Complement Receptor 3 (CR3), a β2 integrin found on neutrophils, plays an important role in fungal recognition and immune response. Co-ligation of CR3 with fibronectin (Fn), an ubiquitous extracellular matrix component, at the I-domain and β-glucan (B), a glucose polymer found in fungal cell walls, at the lectin-like domain is possible due to spatially distinct locations. Dual ligation of CR3 with Fn+B induces homotypic aggregation of primed neutrophils, a response representative of the immune cells encounter with fungi within tissues and that can be blocked by anti-CR3 antibody. Previous findings have shown that CR3-mediated DNA Neutrophillic Extracellular Traps (NETS) coincide with PMN aggregates. To understand the molecular mechanisms of how CR3 coordinates these neutrophil responses, this thesis explores the role of the integrins CR3 as well as the β1 integrin family members VLA3 and VLA5. Using antibody blockade and receptor-FRET, we unexpectedly discovered a CR3-mediated required role for VLA3, the canonical laminin receptor, in aggregate formation. The role of VLA3 in aggregate formation was specific as blockade of other β1 integrin family members such as VLA5, the canonical Fn receptor, failed to prevent aggregation. Exploring the role of VLA5, we were able to show a decrease in overall VLA5 activity on Fn+B and by using an activating anti-VLA5 antibody, that active inhibition of VLA5 activity is necessary for aggregate formation. In assessing NETs formation, we discovered that unlike aggregate formation, VLA5 and CR3 are necessary for NET formation, where VLA3 is not. Furthermore, activation of VLA5 with the activating VLA5 antibody does not inhibit NET formation. Finally, a correlative signaling role for p-ERK and p-GSK-3β was determined in the neutrophil responses to β-glucan and Fn but not to either alone. Within this thesis, a novel, complex and temporally regulated cross-talk pathway was uncovered in which dual ligation of CR3 signals the differential regulation of individual β1 integrins not often associated with anti-fungal activity. Furthermore, it was discovered that NETosis and aggregation are controlled by the activation state of distinct β1 integrins, VLA5 and VLA3, respectively. Advisors/Committee Members: Reichner, Jonathan (Director), Bowen, Wayne (Reader), Bliss, Joseph (Reader), Sanders, Jennifer (Reader), Luscinskas, Francis (Reader), Fast, Loren (Director).

Subjects/Keywords: Complement Receptor 3

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APA (6^th Edition):

Johnson, C. M. (2015). Molecular Mechanisms Underlying The Human Neutrophil Response To Fungal Beta-Glucan In The Context Of The Extracellular Matrix Protein Fibronectin. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:419450/

Chicago Manual of Style (16^th Edition):

Johnson, Courtney Michele. “Molecular Mechanisms Underlying The Human Neutrophil Response To Fungal Beta-Glucan In The Context Of The Extracellular Matrix Protein Fibronectin.” 2015. Doctoral Dissertation, Brown University. Accessed April 11, 2021. https://repository.library.brown.edu/studio/item/bdr:419450/.

MLA Handbook (7^th Edition):

Johnson, Courtney Michele. “Molecular Mechanisms Underlying The Human Neutrophil Response To Fungal Beta-Glucan In The Context Of The Extracellular Matrix Protein Fibronectin.” 2015. Web. 11 Apr 2021.

Vancouver:

Johnson CM. Molecular Mechanisms Underlying The Human Neutrophil Response To Fungal Beta-Glucan In The Context Of The Extracellular Matrix Protein Fibronectin. [Internet] [Doctoral dissertation]. Brown University; 2015. [cited 2021 Apr 11]. Available from: https://repository.library.brown.edu/studio/item/bdr:419450/.

Council of Science Editors:

Johnson CM. Molecular Mechanisms Underlying The Human Neutrophil Response To Fungal Beta-Glucan In The Context Of The Extracellular Matrix Protein Fibronectin. [Doctoral Dissertation]. Brown University; 2015. Available from: https://repository.library.brown.edu/studio/item/bdr:419450/

21. Magruder, Hilary. Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression.

Degree: PhD, Pathobiology, 2014, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:386260/

► Stimulation of estrogen receptor (ER)-negative human breast cancer cells with 17β-estradiol (E2β) results in fibronectin (FN) matrix assembly and transactivation of the epidermal growth factor… (more)

▼ Stimulation of estrogen receptor (ER)-negative human breast cancer cells with 17β-estradiol (E2β) results in fibronectin (FN) matrix assembly and transactivation of the epidermal growth factor receptor (EGFR) via the G protein-coupled estrogen receptor (GPER). This mechanism of action results in the recruitment of FN-engaged integrin α5β1 to fibrillar adhesions and the formation of integrin α5β1-Shc adaptor protein complexes. Here, we show that GPER stimulation of murine 4T1 or human SKBR3 breast cancer cells promotes the formation of focal adhesions, actin stress fibers, and results in increased cellular adhesion and haptotaxis on FN, but not collagen. These actions are also induced by the xenoestrogen, bisphenol A, and the ER antagonist, ICI 182, 780, but not the inactive stereoisomer, 17α-estradiol (E2α). In addition, we show that GPER stimulation of breast cancer cells allows for FN-dependent, anchorage-independent growth and FN fibril formation in hanging drop assays, indicating that these GPER-mediated actions occur independently of adhesion to solid substrata. Furthermore, stable expression of Shc mutant Y317F lacking its primary tyrosyl phosphorylation site disrupts E2β-induced focal adhesion and actin stress fiber formation, and abolishes E2β-enhanced haptotaxis on FN and anchorage-dependent growth. We also show that overexpression of a phosphatase, PTPN12, known to interact with Shc inhibits focal adhesion and FN fibril formation, adhesion and haptotaxis on FN, and anchorage independent growth. Moreover, PTPN12 knockdown positively influences these events associated with cellular survival. Collectively, these data demonstrate that E2β action via GPER enhances cellular adhesivity and FN matrix assembly and allows for anchorage-independent growth, cellular events that may allow for cellular survival and tumor progression. Advisors/Committee Members: Filardo, Edward (Director), Reichner, Jonathan (Reader), Freiman, Richard (Reader), Yang, Wentian (Reader), Prossnitz, Eric (Reader).

Subjects/Keywords: estrogen receptor (ER)

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APA (6^th Edition):

Magruder, H. (2014). Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:386260/

Chicago Manual of Style (16^th Edition):

Magruder, Hilary. “Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression.” 2014. Doctoral Dissertation, Brown University. Accessed April 11, 2021. https://repository.library.brown.edu/studio/item/bdr:386260/.

MLA Handbook (7^th Edition):

Magruder, Hilary. “Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression.” 2014. Web. 11 Apr 2021.

Vancouver:

Magruder H. Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression. [Internet] [Doctoral dissertation]. Brown University; 2014. [cited 2021 Apr 11]. Available from: https://repository.library.brown.edu/studio/item/bdr:386260/.

Council of Science Editors:

Magruder H. Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression. [Doctoral Dissertation]. Brown University; 2014. Available from: https://repository.library.brown.edu/studio/item/bdr:386260/

22. Ellens, Elizabeth Rose. Evolution of the Growth Hormone Receptor: Insights Into the Molecular Basis of the Physiologically Pleiotropic Nature of the Growth Hormone Receptor.

Degree: 2014, North Dakota State University

URL: http://hdl.handle.net/10365/26654

► One of the oldest, extant, lineages of vertebrates, the sea lamprey, was used to clarify the evolutionary origin and divergence of the growth hormone receptor… (more)

Subjects/Keywords: Evolution; Growth hormone receptor; Lamprey; Prolactin receptor; Somatolactin receptor; Type-1 cytokine receptor

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APA (6^th Edition):

Ellens, E. R. (2014). Evolution of the Growth Hormone Receptor: Insights Into the Molecular Basis of the Physiologically Pleiotropic Nature of the Growth Hormone Receptor. (Thesis). North Dakota State University. Retrieved from http://hdl.handle.net/10365/26654

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):

Ellens, Elizabeth Rose. “Evolution of the Growth Hormone Receptor: Insights Into the Molecular Basis of the Physiologically Pleiotropic Nature of the Growth Hormone Receptor.” 2014. Thesis, North Dakota State University. Accessed April 11, 2021. http://hdl.handle.net/10365/26654.

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

MLA Handbook (7^th Edition):

Ellens, Elizabeth Rose. “Evolution of the Growth Hormone Receptor: Insights Into the Molecular Basis of the Physiologically Pleiotropic Nature of the Growth Hormone Receptor.” 2014. Web. 11 Apr 2021.

Vancouver:

Ellens ER. Evolution of the Growth Hormone Receptor: Insights Into the Molecular Basis of the Physiologically Pleiotropic Nature of the Growth Hormone Receptor. [Internet] [Thesis]. North Dakota State University; 2014. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/10365/26654.

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

Council of Science Editors:

Ellens ER. Evolution of the Growth Hormone Receptor: Insights Into the Molecular Basis of the Physiologically Pleiotropic Nature of the Growth Hormone Receptor. [Thesis]. North Dakota State University; 2014. Available from: http://hdl.handle.net/10365/26654

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

Wake Forest University

23. Perry, Rebecca Jane. Evaluation of Adipokinetic Hormone Receptor Function Suggests a Single Tissue is Responsible for Starvation Phenotypes in Drosophila.

Degree: 2016, Wake Forest University

URL: http://hdl.handle.net/10339/62638

► Adipokinetic hormone (AKH) is an insect neurohormone critical in times of metabolic stress. AKH signals to the fat body where it induces both hypertrehalosemia and… (more)

Subjects/Keywords: adipokinetic hormone receptor

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APA (6^th Edition):

Perry, R. J. (2016). Evaluation of Adipokinetic Hormone Receptor Function Suggests a Single Tissue is Responsible for Starvation Phenotypes in Drosophila. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/62638

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):

Perry, Rebecca Jane. “Evaluation of Adipokinetic Hormone Receptor Function Suggests a Single Tissue is Responsible for Starvation Phenotypes in Drosophila.” 2016. Thesis, Wake Forest University. Accessed April 11, 2021. http://hdl.handle.net/10339/62638.

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

MLA Handbook (7^th Edition):

Perry, Rebecca Jane. “Evaluation of Adipokinetic Hormone Receptor Function Suggests a Single Tissue is Responsible for Starvation Phenotypes in Drosophila.” 2016. Web. 11 Apr 2021.

Vancouver:

Perry RJ. Evaluation of Adipokinetic Hormone Receptor Function Suggests a Single Tissue is Responsible for Starvation Phenotypes in Drosophila. [Internet] [Thesis]. Wake Forest University; 2016. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/10339/62638.

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

Council of Science Editors:

Perry RJ. Evaluation of Adipokinetic Hormone Receptor Function Suggests a Single Tissue is Responsible for Starvation Phenotypes in Drosophila. [Thesis]. Wake Forest University; 2016. Available from: http://hdl.handle.net/10339/62638

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

Oregon State University

24. Phillips, Jessica Lynne. Roles for the Aryl Hydrocarbon Receptor in Tumor Suppression.

Degree: PhD, 2017, Oregon State University

URL: http://hdl.handle.net/1957/61709

► The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor of the basic helix-loop-helix PER/ARNT/SIM (bHLH/PAS) family and regulates a diverse set of genes. The… (more)

▼ The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor of the basic helix-loop-helix PER/ARNT/SIM (bHLH/PAS) family and regulates a diverse set of genes. The AhR is best known for directing the transcription of drug-metabolizing enzymes, particularly upon activation by ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polycyclic aromatic hydrocarbons (PAHs). However, the AhR also regulates gene programs upstream of organismal development, cellular differentiation, cell proliferation, and programmed cell death. The roles of AhR in mediating cellular fate coupled with its ability to respond to both exogenous and endogenous chemical signals make its behavior in the context of cancer particularly interesting. Recently, we reported that low expression of AhR correlates with poor prognosis for breast cancer patients, adding to the accumulating evidence that AhR is able to mediate tumor suppressive effects in tissues. The central hypothesis of this research is that the aryl hydrocarbon receptor functions as a tumor suppressor, and that the tumor suppressive activities of AhR can be therapeutically activated with selective AhR ligands. To test our hypothesis, we developed AhR-knockout mice lacking the tumor suppressor protein p53, mimicking the most common mutation event in the development of human cancers. The absence of AhR increased the tumor burden, tumor spectrum and reduced survival in p53-deficient mice, supporting a tumor modifier role for the AhR. Furthermore, the double-knockout of AhR and p53 resulted in reduced embryonic survival and neonatal fitness. These findings suggest important roles for the AhR in tumor suppression and development, and have significant clinical implications. To test the hypothesis that AhR is a molecular target for anti-cancer therapeutics, we screened chemical libraries for small molecules capable of both activating the AhR and inhibiting the growth of cancer cells. Of interest were the compounds that caused growth arrest or apoptosis in triple-negative breast cancer (TNBC) cells, as patients with TNBC have an extremely bleak prognosis characterized by poor responses to currently available therapeutics and a rapid rate of relapse. A short list of compounds that induced AhR-dependent anti-cancer effects was investigated to determine their mechanisms of action. One compound activated AhR-dependent transcription of cyclin-dependent kinase inhibitor 1B (CDKN1B/p27Kip1), a cell cycle inhibitor and a tumor suppressor. As transcriptional regulation of p27Kip1 is a poorly understood phenomenon with implications for cancer treatment, we performed promoter analyses to determine regions critical to regulation of p27Kip1, and found evidence of transcriptional activation of p27Kip1 by the AhR. Given the potential for drug development, we then investigated the structural analogs of the p27Kip1-inducing compound for activation of AhR and subsequent transcriptional induction of p27Kip1, and restriction of TNBC cell growth. We selected ten analogs from a list of… Advisors/Committee Members: Kolluri, Siva K. (advisor), Buermeyer, Andrew B. (committee member).

Subjects/Keywords: Aryl hydrocarbon receptor

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APA (6^th Edition):

Phillips, J. L. (2017). Roles for the Aryl Hydrocarbon Receptor in Tumor Suppression. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/61709

Chicago Manual of Style (16^th Edition):

Phillips, Jessica Lynne. “Roles for the Aryl Hydrocarbon Receptor in Tumor Suppression.” 2017. Doctoral Dissertation, Oregon State University. Accessed April 11, 2021. http://hdl.handle.net/1957/61709.

MLA Handbook (7^th Edition):

Phillips, Jessica Lynne. “Roles for the Aryl Hydrocarbon Receptor in Tumor Suppression.” 2017. Web. 11 Apr 2021.

Vancouver:

Phillips JL. Roles for the Aryl Hydrocarbon Receptor in Tumor Suppression. [Internet] [Doctoral dissertation]. Oregon State University; 2017. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1957/61709.

Council of Science Editors:

Phillips JL. Roles for the Aryl Hydrocarbon Receptor in Tumor Suppression. [Doctoral Dissertation]. Oregon State University; 2017. Available from: http://hdl.handle.net/1957/61709

University of Manitoba

25. Liu, Kun. Identification and characterization of novel ligands for human bitter taste receptor T2R7.

Degree: Oral Biology, 2017, University of Manitoba

URL: http://hdl.handle.net/1993/32876

► Humans have five basic taste sensations which are bitter, sweet, umami, salt and sour. Salt and sour are mediated by ion channel-linked receptors, while bitter,… (more)

▼ Humans have five basic taste sensations which are bitter, sweet, umami, salt and sour. Salt and sour are mediated by ion channel-linked receptors, while bitter, sweet and umami are sensed by cell surface G protein-coupled receptors (GPCRs). Among the five basic taste modalities, the bitter taste signaling mechanism is the most complex and least understood. This is in part due to the large number of bitter taste receptors (T2Rs) in humans (n=25), and the wide range of bitter compounds they detect. The T2Rs are expressed in the oral cavity as well as in many extraoral tissues. The activation of T2Rs in the oral cavity elicits bitter taste sensation, while the activation of the extraoral T2Rs causes various physiological and pathophysiological responses. Recent findings showed that T2R activation caused muscle relaxation and bronchodilation of pre-contracted airway smooth muscle. Moreover, bacterial quorum sensing molecules were shown to activate T2Rs in extraoral tissues. In view of the importance of T2R functions in extraoral tissues, it is of great value to study the structure-function relationship of T2Rs and identify efficient ligands. Hitherto, there have been few studies published involving human bitter taste receptor 7 (T2R7). Only few agonists have been identified for the T2R7 receptor, and no structure-function studies on the T2R7 receptor have been reported. In this study, different compounds including known T2R7 agonists, common bitter compounds, antibiotics and quorum sensing molecules were tested for their ability to activate or inhibit T2R7 heterologously expressed in HEK293T cells. Results suggest that T2R7 is activated by novel ligands including dextromethorphan (DXM), diphenhydramine (DPH), thiamine, tobramycin and erythromycin. In contrast, beef protein hydrolysates purified by RP-HPLC quenched quinine activated T2R7 signal. This suggests that beef hydrolysates may contain potent T2R7 blockers. To understand the structure of the ligand binding pocket in T2R7, molecular model guided site-directed mutagenesis was pursued. Eighteen mutants were made at nine amino acid positions in the ligand binding pocket of T2R7 and their expression was characterized by flow cytometry. All of the mutants were properly expressed on the cell surface. Functional characterization of the mutants including intracellular calcium mobilization in response to quinine and DXM treatment allowed mapping of the ligand binding pocket of T2R7. Taken together, this study identified novel ligands for T2R7 and elucidated the important amino acids involved in T2R7 ligand binding. Advisors/Committee Members: Chelikani, Prashen (Oral Biology) (supervisor), Bhullar, Rajinder (Oral Biology).

Subjects/Keywords: Bitter taste receptor

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

APA (6^th Edition):

Liu, K. (2017). Identification and characterization of novel ligands for human bitter taste receptor T2R7. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/32876

Chicago Manual of Style (16^th Edition):

Liu, Kun. “Identification and characterization of novel ligands for human bitter taste receptor T2R7.” 2017. Masters Thesis, University of Manitoba. Accessed April 11, 2021. http://hdl.handle.net/1993/32876.

MLA Handbook (7^th Edition):

Liu, Kun. “Identification and characterization of novel ligands for human bitter taste receptor T2R7.” 2017. Web. 11 Apr 2021.

Vancouver:

Liu K. Identification and characterization of novel ligands for human bitter taste receptor T2R7. [Internet] [Masters thesis]. University of Manitoba; 2017. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/1993/32876.

Council of Science Editors:

Liu K. Identification and characterization of novel ligands for human bitter taste receptor T2R7. [Masters Thesis]. University of Manitoba; 2017. Available from: http://hdl.handle.net/1993/32876

University of Debrecen

26. Szőllősiné Erdei, Edit. GHRH receptorok, mint molekuláris célpontok vizsgálata a humán rosszindulatú daganatok terápiájában .

Degree: DE – TEK – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, 2013, University of Debrecen

URL: http://hdl.handle.net/2437/166726

► Napjainkban az onkológiai kutatásokban egyre nagyobb szerepet kap a molekulárisan célzott terápia, melynek ígéretes célpontjai a peptidhormon receptorok, mint például a növekedési hormon-releasing hormon (GHRH)… (more)

Subjects/Keywords: GHRH receptor; tüdődaganat

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APA (6^th Edition):

Szőllősiné Erdei, E. (2013). GHRH receptorok, mint molekuláris célpontok vizsgálata a humán rosszindulatú daganatok terápiájában . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/166726

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):

Szőllősiné Erdei, Edit. “GHRH receptorok, mint molekuláris célpontok vizsgálata a humán rosszindulatú daganatok terápiájában .” 2013. Thesis, University of Debrecen. Accessed April 11, 2021. http://hdl.handle.net/2437/166726.

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

MLA Handbook (7^th Edition):

Szőllősiné Erdei, Edit. “GHRH receptorok, mint molekuláris célpontok vizsgálata a humán rosszindulatú daganatok terápiájában .” 2013. Web. 11 Apr 2021.

Vancouver:

Szőllősiné Erdei E. GHRH receptorok, mint molekuláris célpontok vizsgálata a humán rosszindulatú daganatok terápiájában . [Internet] [Thesis]. University of Debrecen; 2013. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/2437/166726.

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

Council of Science Editors:

Szőllősiné Erdei E. GHRH receptorok, mint molekuláris célpontok vizsgálata a humán rosszindulatú daganatok terápiájában . [Thesis]. University of Debrecen; 2013. Available from: http://hdl.handle.net/2437/166726

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

University of Melbourne

27. Trenker, Raphael. Investigating the structure and function of transmembrane domains in MARCH e3 ligases and single-span receptors.

Degree: 2018, University of Melbourne

URL: http://hdl.handle.net/11343/212083

► Single-span receptors play essential roles in mediating communication amongst cells of the haematopoietic system, and their single transmembrane (TM) a-helices are often important determinants for… (more)

▼ Single-span receptors play essential roles in mediating communication amongst cells of the haematopoietic system, and their single transmembrane (TM) a-helices are often important determinants for receptor function. They form specific oligomeric assemblies to communicate extracellular ligand binding into intracellular signalling events, but what the specific interactions are that govern these interfaces and how they control functionality of the full-length receptor remains poorly understood for most systems. Nonetheless, the small number of available structures of isolated TM helical assemblies determined using solution nuclear magnetic resonance (NMR) methods highlight the impact TM domain structures can have on understanding signalling and intra-membrane helix recognition. This thesis describes the development of crystallographic methods and high-throughput mutagenesis to study TM domains of single-span receptors and related systems. Using a lipidic cubic phase (LCP) crystallisation medium, I determined the first crystal structure of the intensively studied glycophorin A TM dimer in a continuous lipid bilayer, showing that hydrophobic TM peptides can be crystallised and maintain native helix-helix interactions within the crystal lattice (chapter 3). Using the same methods, I also determined the structure of a de-novo designed TM assembly that forms a strong trimer in lipid bilayers and made significant progress towards structures of three more designed oligomers (chapter 4). My efforts towards translating this method to study cytokine receptors and a family of membrane-associated RING-CH (MARCH) E3 ligases that regulate the cell-surface expression of important immunoregulatory proteins highlight remaining challenges associated with physiological membrane protein systems (chapter 5). I further show how targeted mutagenesis combined with deep mutational scanning of TM domains in MARCH-substrate interactions can provide a comprehensive mutational landscape for TM helix sequence requirements that govern substrate recognition events (chapter 6). The results presented here provide methodological frameworks to structurally and functionally analyse TM helix interactions by X-ray crystallography and content-rich mutational scanning. These methods are expected to be applicable to other biological systems to yield a better understanding of the role TM a-helices play in receptor biology and immune regulation.

Subjects/Keywords: transmembrane; receptor; MARCH

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APA (6^th Edition):

Trenker, R. (2018). Investigating the structure and function of transmembrane domains in MARCH e3 ligases and single-span receptors. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/212083

Chicago Manual of Style (16^th Edition):

Trenker, Raphael. “Investigating the structure and function of transmembrane domains in MARCH e3 ligases and single-span receptors.” 2018. Doctoral Dissertation, University of Melbourne. Accessed April 11, 2021. http://hdl.handle.net/11343/212083.

MLA Handbook (7^th Edition):

Trenker, Raphael. “Investigating the structure and function of transmembrane domains in MARCH e3 ligases and single-span receptors.” 2018. Web. 11 Apr 2021.

Vancouver:

Trenker R. Investigating the structure and function of transmembrane domains in MARCH e3 ligases and single-span receptors. [Internet] [Doctoral dissertation]. University of Melbourne; 2018. [cited 2021 Apr 11]. Available from: http://hdl.handle.net/11343/212083.

Council of Science Editors:

Trenker R. Investigating the structure and function of transmembrane domains in MARCH e3 ligases and single-span receptors. [Doctoral Dissertation]. University of Melbourne; 2018. Available from: http://hdl.handle.net/11343/212083

28. Maísa Aparecida Costa. Efeito modulatório dos receptores A1 e A2A sobre a neurotransmissão nitrérgica em culturas de células da região dorsomedial do bulbo de ratos normotensos e geneticamente hipertensos.

Degree: 2014, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-16042014-152527/

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Adenosina e óxido nítrico, importantes neuromoduladores endógenos, atuam modulando finamente o controle neural cardiovascular no núcleo de trato solitário (NTS). Embora se tenha conhecimento sobre… (more)

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Adenosina e óxido nítrico, importantes neuromoduladores endógenos, atuam modulando finamente o controle neural cardiovascular no núcleo de trato solitário (NTS). Embora se tenha conhecimento sobre a relação entre adenosina e NO periférica e centralmente, em particular, no bulbo, os mecanismos pelos quais a adenosina interfere na dinâmica da neurotransmissão nitrérgica, ainda não são totalmente conhecidos. Logo, alterações na interação entre esses sistemas podem ser especialmente relevantes para indivíduos predispostos à hipertensão. Dessa forma, os objetivos do presente estudo foram estudar a interação entre o sistema adenosinérgico e nitrérgico em culturas de células da porção dorsomedial do bulbo de ratos normotenso Wistar Kyoto (WKY) e espontaneamente hipertensos (SHR). Para tal, utilizou-se técnicas para quantificação dos níveis de nitrito, PCR em tempo real e RNA de interferência. Foi observada uma redução e um aumento concentração-dependente nos níveis de nitrito e do mRNA da nNOS induzido pelos agonistas dos receptores A1(A1R) e A2A(A>sub>2AR), CPA e CGS21680, respectivamente. Os efeitos nos níveis de nitrito foram atenuados pela administração dos antagonistas seletivos dos A1R e A2AR, CPT e ZM241385. Knockdown dos A1R e A2AR mostraram que a redução da expressão desses receptores aumentaram e diminuíram os níveis de expressão da nNOS, respectivamente. Pré-tratamento com o inibidor não seletivo da nNOS, L-NAME, aboliu os níveis aumentados de nitrito desencadeados pelo CGS21680 em células de WKY e SHR. Por fim, é mostrado que a via cAMP-PKA está envolvida na sinalização que deflaga tantos os níveis reduzidos de nitrito, via A1R, quantos os níveis aumentados de nitrito, via A2AR, em culturas de WKY e SHR. Em síntese, nossos resultados destacam a influência da adenosina sobre a síntese de NO em culturas de células da porção dorsomedial do bulbo de ratos WKY e SHR. Pelo menos em parte, o perfil modulatório é diferenciado em ratos SHR

Adenosine and nitric oxide, important endogenous neuromodulators, act on the fine tuning regulation of neural cardiovascular control in the nucleus tractus solitarius (NTS). Although the relationship between adenosine and NO peripheral and centrally, is well established, in particular, in the oblongata medulla, the mechanisms by which adenosine interferes in the dynamics of nitrergic neurotransmission, is not completely understood. Thus, changes in the interaction between these systems may be especially relevant for individuals predisposed to hypertension. The aim of this study was to evaluate the interaction between the adenosinergic and nitrergic systems in cell culture from the dorsomedial medulla oblongata of Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR). This purpose was performed the quantification of nitrite level, RT-PCR analysis and RNA interference. We observed a concentration-dependent decrease and increase of nitrite and nNOS mRNA levels in cultured cells of WKY and SHR rats induced by agonists of adenosine A1 (A1R) and A2A receptor (A2AR), CPA and…

Advisors/Committee Members: Debora Rejane Fior Chadi, Daniel Carneiro Carrettiero, Merari de Fatima Ramires Ferrari, Zulma Felisbina da Silva Ferreira, Jessica Ruivo Maximino, Cristoforo Scavone.

Subjects/Keywords: Neuromodulação; Óxido nítrico; Receptor A1; Receptor A2A; A1 receptor; A2A receptor; Neuromodulation; Nitric oxide

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

APA (6^th Edition):

Costa, M. A. (2014). Efeito modulatório dos receptores A1 e A2A sobre a neurotransmissão nitrérgica em culturas de células da região dorsomedial do bulbo de ratos normotensos e geneticamente hipertensos. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/41/41135/tde-16042014-152527/

Chicago Manual of Style (16^th Edition):

Costa, Maísa Aparecida. “Efeito modulatório dos receptores A1 e A2A sobre a neurotransmissão nitrérgica em culturas de células da região dorsomedial do bulbo de ratos normotensos e geneticamente hipertensos.” 2014. Doctoral Dissertation, University of São Paulo. Accessed April 11, 2021. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-16042014-152527/.

MLA Handbook (7^th Edition):

Costa, Maísa Aparecida. “Efeito modulatório dos receptores A1 e A2A sobre a neurotransmissão nitrérgica em culturas de células da região dorsomedial do bulbo de ratos normotensos e geneticamente hipertensos.” 2014. Web. 11 Apr 2021.

Vancouver:

Costa MA. Efeito modulatório dos receptores A1 e A2A sobre a neurotransmissão nitrérgica em culturas de células da região dorsomedial do bulbo de ratos normotensos e geneticamente hipertensos. [Internet] [Doctoral dissertation]. University of São Paulo; 2014. [cited 2021 Apr 11]. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-16042014-152527/.

Council of Science Editors:

Costa MA. Efeito modulatório dos receptores A1 e A2A sobre a neurotransmissão nitrérgica em culturas de células da região dorsomedial do bulbo de ratos normotensos e geneticamente hipertensos. [Doctoral Dissertation]. University of São Paulo; 2014. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-16042014-152527/

Universidade do Estado do Rio de Janeiro

29. Jorge Luiz Alves Pereira. Análise molecular e morfométrica da próstata ventral de ratos injetados com leptina.

Degree: Master, 2012, Universidade do Estado do Rio de Janeiro

URL: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=3870 ;

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O objetivo deste estudo foi avaliar o efeito da administração de leptina no lobo ventral da próstata de ratos adultos. Vinte ratos Wistar machos e… (more)

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O objetivo deste estudo foi avaliar o efeito da administração de leptina no lobo ventral da próstata de ratos adultos. Vinte ratos Wistar machos e adultos foram divididos em 2 grupos: L - animais foram injetados com 50 μL diária de leptina (8 μg / 100 g PC, subcutânea) durante quatro dias e C - animais receberam o mesmo volume de solução salina. Perfil lipídico e níveis séricos de testosterona foram avaliados. O lobo ventral da próstata foi processado para análise histomorfométrica. Expressão dos genes da aromatase, receptor de andrógeno, receptores de estrógeno (α e β) e as isoformas dos receptores de leptina longa (Ob-Rb) e curta (Ob-Ra) foram avaliados por PCR em tempo real. Proliferação celular foi avaliada por imuno-histoquímica com PCNA. Os dados foram expressos como média  erro padrão e analisados pelo teste t de Student. Níveis séricos de colesterol aumentaram (C = 39,7 4,2; L = 55,2 4,2, mg / dL, P ≤ 0,02) e de testosterona (C = 1,6 0,43; L = 0,6 0,15, ng / dL, P ≤ 0,03) diminuíram no grupo L. A análise histomorfométrica mostrou uma redução na densidade de células (C = 8868 242; L = 8.211 210, mm2; P ≤ 0,04), na área total (C = 0,24 0,026; L = 0,10 0,009, mm2; P ≤ 0,001) e na área interna dos ácinos (C = 0,16 0,009; L = 0,08 0,006, mm2; P ≤ 0,0002). Por outro lado, houve um aumento na altura do epitélio (C = 17,3 0,3; L = 22,8 0,2 m, P ≤ 0,0001) e no número de ácinos (C = 7,0 0,2; L = 8,7 0,1, mm2; P ≤ 0,0002). As análises histomorfométrica juntamente com os resultados imuno-histoquímicos para PCNA sugerem que a leptina aumenta a proliferação celular. Em relação à expressão gênica, o tratamento de leptina aumentou a expressão de todos os genes, mas ER-α, em mais de 200 vezes em comparação com a expressão no grupo C. Em conclusão, neste trabalho mostramos que a leptina tem um efeito direto sobre a próstata de ratos adultos levando a um aumento na proliferação celular e na expressão gênica da aromatase, receptor de androgênio, nas isoformas dos receptores de leptina e receptores de estrogênios alfa e beta que são importantes para a fisiologia normal do tecido prostático

The aim of this study was to evaluate the effect of leptin administration on the ventral prostate lobe of adult rat. Twenty adult male rats were divided into 2 groups: L - animals were daily injected with 50 μL of leptin (8 g / 100 g BW, subcutaneous) for four days and C -animals received the same volume of saline solution. Lipid profile and testosterone serum levels were evaluated. The prostate ventral lobe was processed for histomorphometric analysis. Gene expression of aromatase, androgen receptor, leptin and estrogen receptors isoforms was evaluated by real-time PCR. Cell proliferation was evaluated by PCNA immunohistochemistry. Data were expressed as mean  standard error and analyzed by students t-test. Serum levels of cholesterol (C = 39.7 4.2; L = 55.2 4.2, mg / dL; P ≤ 0.02) increased and testosterone (C = 1.6 0.43; L = 0.6 …

Advisors/Committee Members: Cristiane da Fonte Ramos, Luciano Alves Favorito, Marcelo Abidu Figueiredo, Tatiane da Silva Faria.

Subjects/Keywords: leptina; próstata; receptor de androgênio; aromatase; receptor de estrogênio; receptor de leptina; leptin; prostate; androgen receptor; aromatase; estrogen receptor; leptin receptor.; CIRURGIA PROCTOLOGICA

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

APA (6^th Edition):

Pereira, J. L. A. (2012). Análise molecular e morfométrica da próstata ventral de ratos injetados com leptina. (Masters Thesis). Universidade do Estado do Rio de Janeiro. Retrieved from http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=3870 ;

Chicago Manual of Style (16^th Edition):

Pereira, Jorge Luiz Alves. “Análise molecular e morfométrica da próstata ventral de ratos injetados com leptina.” 2012. Masters Thesis, Universidade do Estado do Rio de Janeiro. Accessed April 11, 2021. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=3870 ;.

MLA Handbook (7^th Edition):

Pereira, Jorge Luiz Alves. “Análise molecular e morfométrica da próstata ventral de ratos injetados com leptina.” 2012. Web. 11 Apr 2021.

Vancouver:

Pereira JLA. Análise molecular e morfométrica da próstata ventral de ratos injetados com leptina. [Internet] [Masters thesis]. Universidade do Estado do Rio de Janeiro; 2012. [cited 2021 Apr 11]. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=3870 ;.

Council of Science Editors:

Pereira JLA. Análise molecular e morfométrica da próstata ventral de ratos injetados com leptina. [Masters Thesis]. Universidade do Estado do Rio de Janeiro; 2012. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=3870 ;

30. 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 April 11, 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. 11 Apr 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 Apr 11]. 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

Open Access Theses and Dissertations