subject:(signaling pathway)

1. Zhang, Rengjing. Lurking Pathway Prediction And Pathway ODE Model Dynamic Analysis.

Degree: 2013, Texas Digital Library

URL: http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66737

► Signaling pathway analysis is so important to study the causes of diseases and the treatment of drugs. Finding the lurking pathway from ligand to signature… (more)

▼ Signaling pathway analysis is so important to study the causes of diseases and the treatment of drugs. Finding the lurking pathway from ligand to signature is a significant issue in studying the mechanism of how the cell response to the stimulation signal. However, recent literature based pathway analysis methods can only tell about highly differentially expressed pathways related to the experiment data, which may tell nothing about our interested specific ligand and signature. In this paper, we designed an approach to successfully detect the most reliable pathways for specific ligand and signature by solving multi-objective optimization problem on the bridge connecting two signaling pathways where the ligand and sig- nature locate. The pathway bridge consisted of enriched looping patterns refined the complicated entire protein interactions network with 39031 links, which made the approach time-saving. The approach was further applied to study the mod- ulator mechanism of the signal molecule, receptor, intermediate transfer proteins, transcription factor, and signature. With preliminary studied pathways, we then employed Ordinary Differential Equations(ODE) to modeling and dynamic analysis the signaling transduction. The biological reactions were represented in terms of differential equations, and the solu- tions to the group of equations were further be optimized to fit the RPPA experiment data. In order to find the potential signaling paths in specific disease and discovery the best therapy, coefficient variation analysis, system robustness study and system outcomes changes to perturbations were also utilized. Our approach successfully predicted the lurking pathway for the signal molecule T GF ??1 and the nova protein OC I AD2 in cancer microenviroment: T GF ??1 ???T GF ??R1 ??? SM AD2/3 ??? SM AD4/AR ??? OC I AD2, and this result was verified by literature. Better than recent pathway analysis tool, our predicted pathway also took care of significant but relatively less regulated proteins in the transduction pro- cess. And by modeling the CCL2 pathway in MTB infected cells, J N K , cM Y C and P LC showed as the most significant modules. Hence, the drug treatments inhibit- ing J N K , cM Y C and P LC would effectively obstruct the increasing of MMPs and further prevent the Mtb infections. Advisors/Committee Members: Xiong, Zixiang (advisor).

Subjects/Keywords: Signaling Pathway

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Zhang, R. (2013). Lurking Pathway Prediction And Pathway ODE Model Dynamic Analysis. (Thesis). Texas Digital Library. Retrieved from http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66737

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):

Zhang, Rengjing. “Lurking Pathway Prediction And Pathway ODE Model Dynamic Analysis.” 2013. Thesis, Texas Digital Library. Accessed January 28, 2021. http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66737.

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

MLA Handbook (7^th Edition):

Zhang, Rengjing. “Lurking Pathway Prediction And Pathway ODE Model Dynamic Analysis.” 2013. Web. 28 Jan 2021.

Vancouver:

Zhang R. Lurking Pathway Prediction And Pathway ODE Model Dynamic Analysis. [Internet] [Thesis]. Texas Digital Library; 2013. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66737.

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

Council of Science Editors:

Zhang R. Lurking Pathway Prediction And Pathway ODE Model Dynamic Analysis. [Thesis]. Texas Digital Library; 2013. Available from: http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66737

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

2. Yu, Kebing. A Phosphoproteomic Study of Insulin Signaling Pathway Using A Novel High-Throughput Pipeline.

Degree: PhD, Chemistry, 2009, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:199/

► Recent advances in the speed and sensitivity of mass spectrometers and analytical methods, the exponential acceleration of computer powers, and the availability of genomic databases… (more)

▼ Recent advances in the speed and sensitivity of mass spectrometers and analytical methods, the exponential acceleration of computer powers, and the availability of genomic databases from an array of species have led to a deluge of proteomic data. Unfortunately, this enhancement has not been accompanied by a concomitant increase in the availability of tools allowing users to efficiently analyze these data. Often the manual aggregation and analysis of proteomic data in current software distract investigators from the biological meaning of their data, leading to the all-too-frequent deposition of data into scientific literature with little biological interpretation. We seek to fill the gap by providing a high-throughput autonomous proteomic analysis pipeline with the following critical components: liquid chromatography/mass spectrometry (LC/MS) acquisition control, peptide validation, quantitative data exploration, and protein network analysis. The automated LC/MS control tool provides reproducible and sensitive multi-dimensional sample analysis. Instrument acquired data are streamlined to a customized proteomic pipeline for database searching and post-acquisition calculation. The logistic spectral score we developed for high-throughput statistical validation of database assignment outperforms SEQUEST XCorr (3.4-fold more peptides) and X!Tandem E-Value (1.9-fold more peptides) at a 1% false discovery rate estimated by decoy database. All calculation results are directed into a relational database for organization of proteomic results, collation of experimental data with available protein information resources, and visual comparison of multiple proteomic experiments. This platform provides flexible adaptation to diverse workflows for individual proteomics labs and enables proteomic scientists to modify the presentation of the proteomic data, implement extra data-dependent analysis tasks and process additional input formats. The utility of this system is illustrated through analysis of insulin signaling pathway important to liver cancers. We explored changes in phosphorylation quantitatively in hIRS1-transfected NIH3T3 cells in response to insulin stimulation using a label-free/SILAC hybrid quantitation approach. In the NIH3T3-hIRS1/NIH3T3-hIRS1 Y1180F timecourse, we discovered 2201 phosphorylation sites at 1% false discovery rate, among which 84.6% were on Serine, 13.6% were on Threonine and 1.8% were on Tyrosine. Advisors/Committee Members: Salomon, Arthur (director), Sun, Shouheng (reader), Bazemore-Walker, Carthene (reader).

Subjects/Keywords: Signaling Pathway

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Yu, K. (2009). A Phosphoproteomic Study of Insulin Signaling Pathway Using A Novel High-Throughput Pipeline. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:199/

Chicago Manual of Style (16^th Edition):

Yu, Kebing. “A Phosphoproteomic Study of Insulin Signaling Pathway Using A Novel High-Throughput Pipeline.” 2009. Doctoral Dissertation, Brown University. Accessed January 28, 2021. https://repository.library.brown.edu/studio/item/bdr:199/.

MLA Handbook (7^th Edition):

Yu, Kebing. “A Phosphoproteomic Study of Insulin Signaling Pathway Using A Novel High-Throughput Pipeline.” 2009. Web. 28 Jan 2021.

Vancouver:

Yu K. A Phosphoproteomic Study of Insulin Signaling Pathway Using A Novel High-Throughput Pipeline. [Internet] [Doctoral dissertation]. Brown University; 2009. [cited 2021 Jan 28]. Available from: https://repository.library.brown.edu/studio/item/bdr:199/.

Council of Science Editors:

Yu K. A Phosphoproteomic Study of Insulin Signaling Pathway Using A Novel High-Throughput Pipeline. [Doctoral Dissertation]. Brown University; 2009. Available from: https://repository.library.brown.edu/studio/item/bdr:199/

Univerzitet u Beogradu

3. Pantelić, Marija M., 1981-. Утицај пероралне апликације хрома на ендокрини и метаболички статус крава холштајн расе.

Degree: Fakultet veterinarske medicine, 2019, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:19217/bdef:Content/get

►

Ветеринарска медицина - Физиологија / Veterinary medicine - Physiology

Циљ ове докторске дисертације је био да се испита утицај органског комплекса тровалентног хрома на високомлечне… (more)

▼

Ветеринарска медицина - Физиологија / Veterinary medicine - Physiology

Циљ ове докторске дисертације је био да се испита утицај органског комплекса тровалентног хрома на високомлечне краве у периоду касног гравидитета и ране лактације, као и његов утицај на млечност. Тридесет дана пре очекиваног термина тељења је одабрано 20 крава холштајн расе које су подељене у две једнаке групе контролну (–Cr) и огледну (+Cr). У периоду од 25. дана пре очекиваног термина тељења до 30. дана после тељења, +Cr група крава је свакодневно перорално са јутарњим оброком добијала 10 mg, односно 5 g препарата са органски везаним хромом (0,2 % органског препарата тровалентног хрома везаног у квасцу (Co-Factor III Cr Yeast, Alltech). Интравенски тест толеранције глукозе (IVGTT) је урађен на укупно 12 крава (n=6 крава по групи) четири пута током испитиваног периода и то 28. и 7. дана пре очекиваног термина тељења као и 10. и 30. дана после тељења. Крв је узимана 0., 15., 30., 60., 90., 120. минута теста за одређивање концентрација глукозе и инсулина. Коришћењем података добијених током IVGTT урађена је и кинетика глукозе и инсулина. У узорцима крви узетим 0. минута IVGTT одређена је, поред концентрација глукозе и инсулина, концентрација NEFA (non-esterified fatty acids), BHBА (beta hydroxybutyric acid), укупних протеина, албумина, урее, холестерола, триглицерида (TG), укупног билирубина (TB), Mg, Ca, P и кортизола, као и активности AST и GGT. У циљу испитивања инсулинске резистенције периферних ткива обрачунат је RQUICKI (Revised Quantitative Insulin Sensitivity Check Index) који је показатељ осетљивости ткива на инсулин. Узорци мишићног и масног ткива су узимани биопсијом четири пута у току огледног периода и то 30. и 10. дана пре очекиваног термина тељења као и 7. и 28. дана после тељења, када је урађена и процена телесне кондиције (BCS-body condition score)...

Advisors/Committee Members: Kirovski, Danijela, 1969-.

Subjects/Keywords: bovine; chromium; insulin signaling pathway

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Pantelić, Marija M., 1. (2019). Утицај пероралне апликације хрома на ендокрини и метаболички статус крава холштајн расе. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:19217/bdef:Content/get

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

Chicago Manual of Style (16^th Edition):

Pantelić, Marija M., 1981-. “Утицај пероралне апликације хрома на ендокрини и метаболички статус крава холштајн расе.” 2019. Thesis, Univerzitet u Beogradu. Accessed January 28, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:19217/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Pantelić, Marija M., 1981-. “Утицај пероралне апликације хрома на ендокрини и метаболички статус крава холштајн расе.” 2019. Web. 28 Jan 2021.

Vancouver:

Pantelić, Marija M. 1. Утицај пероралне апликације хрома на ендокрини и метаболички статус крава холштајн расе. [Internet] [Thesis]. Univerzitet u Beogradu; 2019. [cited 2021 Jan 28]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:19217/bdef:Content/get.

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

Council of Science Editors:

Pantelić, Marija M. 1. Утицај пероралне апликације хрома на ендокрини и метаболички статус крава холштајн расе. [Thesis]. Univerzitet u Beogradu; 2019. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:19217/bdef:Content/get

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

Virginia Commonwealth University

4. Kim, Seung L. Effect of Manipulation of Notch Signaling Pathway on Neural Stem Cell Proliferation in the Hippocampus Following Traumatic Brain Injury.

Degree: MS, Anatomy & Neurobiology, 2019, Virginia Commonwealth University

URL: https://doi.org/10.25772/TRS0-X522 ; https://scholarscompass.vcu.edu/etd/5777

► Effect of Manipulation of Notch Signaling Pathway on Neural Stem Cell Proliferation in the Hippocampus Following Traumatic Brain Injury By Seung L. Kim A… (more)

▼ Effect of Manipulation of Notch Signaling Pathway on Neural Stem Cell Proliferation in the Hippocampus Following Traumatic Brain Injury By Seung L. Kim A thesis statement submitted for degree requirement in Mater of Science Virginia Commonwealth University, 2019 Advisor: Dong Sun, MD. PhD. Department of Anatomy & Neurobiology The Notch signaling pathway is known as a core signaling system in maintaining neural stem cells (NSCs) in embryonic development and adulthood including cell proliferation, maturation, and cell fate decision. Proliferation of NSCs persists throughout lifespan in neurogenic niches and is often upregulated following neurological insults including traumatic brain injury (TBI). Therefore, NSCs are viewed as the brain’s endogenous source for repair and regeneration. We speculate Notch signaling pathway is also involved in injury-induced cell proliferation in the neurogenic niche following TBI. TBI, which is a leading cause of death and disability, has been a huge burden to our society. Many efforts have been made in attempt to treat and manage TBI. In this study, we examined the involvement of Notch signaling pathway in injury induced NSC proliferation in the neurogenic niche, by administering exogenous Notch ligands including, Notch agonist or antagonist. Adult rats were intraventricularly infused with Notch1 receptor agonists (anti-Notch1 antibody at the dose of 0.5, 2 or 4μg/ml), Notch1 receptor antagonist (recombinant Jagged1 fusion protein at the dose of 25, 50 or 100μg/ml) or vehicle for 7 days following TBI. 5-bromo-2-deoxyuridine (BrdU) was administered single daily via intraperitoneal injection to label proliferating cells for 7 days post injury. The animals were sacrificed on the 7th day at 2 hours after the last BrdU injection. Sequential vibratome sliced coronal brain sections were processed for proliferation marker BrdU, Ki67 or immature neuronal marker DCX staining. BrdU, Ki67 or DCX-labeled cells in the dentate gyrus of the hippocampus were quantified using unbiased stereological method. We found TBI in the form of moderate lateral fluid percussion injury (LFPI) induced cell proliferation was further augmented by 7-day infusion of Notch agonist (Notch1-2μg/ml) as shown by BrdU and Ki67 labeling. Further, 7-day infusion of Notch antagonist (Jagged1-50μg/ml) post-injury greatly reduced the number of BrdU+ cells. However, ambiguous dose related responses were also observed where 7-day infusion of higher dose of Notch agonist (Notch1-4μg/ml) resulted in reduced cell proliferation. No major changes in the numbers of newly generated neurons were observed across the animals, except a slight reduction in Notch agonist (Notch1-2μg/ml) and Notch antagonist (Jagged1-50μg/ml) infused animals as shown by DCX labeling. Infusion of Notch agonist or antagonist affects NSC proliferation following TBI suggesting the involvement of Notch signaling pathway in regulating post-TBI NSC proliferation in the neurogenic niche. For the unexpected opposite… Advisors/Committee Members: Dong Sun.

Subjects/Keywords: Notch Signaling Pathway; Neuroscience and Neurobiology

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kim, S. L. (2019). Effect of Manipulation of Notch Signaling Pathway on Neural Stem Cell Proliferation in the Hippocampus Following Traumatic Brain Injury. (Thesis). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/TRS0-X522 ; https://scholarscompass.vcu.edu/etd/5777

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):

Kim, Seung L. “Effect of Manipulation of Notch Signaling Pathway on Neural Stem Cell Proliferation in the Hippocampus Following Traumatic Brain Injury.” 2019. Thesis, Virginia Commonwealth University. Accessed January 28, 2021. https://doi.org/10.25772/TRS0-X522 ; https://scholarscompass.vcu.edu/etd/5777.

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

MLA Handbook (7^th Edition):

Kim, Seung L. “Effect of Manipulation of Notch Signaling Pathway on Neural Stem Cell Proliferation in the Hippocampus Following Traumatic Brain Injury.” 2019. Web. 28 Jan 2021.

Vancouver:

Kim SL. Effect of Manipulation of Notch Signaling Pathway on Neural Stem Cell Proliferation in the Hippocampus Following Traumatic Brain Injury. [Internet] [Thesis]. Virginia Commonwealth University; 2019. [cited 2021 Jan 28]. Available from: https://doi.org/10.25772/TRS0-X522 ; https://scholarscompass.vcu.edu/etd/5777.

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

Council of Science Editors:

Kim SL. Effect of Manipulation of Notch Signaling Pathway on Neural Stem Cell Proliferation in the Hippocampus Following Traumatic Brain Injury. [Thesis]. Virginia Commonwealth University; 2019. Available from: https://doi.org/10.25772/TRS0-X522 ; https://scholarscompass.vcu.edu/etd/5777

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

University of Southern California

5. Ramanathan, Anita. Defining function of an autism pathway in human neuronal cells.

Degree: MS, Biochemistry and Molecular Biology, 2011, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/627881/rec/1819

► Autism is a neurodevelopmental disorder that affects 1% of the population and causes deficits in social interaction, communication and behavioral flexibility. Autism is highly heritable,… (more)

Subjects/Keywords: autism; luminex; PI3K signaling; PI3K Akt pathway

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Ramanathan, A. (2011). Defining function of an autism pathway in human neuronal cells. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/627881/rec/1819

Chicago Manual of Style (16^th Edition):

Ramanathan, Anita. “Defining function of an autism pathway in human neuronal cells.” 2011. Masters Thesis, University of Southern California. Accessed January 28, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/627881/rec/1819.

MLA Handbook (7^th Edition):

Ramanathan, Anita. “Defining function of an autism pathway in human neuronal cells.” 2011. Web. 28 Jan 2021.

Vancouver:

Ramanathan A. Defining function of an autism pathway in human neuronal cells. [Internet] [Masters thesis]. University of Southern California; 2011. [cited 2021 Jan 28]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/627881/rec/1819.

Council of Science Editors:

Ramanathan A. Defining function of an autism pathway in human neuronal cells. [Masters Thesis]. University of Southern California; 2011. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/627881/rec/1819

6. Kachrilas, Stefanos. Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως.

Degree: 2018, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/43242

►

The purpose of this PhD thesis was to examine the involvement of specific components of the PI3K/AKT pathway in urinary bladder cancer. Samples from sixty-five… (more)

▼

The purpose of this PhD thesis was to examine the involvement of specific components of the PI3K/AKT pathway in urinary bladder cancer. Samples from sixty-five tumors and thirteen normal bladder tissues were collected. Genomic DNA isolation from snap-frozen and paraffin-embedded laser-microdissected tissues was followed by Sanger sequencing, whereas total RNA was purified for use in RT-PCR analyses. Immunohistochemistry was carried out on sections of paraffin-embedded biopsy material.Three pathogenic mutations (two missense and one frameshift) were identified in exon 20 of PIK3CA {c.3140A>G (p.His1047Arg), c.[3172A>T(;)3174C>T] (p.lle1058Phe), c.3203dupA (p.Asn1068Lysfs*5)} after laser capture microdissection, whereas PTEN mRNA expression was found to be downregulated in bladder cancer tissues compared to normal bladder urothelium. Upregulation of cytoplasmic and nuclear p-AKT expression was detected in low grade tumors, whereas in muscle invasive tumors, p-AKT was shown to be downregulated and confined to the cytoplasm. PTEN expression was weak and mainly cytoplasmic in superficial tumors, but stronger and nuclear in the muscle invasive tumors.In conclusion, PI3K/AKT pathway activation is involved in bladder cancer initiation and progression. In this context, PIK3CA, p-AKT and nuclear PTEN could be used along with other biomarkers for prognostic purposes and for the selection of appropriate therapy in the clinical management of bladder cancer.

Σκοπός αυτής της διδακτορικής διατριβής ήταν να εξετάσει τη πιθανή εμπλοκή του μοριακού μονοπατιού PI3K/AKT στο καρκίνο της ουροδόχου κύστης. Πραγματοποιήθηκε λήψη δειγμάτων από εξήντα πέντε όγκους κύστης και από δεκατρία φυσιολογικούς ιστούς ουροθηλίου της κύστης. Πραγματοποιήθηκε απομόνωση DNA, ακολουθία Sanger, εξέταση RNA, RT-PCR, καθώς και ανοσοιστοχημεία. Διαπιστώθηκαν τρεις παθογενετικές μεταλλάξεις (2 missense, 1 frameshift) στο εξόνιο 20 του PIK3CA {c.3140A>G (p.His1047Arg), c.[3172A>T(;)3174C>T] (p.lle1058Phe), c.3203dupA (p.Asn1068Lysfs*5). Η έκφραση του PTEN mRNA διαπιστώθηκε ότι ήταν μειωμένη στο καρκίνο της κύστης σε σύγκριση με το φυσιολογικό ουροθήλιο της κύστης. Η έκφραση του p-AKT βρέθηκε αυξημένη στο κυτταρόπλασμα και το πυρήνα σε όγκους επιφανειακούς (μη μυοδηιθητικούς) σε αντίθεση με τους μυοδηιθητικούς όγκους όπου η έκφραση του p-AKT βρέθηκε μειωμένη και περιορισμένη κυρίως στο κυτταρόπλασμα. Η έκφραση του PTEN διαπιστώθηκε ότι ήταν ασθενής και κυρίως κυτταροπλασματική στους επιφανειακούς όγκους (μη μυοδηιθητικούς), ενώ στους μυοδιηθητικούς ήταν ισχυρότερη και κυρίως πυρηνική.Συμπερασματικά, το μοριακό μονοπάτι PI3K/AKT εμπλέκεται στην εξέλιξη του καρκίνου της ουροδόχου κύστης και η μέτρηση μορίων του (PIK3CA, p-AKT, PTEN) σε συνδυασμό και με άλλους βιοδείκτες θα μπορύσε να έχει προγνωστικό και θεραπευτικό ρόλο.

Subjects/Keywords: PI3K / Akt signaling pathway; Cancer; Bladder cancer

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kachrilas, S. (2018). Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/43242

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):

Kachrilas, Stefanos. “Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως.” 2018. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed January 28, 2021. http://hdl.handle.net/10442/hedi/43242.

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

MLA Handbook (7^th Edition):

Kachrilas, Stefanos. “Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως.” 2018. Web. 28 Jan 2021.

Vancouver:

Kachrilas S. Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2018. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/10442/hedi/43242.

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

Council of Science Editors:

Kachrilas S. Γενετικές και επιγενετικές αλλαγές στο μονοπάτι σηματοδότησης p13k / akt στον καρκίνο της ουροδόχου κύστεως. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2018. Available from: http://hdl.handle.net/10442/hedi/43242

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

University of Notre Dame

7. Anthony E Clemons. Conserved Developmental Cues of Aedes aegypti and their Impact on the Mosquito Vector</h1>.

Degree: Biological Sciences, 2014, University of Notre Dame

URL: https://curate.nd.edu/show/w089280462m

► Gene expression during embryogenesis impacts adult mosquito fitness, the ability of an organism to survive and transmit its genotype to offspring as compared to… (more)

▼ Gene expression during embryogenesis impacts adult mosquito fitness, the ability of an organism to survive and transmit its genotype to offspring as compared to competing organisms. Sequencing of the Ae. aegypti genome has made possible the characterization of many genes, but analysis of developmental genes has proven challenging, largely as a result of technical difficulties encountered when manipulating mosquito embryos. First, techniques that focused on handling/manipulation of embryos and various analytics were designed (Chapter 2). With these techniques I was able to properly rear, fix, stain and perform functional analyses on embryos. Even with these techniques, genes important to organismal development remained fairly uncharacterized. Second, we used comparative genomics to study genes in Ae. aegypti that are found to be homologous to developmental genes in Drosophila melanogaster, a genetic model organism. Doing so I was able to show that Netrin/Frazzled signaling at the CNS midline was conserved (Chapter 3) between the mosquito and fruit fly. I showed via RNAi, immunohistochemistry and in situ hybridization that frazzled (fra) expression is important for proper axon guidance. In D. melanogaster axon guidance genes are known to control salivary gland migration during development. Salivary glands are critical to disease transmission in mosquitoes. Although there was a level of gene conservation shown in CNS development, development of the salivary glands is different (Chapter 4). Lastly, there are populations of Ae. aegypti, that show differences in susceptibilities to pathogens. The noticeable physiological difference between the two is body size. Body size in all organisms is controlled by Insulin Signaling (IIS). Developmental stressors are shown to decrease overall body size, but increase longevity and pathogen resistance. Stress during development modulates IIS. Stress Signaling is activated by c-Jun N-Terminal Kinase (Jnk) and regulated by Puckered (Puc) phosphatase. I found the smaller less susceptible Moyo-R subpopulation expresses higher levels of jnk at all stages of development when compared to the larger more susceptible Moyo-S subpopulation (Chapter 5). In future studies, we intend to show RNAi of puc in Moyo-S will lead to smaller and less susceptible mosquitoes. Advisors/Committee Members: David W Severson, Committee Co-Chair, Michael Ferdig, Committee Member, Molly Duman-Scheel, Committee Co-Chair, John Duman, Committee Member, Frank Collins, Committee Member.

Subjects/Keywords: Aeded aegypti; Puckered; C-Jun N-terminal Kinase; insulin signaling pathway; stress signaling pathway

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Clemons, A. E. (2014). Conserved Developmental Cues of Aedes aegypti and their Impact on the Mosquito Vector</h1>. (Thesis). University of Notre Dame. Retrieved from https://curate.nd.edu/show/w089280462m

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):

Clemons, Anthony E. “Conserved Developmental Cues of Aedes aegypti and their Impact on the Mosquito Vector</h1>.” 2014. Thesis, University of Notre Dame. Accessed January 28, 2021. https://curate.nd.edu/show/w089280462m.

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

MLA Handbook (7^th Edition):

Clemons, Anthony E. “Conserved Developmental Cues of Aedes aegypti and their Impact on the Mosquito Vector</h1>.” 2014. Web. 28 Jan 2021.

Vancouver:

Clemons AE. Conserved Developmental Cues of Aedes aegypti and their Impact on the Mosquito Vector</h1>. [Internet] [Thesis]. University of Notre Dame; 2014. [cited 2021 Jan 28]. Available from: https://curate.nd.edu/show/w089280462m.

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

Council of Science Editors:

Clemons AE. Conserved Developmental Cues of Aedes aegypti and their Impact on the Mosquito Vector</h1>. [Thesis]. University of Notre Dame; 2014. Available from: https://curate.nd.edu/show/w089280462m

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

University of Iowa

8. Zheng, Chaoqun. Molecular mechanisms of the anti-cancer action of schweinfurthins.

Degree: PhD, Molecular and Cellular Biology, 2015, University of Iowa

URL: https://ir.uiowa.edu/etd/1815

► Schweinfurthins are a family of natural products with significant anti-cancer activities. They were originally identified in the National Cancer Institute (NCI) human 60 cancer… (more)

▼ Schweinfurthins are a family of natural products with significant anti-cancer activities. They were originally identified in the National Cancer Institute (NCI) human 60 cancer cell line screening. The growth inhibition profile of schweinfurthins is distinct from other clinically used anti-cancer agents, indicating that they have a novel mechanism of action or have a previously unrecognized protein target. Previous studies showed that schweinfurthins affect multiple cellular processes in cancer cells. For example, schweinfurthins can alter cytoskeleton organization, induce ER stress and apoptosis, and inhibit the mevalonate pathway. The mevalonate pathway is responsible for the production of isoprenoids and cholesterol, which have been shown to play regulatory roles in the Hedgehog (Hh) signaling pathway. In this study, we found that the Hh signaling pathway in NIH-3T3 and SF-295 cells was inhibited by schweinfurthins. The supplementation of mevalonate and cholesterol partially restored Hh signaling, indicating that schweinfurthins inhibit Hh signaling partially by down-regulating the products from the mevalonate pathway. Interestingly, schweinfurthins in combination with cyclopamine, an inhibitor of the Hh singaling pathway, synergistically decreased cell viability. In order to better understand the underlying mechanism of the anti-cancer action of schweinfurthins, we attempted to identify the protein target of schweifnurthins. Affinity chromatography was performed to pull down the protein target. We found that schweinfurhtins bound to the M2 isoform of pyruvate kinase (PKM2) and inhibit its pyruvate kinase activity. Knockdown of PKM2 by siRNA increased the sensitivity of SF-295 cells to schweinfurthins. The inhibition of PKM2 by schweinfurthins led to a reduction in the rate of glycolysis in cancer cells. Fructose 1,6-bisphosphate (FBP), an activator of PKM2, could alleviate schweinfurthin-mediated inhibition on PKM2 and glycolysis. Notably, FBP could also partially reverse the reduction of cell viability in the presence of schweinfurthins. Taken together, these studies revealed the mechanism by which schweinfurthins inhibit Hh signaling. In addition, we uncovered PKM2 as a schwienfurthin target and highlighted the importance of glycolysis suppression as a mechanism of the anti-cancer action of schweinfurthins. Advisors/Committee Members: Hohl, Raymond J. (supervisor).

Subjects/Keywords: publicabstract; glioblastoma; glycolysis; PKM2; schweinfurthins; the Hedgehog signaling pathway; the mevalonate pathway; Cell Biology

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Zheng, C. (2015). Molecular mechanisms of the anti-cancer action of schweinfurthins. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/1815

Chicago Manual of Style (16^th Edition):

Zheng, Chaoqun. “Molecular mechanisms of the anti-cancer action of schweinfurthins.” 2015. Doctoral Dissertation, University of Iowa. Accessed January 28, 2021. https://ir.uiowa.edu/etd/1815.

MLA Handbook (7^th Edition):

Zheng, Chaoqun. “Molecular mechanisms of the anti-cancer action of schweinfurthins.” 2015. Web. 28 Jan 2021.

Vancouver:

Zheng C. Molecular mechanisms of the anti-cancer action of schweinfurthins. [Internet] [Doctoral dissertation]. University of Iowa; 2015. [cited 2021 Jan 28]. Available from: https://ir.uiowa.edu/etd/1815.

Council of Science Editors:

Zheng C. Molecular mechanisms of the anti-cancer action of schweinfurthins. [Doctoral Dissertation]. University of Iowa; 2015. Available from: https://ir.uiowa.edu/etd/1815

Baylor University

9. Hudson, Geoffrey Marcus. The effects of resveratrol supplementation on glucose/insulin kinetics and transcription of the AMPK and insulin signaling pathway at rest and following an oral glucose tolerance and graded exercise test in overweight women.

Degree: PhD, Health, Human Performance and Recreation., 2010, Baylor University

URL: http://hdl.handle.net/2104/8033

► The AMPK pathway plays a critical role in glucose metabolism and can potentially improve insulin resistance. Resveratrol is a natural polyphenolic compound that activates this… (more)

▼ The AMPK pathway plays a critical role in glucose metabolism and can potentially improve insulin resistance. Resveratrol is a natural polyphenolic compound that activates this pathway. Therefore, the primary purpose of this study was to determine the effects of daily activation of the AMPK pathway by resveratrol supplementation on glucose/insulin kinetics and transcriptional changes in the AMPK and insulin signaling pathway at rest and following an oral glucose tolerance test (OGTT) and graded exercise test (GXT). Sixteen sedentary, overweight women were recruited for the study. In a randomized and double blind fashion, participants were divided into groups that consumed either 500 mg of resveratrol or a cellulose placebo twice daily for 7 days. On the sixth and seventh day, they returned for an OGTT and a GXT, respectively. Blood and muscle tissue was sampled prior to, and following both the OGTT and GXT. Multivariate analyses revealed no significant changes in resting serum glucose and insulin concentrations (p = 0.255), clinical chemistry safety markers (p = 0.309), or lipid profile panels (p = 0.051) following 7 days of resveratrol supplementation. Following the OGTT, serum glucose concentration was significantly increased 30 min (p < 0.001) and at 1 hr compared to baseline (p = 0.001). However, only a strong trend (p = 0.051) for increased serum insulin concentration was observed following the OGTT. The GXT protocol produced significant changes in serum glucose and insulin concentration. Glucose concentrations were significantly decreased at 1 hr when compared to baseline (p = 0.01) and 30 min (p = 0.032) post-exercise. Insulin concentrations were decreased at 1 hr (p = 0.012) and 2 hrs (p = 0.003) post-exercise. Resveratrol supplementation was unable to enhance such responses. No significant changes were observed with any of the genes analyzed. As a result, it appears that one week of resveratrol supplementation (500 mg/day) is not sufficient to enhance glucose/insulin homeostasis or transcription of metabolically-relevant genes in sedentary, overweight women. Since diabetes is still an increasing global health concern, it is evident that more research is needed to find ways to prevent and/or treat insulin resistance. Advisors/Committee Members: Willoughby, Darryn Scott, 1963- (advisor), Cooke, Matthew B. (advisor).

Subjects/Keywords: Resveratrol.; Exercise physiology.; AMPK signaling pathway.; Insulin signaling pathway.

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Hudson, G. M. (2010). The effects of resveratrol supplementation on glucose/insulin kinetics and transcription of the AMPK and insulin signaling pathway at rest and following an oral glucose tolerance and graded exercise test in overweight women. (Doctoral Dissertation). Baylor University. Retrieved from http://hdl.handle.net/2104/8033

Chicago Manual of Style (16^th Edition):

Hudson, Geoffrey Marcus. “The effects of resveratrol supplementation on glucose/insulin kinetics and transcription of the AMPK and insulin signaling pathway at rest and following an oral glucose tolerance and graded exercise test in overweight women.” 2010. Doctoral Dissertation, Baylor University. Accessed January 28, 2021. http://hdl.handle.net/2104/8033.

MLA Handbook (7^th Edition):

Hudson, Geoffrey Marcus. “The effects of resveratrol supplementation on glucose/insulin kinetics and transcription of the AMPK and insulin signaling pathway at rest and following an oral glucose tolerance and graded exercise test in overweight women.” 2010. Web. 28 Jan 2021.

Vancouver:

Hudson GM. The effects of resveratrol supplementation on glucose/insulin kinetics and transcription of the AMPK and insulin signaling pathway at rest and following an oral glucose tolerance and graded exercise test in overweight women. [Internet] [Doctoral dissertation]. Baylor University; 2010. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/2104/8033.

Council of Science Editors:

Hudson GM. The effects of resveratrol supplementation on glucose/insulin kinetics and transcription of the AMPK and insulin signaling pathway at rest and following an oral glucose tolerance and graded exercise test in overweight women. [Doctoral Dissertation]. Baylor University; 2010. Available from: http://hdl.handle.net/2104/8033

University of Maine

10. Muthukrishnan, Sree Deepthi. Combinatorial Growth Factor Signaling Controls Nephron Progenitor Renewal and Differentiation.

Degree: PhD, Biomedical Sciences, 2016, University of Maine

URL: https://digitalcommons.library.umaine.edu/etd/2703

► Self-renewal and differentiation of nephron progenitor cells (NPCs) in the developing kidney is governed by three major growth factor pathways: BMP, FGF and WNT.… (more)

Subjects/Keywords: kidney development; nephron progenitors; BMP7 signaling; MAPK andSMAD pathway; AP-1 transcription factors; FGF signaling

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Muthukrishnan, S. D. (2016). Combinatorial Growth Factor Signaling Controls Nephron Progenitor Renewal and Differentiation. (Doctoral Dissertation). University of Maine. Retrieved from https://digitalcommons.library.umaine.edu/etd/2703

Chicago Manual of Style (16^th Edition):

Muthukrishnan, Sree Deepthi. “Combinatorial Growth Factor Signaling Controls Nephron Progenitor Renewal and Differentiation.” 2016. Doctoral Dissertation, University of Maine. Accessed January 28, 2021. https://digitalcommons.library.umaine.edu/etd/2703.

MLA Handbook (7^th Edition):

Muthukrishnan, Sree Deepthi. “Combinatorial Growth Factor Signaling Controls Nephron Progenitor Renewal and Differentiation.” 2016. Web. 28 Jan 2021.

Vancouver:

Muthukrishnan SD. Combinatorial Growth Factor Signaling Controls Nephron Progenitor Renewal and Differentiation. [Internet] [Doctoral dissertation]. University of Maine; 2016. [cited 2021 Jan 28]. Available from: https://digitalcommons.library.umaine.edu/etd/2703.

Council of Science Editors:

Muthukrishnan SD. Combinatorial Growth Factor Signaling Controls Nephron Progenitor Renewal and Differentiation. [Doctoral Dissertation]. University of Maine; 2016. Available from: https://digitalcommons.library.umaine.edu/etd/2703

Purdue University

11. Karim, Md Shahriar. QUANTITATIVE MODELING OF SCALING OF PATTERNS AND RECEPTOR SIGNALING IN MORPHOGENESIS.

Degree: PhD, Agricultural and Biological Engineering, 2016, Purdue University

URL: https://docs.lib.purdue.edu/open_access_dissertations/1368

► Organs and tissue development often experience perturbations, but developmental processes seem to replicate a common body template to maintain appropriate proportions and positions. The key… (more)

Subjects/Keywords: BMP signaling pathway; Computational models; Morphogen signaling; Noise in BMP signaling; Pattern formation and scaling; Reaction-diffusion systems

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Karim, M. S. (2016). QUANTITATIVE MODELING OF SCALING OF PATTERNS AND RECEPTOR SIGNALING IN MORPHOGENESIS. (Doctoral Dissertation). Purdue University. Retrieved from https://docs.lib.purdue.edu/open_access_dissertations/1368

Chicago Manual of Style (16^th Edition):

Karim, Md Shahriar. “QUANTITATIVE MODELING OF SCALING OF PATTERNS AND RECEPTOR SIGNALING IN MORPHOGENESIS.” 2016. Doctoral Dissertation, Purdue University. Accessed January 28, 2021. https://docs.lib.purdue.edu/open_access_dissertations/1368.

MLA Handbook (7^th Edition):

Karim, Md Shahriar. “QUANTITATIVE MODELING OF SCALING OF PATTERNS AND RECEPTOR SIGNALING IN MORPHOGENESIS.” 2016. Web. 28 Jan 2021.

Vancouver:

Karim MS. QUANTITATIVE MODELING OF SCALING OF PATTERNS AND RECEPTOR SIGNALING IN MORPHOGENESIS. [Internet] [Doctoral dissertation]. Purdue University; 2016. [cited 2021 Jan 28]. Available from: https://docs.lib.purdue.edu/open_access_dissertations/1368.

Council of Science Editors:

Karim MS. QUANTITATIVE MODELING OF SCALING OF PATTERNS AND RECEPTOR SIGNALING IN MORPHOGENESIS. [Doctoral Dissertation]. Purdue University; 2016. Available from: https://docs.lib.purdue.edu/open_access_dissertations/1368

NSYSU

12. Tai , Po-han. Therapeutic potential and mechanism of LECT2 for liver cancer.

Degree: Master, Institute of Biomedical Sciences, 2014, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0621114-111413

► Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. However, current therapeutic modalities for HCC, including surgery, transendothelial embolization (TAE) and… (more)

Subjects/Keywords: Î²-catenin; Hepatocellular carcinoma; Wnt signaling pathway; Cancer stem cell; LECT2

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Tai , P. (2014). Therapeutic potential and mechanism of LECT2 for liver cancer. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0621114-111413

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):

Tai , Po-han. “Therapeutic potential and mechanism of LECT2 for liver cancer.” 2014. Thesis, NSYSU. Accessed January 28, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0621114-111413.

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

MLA Handbook (7^th Edition):

Tai , Po-han. “Therapeutic potential and mechanism of LECT2 for liver cancer.” 2014. Web. 28 Jan 2021.

Vancouver:

Tai P. Therapeutic potential and mechanism of LECT2 for liver cancer. [Internet] [Thesis]. NSYSU; 2014. [cited 2021 Jan 28]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0621114-111413.

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

Council of Science Editors:

Tai P. Therapeutic potential and mechanism of LECT2 for liver cancer. [Thesis]. NSYSU; 2014. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0621114-111413

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

NSYSU

13. Wu, Ping-Hsuan. The role of LECT2 in liver carcinogenesis.

Degree: Master, Biological Sciences, 2011, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0824111-001511

► Leukocyte cell-derived chemotaxin 2 (LECT2) is first isolated as a 16-kDa secreted protein from cultured fluid of phytohemagglutinin-activated human T-cell leukemia SKW-3 cells. Recently LECT2… (more)

Subjects/Keywords: Wnt pathway; Î²-catenin; Hepatocellular carcinoma; cellular signaling; LECT2

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Wu, P. (2011). The role of LECT2 in liver carcinogenesis. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0824111-001511

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):

Wu, Ping-Hsuan. “The role of LECT2 in liver carcinogenesis.” 2011. Thesis, NSYSU. Accessed January 28, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0824111-001511.

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

MLA Handbook (7^th Edition):

Wu, Ping-Hsuan. “The role of LECT2 in liver carcinogenesis.” 2011. Web. 28 Jan 2021.

Vancouver:

Wu P. The role of LECT2 in liver carcinogenesis. [Internet] [Thesis]. NSYSU; 2011. [cited 2021 Jan 28]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0824111-001511.

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

Council of Science Editors:

Wu P. The role of LECT2 in liver carcinogenesis. [Thesis]. NSYSU; 2011. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0824111-001511

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

University of Otago

14. Kőszegi, Zsombor. Restorative effect of estrogen on basal forebrain cholinergic neurons .

Degree: 2011, University of Otago

URL: http://hdl.handle.net/10523/1887

► The basal forebrain cholinergic (BFC) system is one of the most important neurotransmitter systems in the brain. It has received much attention in the past… (more)

▼ The basal forebrain cholinergic (BFC) system is one of the most important neurotransmitter systems in the brain. It has received much attention in the past two decades, primarily for its role in learning, memory, attention and behavior. The BFC system has also been reported to be particularly vulnerable in neurodegenerative diseases, such as in Alzheimer’s disease (AD). The gonadal steroid, estrogen, is an essential contributor in controlling the vulnerability of the BFC system. Besides its classical or genomic mechanism, estrogen is known to have non-classical actions on intracellular signaling pathways. In this study, we investigated the ameliorative effects of estrogen treatment and the role of non-classical estrogen actions on BFC neurons in a neurodegenerative mouse model, in vivo. N-methyl-D-aspartate (NMDA) was injected unilaterally into the substantia innominata - nucleus basalis magnocellularis (SI-NBM) complex of the basal forebrain to elicit cholinergic cell death in the injected area and thus fiber loss in the ipsilateral cortex. An acute treatment of 17β-estradiol (E2) after the NMDA-induced lesion restored the ipsilateral cholinergic fiber density in the cortex in a time- and dose-dependent manner. Conversely, it did not have any effect on the cholinergic cell loss in the SI-NBM. The ameliorative action of E2 on cholinergic fiber loss was detected in both intact and gonadectomized young male and female mice, but not in aged animals. The E2-induced cholinergic fiber density restoration was also absent in neuron-specific estrogen receptor α (ERα) knockout mice. Selective blockade of the mitogen activated protein kinase (MAPK) and protein kinase A (PKA) pathways prevented E2’s ability to restore the cholinergic fiber density. Furthermore, activation of non-classical estrogen signaling by a non-classical pathway activator (estren) induced E2-like fiber restoration. Our findings demonstrate that estrogen restores the cholinergic fiber density in the cortex through a non-classical signaling mechanism after the loss of subcortical cholinergic input. Similar restorative effects were observed in young animals, irrespective of sex or endogenous estrogen levels. These observations reveal a critical role for non-classical estrogen signaling via ERα and MAPK-PKA pathways in BFC neurons, in vivo. Taken together, our study discloses important aspects relating to the vulnerability of the BFC system in neurodegenerative processes, such as AD or traumatic brain injury and might shed light on future medical treatments through the use of non-classical estrogen pathway activators. Advisors/Committee Members: Ábrahám, István (advisor).

Subjects/Keywords: estrogen; cholinergic; basal forebrain; neurodegeneration; non-classical; signaling pathway

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kőszegi, Z. (2011). Restorative effect of estrogen on basal forebrain cholinergic neurons . (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/1887

Chicago Manual of Style (16^th Edition):

Kőszegi, Zsombor. “Restorative effect of estrogen on basal forebrain cholinergic neurons .” 2011. Doctoral Dissertation, University of Otago. Accessed January 28, 2021. http://hdl.handle.net/10523/1887.

MLA Handbook (7^th Edition):

Kőszegi, Zsombor. “Restorative effect of estrogen on basal forebrain cholinergic neurons .” 2011. Web. 28 Jan 2021.

Vancouver:

Kőszegi Z. Restorative effect of estrogen on basal forebrain cholinergic neurons . [Internet] [Doctoral dissertation]. University of Otago; 2011. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/10523/1887.

Council of Science Editors:

Kőszegi Z. Restorative effect of estrogen on basal forebrain cholinergic neurons . [Doctoral Dissertation]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/1887

Mississippi State University

15. Song, Jie. Molecular and proteomic analysis of components involved in abscisic acid (ABA) signaling network.

Degree: PhD, Biochemistry, Molecular Biology, Entomology and Plant Pathology, 2014, Mississippi State University

URL: http://sun.library.msstate.edu/ETD-db/theses/available/etd-10152014-032027/ ;

► Abscisic acid is an important plant hormone in the responses to biotic and abiotic stresses, which also regulates various growth and developmental processes in… (more)

▼ Abscisic acid is an important plant hormone in the responses to biotic and abiotic stresses, which also regulates various growth and developmental processes in plants. Three major components-receptors (PYRs), the PP2C type phosphatases and the SnRK2 subtype kinases form a double negative regulatory system: PYR/PYL/RCARs inhibit the activity of PP2Cs while PP2Cs inhibit that of SnRK2s in ABA signaling pathway. The results of my studies showed that ABA would directly affect the interaction between SnRK2.2 and ABI1 in absence of PYRs. Furthermore, ABA can inhibit the catalytic activity of the SnRK2.2 kinase. These findings indicated that ABA may directly interact with SnRK2.2. Posttranslational modifications play a key role in signal transduction. Phosphorylation is the most important posttranscriptional modification in ABA signal transduction. To dissect new components in ABA signaling network in plants, proteomics studies were carried out in Arabidopsis for identifying ABA- responsive phosphoproteins. Ten phosphoproteins, ATPB, ATPC1, FBA1, CTIMC, GGAT1, GAPC1, GAPC2, GAPA1 and ALDH11A3, were identified by 2-DE proteomic approach and LC-MS/MS analysis. These proteins are likely to be the potential phosphorylated targets of SnRK2s in ABA signaling network. Lysine acetylation (LysAc) also emerges as one of the important posttranslational modifications for protein regulation in plants. Eleven lysine acetylated proteins with altered acetylation in response to ABA were identified in Arabidopsis using proteomic approach. The increased LysAc of Rubisco and the decreased Rubisco activity by ABA treatment indicates the acetylation of Rubisco caused by ABA resulted in the inhibition of Rubisco activity. ABA has also been shown to exist and function in both lower animals and mammalians. The medical application of ABA has become a new area of investigation. To explore the role of protein phosphorylation in ABA-mediated function in mammalians, phosphoproteomic study was conducted in mouse 3T3-L1 cells. Ten phosphoproteins with significant changes in serine/threonine phosphorylation in response to ABA were identified. These results suggest these phosphoproteins are involved in ABA signaling network in mouse cells. The significance of the function of SFRS1, ANXA1 and Galectin-3 on human diseases indicated that ABA could be a potential treatment for some human diseases, such as cancer. Advisors/Committee Members: Jiaxu Li (chair), Din-Pow Ma (committee member), Zhaohua Peng (committee member), Daniel G. Peterson (committee member), Scott T. Willard (committee member).

Subjects/Keywords: ABACABA signaling pathway; Arabidopsis; proteomics; phosphorylation; acetylation; 3T3-L1 mouse cells

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Song, J. (2014). Molecular and proteomic analysis of components involved in abscisic acid (ABA) signaling network. (Doctoral Dissertation). Mississippi State University. Retrieved from http://sun.library.msstate.edu/ETD-db/theses/available/etd-10152014-032027/ ;

Chicago Manual of Style (16^th Edition):

Song, Jie. “Molecular and proteomic analysis of components involved in abscisic acid (ABA) signaling network.” 2014. Doctoral Dissertation, Mississippi State University. Accessed January 28, 2021. http://sun.library.msstate.edu/ETD-db/theses/available/etd-10152014-032027/ ;.

MLA Handbook (7^th Edition):

Song, Jie. “Molecular and proteomic analysis of components involved in abscisic acid (ABA) signaling network.” 2014. Web. 28 Jan 2021.

Vancouver:

Song J. Molecular and proteomic analysis of components involved in abscisic acid (ABA) signaling network. [Internet] [Doctoral dissertation]. Mississippi State University; 2014. [cited 2021 Jan 28]. Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-10152014-032027/ ;.

Council of Science Editors:

Song J. Molecular and proteomic analysis of components involved in abscisic acid (ABA) signaling network. [Doctoral Dissertation]. Mississippi State University; 2014. Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-10152014-032027/ ;

University of Alberta

16. Bostan, Babak. Predicting homologous signaling pathways using machine learning.

Degree: MS, Department of Computing Science, 2009, University of Alberta

URL: https://era.library.ualberta.ca/files/765372669

► Understanding biochemical reactions inside cells of individual organisms is a key factor for improving our biological knowledge. Signaling pathways provide a road map for a… (more)

Subjects/Keywords: signaling pathway; machine learning; prediction; support vector machine

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Bostan, B. (2009). Predicting homologous signaling pathways using machine learning. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/765372669

Chicago Manual of Style (16^th Edition):

Bostan, Babak. “Predicting homologous signaling pathways using machine learning.” 2009. Masters Thesis, University of Alberta. Accessed January 28, 2021. https://era.library.ualberta.ca/files/765372669.

MLA Handbook (7^th Edition):

Bostan, Babak. “Predicting homologous signaling pathways using machine learning.” 2009. Web. 28 Jan 2021.

Vancouver:

Bostan B. Predicting homologous signaling pathways using machine learning. [Internet] [Masters thesis]. University of Alberta; 2009. [cited 2021 Jan 28]. Available from: https://era.library.ualberta.ca/files/765372669.

Council of Science Editors:

Bostan B. Predicting homologous signaling pathways using machine learning. [Masters Thesis]. University of Alberta; 2009. Available from: https://era.library.ualberta.ca/files/765372669

McMaster University

17. Law, Fiona. Characterization of RanBPM in Drosophila melanogaster.

Degree: MSc, 2011, McMaster University

URL: http://hdl.handle.net/11375/11477

►

RanBPM is a conserved putative scaffold protein of unknown function. Loss-of-function in RanBPM leads to pleiotropic phenotypes such as reduced locomotion, decreased size and… (more)

Subjects/Keywords: Drosophila melanogaster; RanBPM; NMJ; insulin signaling pathway; Developmental Biology; Developmental Biology

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Law, F. (2011). Characterization of RanBPM in Drosophila melanogaster. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/11477

Chicago Manual of Style (16^th Edition):

Law, Fiona. “Characterization of RanBPM in Drosophila melanogaster.” 2011. Masters Thesis, McMaster University. Accessed January 28, 2021. http://hdl.handle.net/11375/11477.

MLA Handbook (7^th Edition):

Law, Fiona. “Characterization of RanBPM in Drosophila melanogaster.” 2011. Web. 28 Jan 2021.

Vancouver:

Law F. Characterization of RanBPM in Drosophila melanogaster. [Internet] [Masters thesis]. McMaster University; 2011. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/11375/11477.

Council of Science Editors:

Law F. Characterization of RanBPM in Drosophila melanogaster. [Masters Thesis]. McMaster University; 2011. Available from: http://hdl.handle.net/11375/11477

University of Texas Southwestern Medical Center

18. Kulak, Ozlem. Chemical Disruption of Wnt Signaling and Telomere Length Maintenance.

Degree: 2015, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/4110

►

Pages xvii-xviii of the dissertation are incorrectly numbered as pages xvi-xvii.

A nearly universal feature of colorectal cancer (CRC) incidents is the presence of genetic… (more)

Subjects/Keywords: Enzyme Inhibitors; Tankyrases; Telomere Shortening; Wnt Signaling Pathway

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kulak, O. (2015). Chemical Disruption of Wnt Signaling and Telomere Length Maintenance. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/4110

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):

Kulak, Ozlem. “Chemical Disruption of Wnt Signaling and Telomere Length Maintenance.” 2015. Thesis, University of Texas Southwestern Medical Center. Accessed January 28, 2021. http://hdl.handle.net/2152.5/4110.

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

MLA Handbook (7^th Edition):

Kulak, Ozlem. “Chemical Disruption of Wnt Signaling and Telomere Length Maintenance.” 2015. Web. 28 Jan 2021.

Vancouver:

Kulak O. Chemical Disruption of Wnt Signaling and Telomere Length Maintenance. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2015. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/2152.5/4110.

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

Council of Science Editors:

Kulak O. Chemical Disruption of Wnt Signaling and Telomere Length Maintenance. [Thesis]. University of Texas Southwestern Medical Center; 2015. Available from: http://hdl.handle.net/2152.5/4110

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

Wayne State University

19. Donato, Michele. Systems Biology Approaches For The Analysis Of High-Throughput Biological Data.

Degree: PhD, Computer Science, 2016, Wayne State University

URL: https://digitalcommons.wayne.edu/oa_dissertations/1396

► The identification of biological processes involved with a certain phenotype, such as a disease or drug treatment, is the goal of the majority of… (more)

Subjects/Keywords: Impact Analysis; Microarrays; Pathway Analysis; Signaling Pathways; Systems Biology; Bioinformatics

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Donato, M. (2016). Systems Biology Approaches For The Analysis Of High-Throughput Biological Data. (Doctoral Dissertation). Wayne State University. Retrieved from https://digitalcommons.wayne.edu/oa_dissertations/1396

Chicago Manual of Style (16^th Edition):

Donato, Michele. “Systems Biology Approaches For The Analysis Of High-Throughput Biological Data.” 2016. Doctoral Dissertation, Wayne State University. Accessed January 28, 2021. https://digitalcommons.wayne.edu/oa_dissertations/1396.

MLA Handbook (7^th Edition):

Donato, Michele. “Systems Biology Approaches For The Analysis Of High-Throughput Biological Data.” 2016. Web. 28 Jan 2021.

Vancouver:

Donato M. Systems Biology Approaches For The Analysis Of High-Throughput Biological Data. [Internet] [Doctoral dissertation]. Wayne State University; 2016. [cited 2021 Jan 28]. Available from: https://digitalcommons.wayne.edu/oa_dissertations/1396.

Council of Science Editors:

Donato M. Systems Biology Approaches For The Analysis Of High-Throughput Biological Data. [Doctoral Dissertation]. Wayne State University; 2016. Available from: https://digitalcommons.wayne.edu/oa_dissertations/1396

University of Adelaide

20. Alanazi, Ibrahim Oqla. Understanding the apoptotic signaling pathways in breast cancer using microarrays, proteomics and bioinformatics.

Degree: 2014, University of Adelaide

URL: http://hdl.handle.net/2440/92350

► Breast cancer is one of the most common causes of cancer death to women worldwide. In this study A431 cells, derived from epidermoid carcinoma, are… (more)

▼ Breast cancer is one of the most common causes of cancer death to women worldwide. In this study A431 cells, derived from epidermoid carcinoma, are used as a model to study breast cancer. This cell line over-expresses the Epidermal Growth Factor Receptor (EGFR/HER1) and when treated with a high dose of EGF will undergo apoptosis via the activation of EGFR/HER1 signaling. However, little work has been conducted to identify the underlying molecular mechanisms. The limited available data implicates components of the interferon response pathway as mediators of the apoptotic signal in cancer cells. The genetic network through which EGFR/HER1 can induce apoptosis is not known at the present time. With understanding of the genetic regulatory hierarchy and the molecular mechanisms linking EGFR/HER1 signaling and apoptosis, better drug targets that might regulate apoptosis in cancers that over express HERs can be identified. This thesis focuses on the hypothesis that an apoptosis specific signalling cascade can be triggered by HERs in A431cells. Activation of HER receptors has led us to identify downstream components by global analyses of gene expression and associated regulatory miRNAs and protein levels using microarray and proteomics platforms. A high dose of EGF leads to the induction of apoptosis in A431 cells by activating a number of pathways, which are known to promote apoptosis. These include the STAT pathway and downstream components including cytokines and suppressors of cytokine signalling, cleavage of serpinb1 into L-DNAaseII and down regulation of mutant TP53, which may perturb the cytoskeleton and cell adhesion proteins. Furthermore, our data showed that gene expression and proteomic data were quite different, with very little overlap in terms of transcripts and proteins. Therefore, we considered that post-transcriptional regulation might be crucial. MicroRNAs are known to be important post-transcriptional regulators; as a result, we sought to identify potential regulatory miRNAs with respect to induction of cell death by EGF. We identified novel interaction regulatory networks based on the crosstalk between miRNAs and mRNA/protein that resulted in the induction of apoptosis in A431 cells. We also identified a number of miRNAs that may play an important role in the regulation of apoptosis in A431 cells after EGF treatment. We have used bioinformatics databases and in silico analysis tools to create a comprehensive catalogue of genes/proteins that may induce apoptosis in A431 cell after EGF treatment. We have shown that using various complimentary platforms including gene expression, miRNA expression, proteomics, and network prediction to analyse the induction of apoptosis in treated A431 cells, we have achieved a greater understanding of the molecular mechanisms at work. This in turn may provide strategies for combined therapies and/or predict novel potential mechanisms/targets for chemotherapy aimed at inducing cell death in tumor cells. Advisors/Committee Members: Adelson, David Louis (advisor), Hoffmann, Peter (advisor), School of Molecular and Biomedical Science (school).

Subjects/Keywords: breast cancer; apoptotic signaling pathway; microarray; proteomics; bioinformatics

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Alanazi, I. O. (2014). Understanding the apoptotic signaling pathways in breast cancer using microarrays, proteomics and bioinformatics. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/92350

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):

Alanazi, Ibrahim Oqla. “Understanding the apoptotic signaling pathways in breast cancer using microarrays, proteomics and bioinformatics.” 2014. Thesis, University of Adelaide. Accessed January 28, 2021. http://hdl.handle.net/2440/92350.

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

MLA Handbook (7^th Edition):

Alanazi, Ibrahim Oqla. “Understanding the apoptotic signaling pathways in breast cancer using microarrays, proteomics and bioinformatics.” 2014. Web. 28 Jan 2021.

Vancouver:

Alanazi IO. Understanding the apoptotic signaling pathways in breast cancer using microarrays, proteomics and bioinformatics. [Internet] [Thesis]. University of Adelaide; 2014. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/2440/92350.

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

Council of Science Editors:

Alanazi IO. Understanding the apoptotic signaling pathways in breast cancer using microarrays, proteomics and bioinformatics. [Thesis]. University of Adelaide; 2014. Available from: http://hdl.handle.net/2440/92350

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

University of Miami

21. Sun-Suslow, Ni. The Oxytocin Receptor as an Acute Phase Protein and its Signaling Pathways in Response to Inflammation.

Degree: MS, Psychology (Arts and Sciences), 2015, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_theses/566

► Social environment influences the progression of atherosclerosis, a chronic inflammatory process. Oxytocin (OT) has been associated with pro-social behavior; however, plasma OT levels are not… (more)

▼ Social environment influences the progression of atherosclerosis, a chronic inflammatory process. Oxytocin (OT) has been associated with pro-social behavior; however, plasma OT levels are not elevated in a pro-social environment in animal models of disease. Infusion of exogenous OT in these disease models attenuates inflammation and arterial plaque, which raises the possibility that OT’s anti-inflammatory effects may be regulated at the level of the OT receptor (OTR) rather than by changes in plasma OT titers as a function of social environment. The current study investigated OTR and signaling pathways in human macrophages to understand how inflammation affects the OT/OTR system at the molecular level. We hypothesized that OTR is an acute phase protein, whose expression is increased during the inflammatory response though a nuclear factor κB (NF-κB) mediated pathway. We further evaluated whether inflammation alters OTR signaling pathways, which can occur through either the phosphatidylinositol (PI) (Gαq/11) or the cAMP (Gαs) pathways. Inflammation was induced by treating THP-1 macrophages with lipopolysaccharide (LPS) and monitored by expression of the inflammatory cytokine, interleukin-6 (IL-6). Cells were treated with exogenous IL-6 and NF- κB inhibitor and OTR gene expression was measured by RT-PCR. OTR signaling was evaluated by phosphorylation of downstream targets, ERK1/2 from the PI pathway, and CREB from the cAMP pathway, by immunoblotting after LPS and OT treatments. Induction of inflammation by LPS stimulation of macrophages significantly up-regulated OTR transcription 150-fold relative to control cell, however IL-6 had no effect on OTR expression. Blocking NF-κB activation prevented the increase in OTR transcription. Our data also confirmed OT-treatment of macrophages inhibits LPS stimulated IL-6 secretion. Incubation of LPS-treated cells with OT caused increased phosphorylation of ERK1/2 and CREB. Individual blocking of Gαq/11 and Gαs RNA resulted in a loss of OT’s ability to down-regulate IL-6. Together these results demonstrate receptor function through both Gαq/11 and Gαs signaling pathways during inflammation. OTR is an acute phase protein, whose expression can be regulated by NF-κB. Current data suggest both the PI and cAMP signaling pathways are activated by OTR during an inflammatory response and that the receptor may be responsible for attenuating the inflammatory response of the macrophage. This study is the first to demonstrate OT's effect on the non-conventional cAMP signaling pathway in this cell line and the importance of OTR in regulating inflammation. This suggests OTR regulation/function should be considered in addition to measurement of plasma OT. Advisors/Committee Members: Philip M. McCabe, Armando J. Mendez, Neil Schneiderman.

Subjects/Keywords: Oxytocin Receptor; Oxytocin; Inflammation; Acute Phase Protein; Signaling Pathway

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Sun-Suslow, N. (2015). The Oxytocin Receptor as an Acute Phase Protein and its Signaling Pathways in Response to Inflammation. (Thesis). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_theses/566

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):

Sun-Suslow, Ni. “The Oxytocin Receptor as an Acute Phase Protein and its Signaling Pathways in Response to Inflammation.” 2015. Thesis, University of Miami. Accessed January 28, 2021. https://scholarlyrepository.miami.edu/oa_theses/566.

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

MLA Handbook (7^th Edition):

Sun-Suslow, Ni. “The Oxytocin Receptor as an Acute Phase Protein and its Signaling Pathways in Response to Inflammation.” 2015. Web. 28 Jan 2021.

Vancouver:

Sun-Suslow N. The Oxytocin Receptor as an Acute Phase Protein and its Signaling Pathways in Response to Inflammation. [Internet] [Thesis]. University of Miami; 2015. [cited 2021 Jan 28]. Available from: https://scholarlyrepository.miami.edu/oa_theses/566.

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

Council of Science Editors:

Sun-Suslow N. The Oxytocin Receptor as an Acute Phase Protein and its Signaling Pathways in Response to Inflammation. [Thesis]. University of Miami; 2015. Available from: https://scholarlyrepository.miami.edu/oa_theses/566

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

University of Toronto

22. Martin, Tonya. Glypican-3 Stimulates the WNT Signaling Pathway by Facilitating/Stabilizing the Interaction of WNT LIigand and Frizzled Receptor.

Degree: 2010, University of Toronto

URL: http://hdl.handle.net/1807/25850

►

Glypican-3 (GPC3) belongs to a family of cell surface proteoglycans. GPC3 regulates the activity of several morphogens and growth factors that play critical roles during… (more)

Subjects/Keywords: Glypican-3; Glypicans; Frizzled; Wnt pathway; Cell Signaling; 0379; 0307

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Martin, T. (2010). Glypican-3 Stimulates the WNT Signaling Pathway by Facilitating/Stabilizing the Interaction of WNT LIigand and Frizzled Receptor. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/25850

Chicago Manual of Style (16^th Edition):

Martin, Tonya. “Glypican-3 Stimulates the WNT Signaling Pathway by Facilitating/Stabilizing the Interaction of WNT LIigand and Frizzled Receptor.” 2010. Masters Thesis, University of Toronto. Accessed January 28, 2021. http://hdl.handle.net/1807/25850.

MLA Handbook (7^th Edition):

Martin, Tonya. “Glypican-3 Stimulates the WNT Signaling Pathway by Facilitating/Stabilizing the Interaction of WNT LIigand and Frizzled Receptor.” 2010. Web. 28 Jan 2021.

Vancouver:

Martin T. Glypican-3 Stimulates the WNT Signaling Pathway by Facilitating/Stabilizing the Interaction of WNT LIigand and Frizzled Receptor. [Internet] [Masters thesis]. University of Toronto; 2010. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1807/25850.

Council of Science Editors:

Martin T. Glypican-3 Stimulates the WNT Signaling Pathway by Facilitating/Stabilizing the Interaction of WNT LIigand and Frizzled Receptor. [Masters Thesis]. University of Toronto; 2010. Available from: http://hdl.handle.net/1807/25850

Univerzitet u Beogradu

23. Popić, Jelena. 1978-. Uticaj propofola na signalni put neurotrofina u prednjem mozgu pacova starih 14 dana.

Degree: Biološki fakultet, 2012, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:2344/bdef:Content/get

►

Biologija - molekularna neurobiologija / Biology - molecular neurobiology

Neurotrofini čine familiju signalnih molekula sa brojnim uticajima na rast, preživljavanje, diferencijaciju i sinaptičku plastičnost postmitotskih… (more)

▼

Biologija - molekularna neurobiologija / Biology - molecular neurobiology

Neurotrofini čine familiju signalnih molekula sa brojnim uticajima na rast, preživljavanje, diferencijaciju i sinaptičku plastičnost postmitotskih neurona, kako u adultnom mozgu, tako i u mozgu tokom razvića. Neurotrofini (BDNF, NGF) se sa određenim afinitetom vezuju za Trk receptore, iniciraju njihovu dimerizaciju i autofosforilaciju i na taj način se pokreće aktivacija signalnih puteva kao što su PI3K/Akt i MAPK/ERK. Akt i ERK kinaze imaju ključne regulatorne uloge u mozgu u procesima kao što su neuronalna proliferacija, diferencijacija, razviće, migracija, preživljavanje i dugotrajna sinaptička plastičnost. Aktivan (fosforilisan) Akt štiti ćeliju od apoptoze tako što stimuliše ekspresiju proteina koji favorizuju preživljavanje ćelija i sa druge strane inhibira egzekutorske kaspaze. Aktivacija ERK1/2 kinaze pomoviše preživljavanje, međutim u određenim uslovima ERK1/2 može imati i pro-apoptotske odlike. S obzirom da je uloga neurotrofina u neurotoksičnosti koja je indukovana anestezijom tokom ranog postnatalnog razvića pokazana u nekoliko studija, cilj ove doktorske disertacije je bio da se na molekulskom nivou ispitaju promene u signalnom putu neurotrofina koje nastaju u kori i talamusu postnatalnih pacova nakon primene anestetske doze propofola, kao i da se utvrdi potencijal tretmana da indukuje ćelijsku smrt i/ili promene u sinaptičkoj plastičnosti. Nakon jednokratne primene propofola (25 mg/kg i.p.) ispitana je vremenska i prostorna ekspresija neurotrofina BDNF i NGF, njihovih aktiviranih receptora TrkB, TrkA i p75 receptora, kao i nishodnih kinaza Akt i ERK kod 14 dana starih (PND14) pacova. Ispitan je i potencijal propofolskog tretman da indukuje ćelijsku smrt, praćenjem ekspresije TNF-α, TNFR1, aktivnog fragmenta kaspaze-3, njegovog inhibitora XIAP proteina, kao i transkripcionog faktora NFκB. Finalno je ispitivan potencijal propofolskog tretmana da indukuje promene u ekspresiji markera sinaptičke plastičnosti (MAP-2, drebrina, GAP-43, sinaptofizina, sinukleina-1 i N-kadherina). Promene su praćene u kori i talamusu kao primarnim ciljevima dejstva anestetskog delovanja. Primenom sledećih metoda Western blot analize, RT- i PCR-a u realnom vremenu ispitivane su promene u ekspresiji ciljnih proteina i iRNK, a primenom Fluoro-žad B histološkog bojenja analizirana je pojava neurona u degeneraciji...

Advisors/Committee Members: Kanazir, Selma.

Subjects/Keywords: Propofol; cortex; thalamus; postnatal development; neurotrophic signaling pathway; neuroapoptosis; synaptic plasticity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Popić, J. 1. (2012). Uticaj propofola na signalni put neurotrofina u prednjem mozgu pacova starih 14 dana. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:2344/bdef:Content/get

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

Chicago Manual of Style (16^th Edition):

Popić, Jelena 1978-. “Uticaj propofola na signalni put neurotrofina u prednjem mozgu pacova starih 14 dana.” 2012. Thesis, Univerzitet u Beogradu. Accessed January 28, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:2344/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Popić, Jelena 1978-. “Uticaj propofola na signalni put neurotrofina u prednjem mozgu pacova starih 14 dana.” 2012. Web. 28 Jan 2021.

Vancouver:

Popić J1. Uticaj propofola na signalni put neurotrofina u prednjem mozgu pacova starih 14 dana. [Internet] [Thesis]. Univerzitet u Beogradu; 2012. [cited 2021 Jan 28]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:2344/bdef:Content/get.

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

Council of Science Editors:

Popić J1. Uticaj propofola na signalni put neurotrofina u prednjem mozgu pacova starih 14 dana. [Thesis]. Univerzitet u Beogradu; 2012. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:2344/bdef:Content/get

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

Univerzitet u Beogradu

24. Milivojević, Milena C., 1979-. Uloga Sonic Hedgehog signalnog puta u regulaciji ekspresije SOX18 gena u HeLa ćelijama, kao model sistemu karcinoma grlića materice.

Degree: Biološki fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:10796/bdef:Content/get

►

Biologija - Molekularna biologija / Biology - Molecular biology

Sonic Hedgehog (SHH) signalni put ima važnu ulogu u procesima koji se odvijaju tokom embrionalnog razvića… (more)

▼

Biologija - Molekularna biologija / Biology - Molecular biology

Sonic Hedgehog (SHH) signalni put ima važnu ulogu u procesima koji se odvijaju tokom embrionalnog razvića u kojima kontroliše proliferaciju i diferencijaciju ćelija i učestvuje u održavanju polarnosti tkiva. Poslednjih godina mnogobrojni literaturni podaci pokazuju da promena u regulaciji SHH signalnog puta dovodi do nastanka i progresije različitih vrsta tumora kod čoveka. SHH signalni put je povezan sa meduloblastomom, leukemijom, karcinomom bazalnih ćelija, tumorima pluća, prostate, pancreasa, dojke i jajnika. Takođe, povećana ekspresija komponenti SHH signalnog puta je primećena u premalignim lezijama i ćelijama karcinoma grlića materice. SOX18 gen pripada familiji SOX gena koji kodiraju transkripcione faktore uključene u kontrolu različitih procesa tokom embrionalnog razvića. SOX18 protein ima važnu ulogu u razviću vaskularnog sistema kao i u adultnoj neovaskularizaciji. Uloga SOX18 proteina u vaskularnom razviću otkrivena je na osnovu poremećaja u razvoju vaskularnog sistema koji su uočeni kod prirodnih mutanata miša i čoveka. Osim toga, kod adultnog organizma SOX18 protein učestvuje u regulaciji angiogeneze i limfangiogeneze kako u fiziološkim stanjima organizma, tako i tokom patofizioloških promena kao što su zarastanje rana i tumorska angiogeneza. Takođe, pokazano je da se inhibicijom SOX18 funkcije utiče na limfangiogenezu čime se sprečava metastaza ćelija tumora. Najnoviji podaci pokazuju da je ekspresija SOX18 gena, detektovana u ćelijama invazivnog karcinoma dojke i tumora jajnika, a nivo ekspresije je u direktnoj korelaciji sa stadijumom tumora i može predstavljati prognostički marker. Predmet istraživanja prikazanog u ovom radu je bila analiza uloge SHH signalnog puta u regulaciji ekspresije SOX18 gena u HeLa ćelijama, in vitro model sistemu karcinoma grlića materice. Prvo je analizirana uloga GLI regulatornih proteina, finalnih efektora SHH signalne kaskade, u regulaciji transkripcije SOX18 gena. Prikazani rezultati su pokazali da su GLI1 i GLI2 pozitivni regulatori promotorske aktivnosti SOX18 gena kao i da povećavaju endogenu ekspresiju SOX18 gena, dok GLI3 transkripcioni faktor nije uticao na aktivnost SOX18 promotorskog konstrukta niti na nivo endogene ekspresije SOX18 gena u HeLa ćelijama...

Advisors/Committee Members: Petrović, Isidora.

Subjects/Keywords: SHH signaling pathway; SOX18; transcription factor; transcription regulation; migration; proliferation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Milivojević, Milena C., 1. (2016). Uloga Sonic Hedgehog signalnog puta u regulaciji ekspresije SOX18 gena u HeLa ćelijama, kao model sistemu karcinoma grlića materice. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:10796/bdef:Content/get

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

Chicago Manual of Style (16^th Edition):

Milivojević, Milena C., 1979-. “Uloga Sonic Hedgehog signalnog puta u regulaciji ekspresije SOX18 gena u HeLa ćelijama, kao model sistemu karcinoma grlića materice.” 2016. Thesis, Univerzitet u Beogradu. Accessed January 28, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:10796/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Milivojević, Milena C., 1979-. “Uloga Sonic Hedgehog signalnog puta u regulaciji ekspresije SOX18 gena u HeLa ćelijama, kao model sistemu karcinoma grlića materice.” 2016. Web. 28 Jan 2021.

Vancouver:

Milivojević, Milena C. 1. Uloga Sonic Hedgehog signalnog puta u regulaciji ekspresije SOX18 gena u HeLa ćelijama, kao model sistemu karcinoma grlića materice. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Jan 28]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:10796/bdef:Content/get.

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

Council of Science Editors:

Milivojević, Milena C. 1. Uloga Sonic Hedgehog signalnog puta u regulaciji ekspresije SOX18 gena u HeLa ćelijama, kao model sistemu karcinoma grlića materice. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:10796/bdef:Content/get

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

University of Washington

25. Fagnan, Erin. Mechanisms for Scaffold-Mediated Regulation of Kinase Activity in the Wnt Signaling Pathway.

Degree: PhD, 2019, University of Washington

URL: http://hdl.handle.net/1773/44746

► Cellular signaling is a complex process involving numerous pathways. Many of these pathways are connected through shared proteins, creating branch points that may result in… (more)

Subjects/Keywords: Axin; Cell Signaling; GSK3; Scaffold Proteins; Wnt pathway; Chemistry; Biochemistry; Chemistry

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Fagnan, E. (2019). Mechanisms for Scaffold-Mediated Regulation of Kinase Activity in the Wnt Signaling Pathway. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/44746

Chicago Manual of Style (16^th Edition):

Fagnan, Erin. “Mechanisms for Scaffold-Mediated Regulation of Kinase Activity in the Wnt Signaling Pathway.” 2019. Doctoral Dissertation, University of Washington. Accessed January 28, 2021. http://hdl.handle.net/1773/44746.

MLA Handbook (7^th Edition):

Fagnan, Erin. “Mechanisms for Scaffold-Mediated Regulation of Kinase Activity in the Wnt Signaling Pathway.” 2019. Web. 28 Jan 2021.

Vancouver:

Fagnan E. Mechanisms for Scaffold-Mediated Regulation of Kinase Activity in the Wnt Signaling Pathway. [Internet] [Doctoral dissertation]. University of Washington; 2019. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/1773/44746.

Council of Science Editors:

Fagnan E. Mechanisms for Scaffold-Mediated Regulation of Kinase Activity in the Wnt Signaling Pathway. [Doctoral Dissertation]. University of Washington; 2019. Available from: http://hdl.handle.net/1773/44746

University of Minnesota

26. Baik, June. The role of endoglin during mesoderm specification.

Degree: PhD, Molecular, Cellular, Developmental Biology and Genetics, 2015, University of Minnesota

URL: http://hdl.handle.net/11299/181778

► Embryogenesis requires spatiotemporally regulated cellular signals and gene expressions that influence lineage specification, progenitor patterning, and morphogenesis. However the molecular mechanisms that explain how the… (more)

Subjects/Keywords: Cardiogenesis; Embryoid bodies; Endoglin; Hematopoiesis; Mesoderm; Signaling pathway

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Baik, J. (2015). The role of endoglin during mesoderm specification. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/181778

Chicago Manual of Style (16^th Edition):

Baik, June. “The role of endoglin during mesoderm specification.” 2015. Doctoral Dissertation, University of Minnesota. Accessed January 28, 2021. http://hdl.handle.net/11299/181778.

MLA Handbook (7^th Edition):

Baik, June. “The role of endoglin during mesoderm specification.” 2015. Web. 28 Jan 2021.

Vancouver:

Baik J. The role of endoglin during mesoderm specification. [Internet] [Doctoral dissertation]. University of Minnesota; 2015. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/11299/181778.

Council of Science Editors:

Baik J. The role of endoglin during mesoderm specification. [Doctoral Dissertation]. University of Minnesota; 2015. Available from: http://hdl.handle.net/11299/181778

University of Southern California

27. He, Kaijie. The cancer stem-like phenotype: therapeutics, phenotypic plasticity and mechanistic studies.

Degree: PhD, Genetic, Molecular and Cellular Biology, 2012, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/61631/rec/6485

► Cancer claims over 500,000 lives in the U.S. annually, a mortality rate that is largely attributable to solid tumors that have metastasized and become resistant… (more)

▼ Cancer claims over 500,000 lives in the U.S. annually, a mortality rate that is largely attributable to solid tumors that have metastasized and become resistant to available treatments. This type of disease progression may be mediated by cancer stem cells (CSC), rare and unique cancer cells recently identified in many types of malignancies, and these CSC are thought to play a central role in tumor formation, therapy-resistance, and ultimately cancer progression and metastasis. ❧ Unfortunately, however, to date there are very few effective CSC-targeting therapies. To address this question, we isolated a putative CSC population from human prostate tumors and cell lines, and we showed for the first time that these cells possess extremely high telomerase activity relative to the bulk, unselected cancer cells. Strikingly, telomerase interference – reprogramming telomerase to add incorrect “toxic” telomeres – could induce rapid apoptosis and marked growth inhibition in prostate CSC and abrogated their ability to form new tumors in SCID mice, which offers the first tumor-derived and in vivo evidence that telomerase may ultimately form the basis for more effective new CSC-targeting therapies. ❧ The drug resistant and brisk tumor initiation abilities have been viewed as pre-existing phenotypes only present in the small subpopulation of cancer stem cells, and they have been intuitively conceptualized as self-renewing founder cells from which more differentiated cancer cells derive. However, recent work in cancer cell lines has demonstrated that drug-resistant tumor initiating features can emerge de novo within fractionated subpopulations of cells initially lacking these phenotypes. In our study, we used a “side population” cancer stem cell model with GFP-labeling technique, and demonstrated for the first time that adaptive, cancer-promoting traits like drug-resistance and brisk tumor initiation arise not only as solitary events under selective pressures, but also as highly orchestrated transitions occurring concurrently in large numbers of cells even without specifically-induced drug selection, ectopic gene expression, or fractionation into subpopulations. In addition, our follow-up mechanistic studies have identified the PI3K/Akt/b-catenin/CBP pathway to play a critical role in regulating this dynamic equilibrium and regeneration of CSC. We hope our findings would contribute to a better understanding of CSC, and can potentially offer new strategies for targeting these drug-resistant, tumor-forming cells, ultimately leading to more effective treatments for patients. Advisors/Committee Members: Pinski, Jacek K. (Committee Chair), Goldkorn, Amir (Committee Member), Adams, Gregor B. (Committee Member), Kobielak, Agnieszka (Committee Member), Kahn, Michael (Committee Member).

Subjects/Keywords: cancer stem cell; telomerase; side population; plasticity; signaling pathway

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

He, K. (2012). The cancer stem-like phenotype: therapeutics, phenotypic plasticity and mechanistic studies. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/61631/rec/6485

Chicago Manual of Style (16^th Edition):

He, Kaijie. “The cancer stem-like phenotype: therapeutics, phenotypic plasticity and mechanistic studies.” 2012. Doctoral Dissertation, University of Southern California. Accessed January 28, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/61631/rec/6485.

MLA Handbook (7^th Edition):

He, Kaijie. “The cancer stem-like phenotype: therapeutics, phenotypic plasticity and mechanistic studies.” 2012. Web. 28 Jan 2021.

Vancouver:

He K. The cancer stem-like phenotype: therapeutics, phenotypic plasticity and mechanistic studies. [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2021 Jan 28]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/61631/rec/6485.

Council of Science Editors:

He K. The cancer stem-like phenotype: therapeutics, phenotypic plasticity and mechanistic studies. [Doctoral Dissertation]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/61631/rec/6485

University of Arizona

28. Gao, Yang. Lithium-Induced Nephropathy: The Role Of mTOR Signaling, Primary Cilia And Hedgehog Pathway .

Degree: 2014, University of Arizona

URL: http://hdl.handle.net/10150/347188

► Lithium is given to millions of bipolar disorder or post-traumatic disorder patients. The recent studies also support a role for lithium in treating neurodegenerative disease… (more)

▼ Lithium is given to millions of bipolar disorder or post-traumatic disorder patients. The recent studies also support a role for lithium in treating neurodegenerative disease such as Parkinson's disease and stroke. Lithium treatment leads to lithium nephropathy, which includes lithium-induced nephrogenic diabetic insipidus (NDI), lithium-induced renal cell proliferation leading to the formation of microcysts in the kidney, and lithium-induced renal fibrosis. However, there is still a gap in understanding the mechanisms and signaling pathways involved in regulating lithium-induced nephropathy. mTOR pathway activation and primary cilia are known to be associated with the abnormal renal cell proliferation and the formation of renal cysts in polycystic kidney disease, a renal disease model similar to our lithium model. The activation of hedgehog pathway is associated with the renal fibrosis observed in the unilateral ureteral obstruction and unilateral ischemia reperfusion injury models of chronic renal injury. Thus, I hypothesize that mTOR signaling pathway, primary cilia and hedgehog pathway may all contribute to lithium-induced nephropathy. To address the hypothesis that the mTOR signaling pathway may be responsible for lithium-induced renal collecting duct proliferation, mTOR pathway activation was assessed in lithium-treated mice and lithium-treated mouse inner medullary collecting duct (mIMCD3) cells. Lithium activated mTOR signaling pathway in renal collecting duct cells both in vivo and in vitro. Rapamycin, an inhibitor of mTOR, blocked lithium-induced renal cell proliferation in renal cortex and medulla in vivo and in renal collecting duct cells in vitro, supporting the hypothesis. However, rapamycin did not improve lithium-induced reduction of urine osmolality, suggesting mTOR signaling pathway may not contribute to lithium-induced NDI. To address the hypothesis that primary cilia may be necessary for lithium-induced mTOR activation and renal cell proliferation, primary cilia deficient cells were used to assess mTOR pathway activation and cell proliferation in response to lithium treatment. The absence of primary cilia abolished lithium-induced activation of mTOR pathway and cell proliferation, which supports the hypothesis. To address the hypothesis that lithium elongates primary cilia length, which is mediated by mTOR signaling pathway, primary cilia length alternation was assessed in the kidney and in mIMCD3 cells in response to lithium treatment. Lithium increased primary cilia length in renal collecting duct cells of cortex, outer medulla, and inner medulla kidney regions in vivo and in mIMCD3 cells in vitro. Rapamycin reversed lithium-induced elongation of primary cilia in renal cortical and outer medullary collecting duct cells in vivo, and blocked the increase of primary cilia length in mIMCD3 cells in vitro, which support the hypothesis. To address the hypothesis that lithium activates the hedgehog pathway in a Smoothened (smo, a key regulator of the hedgehog pathway)-dependent manner in renal… Advisors/Committee Members: Brooks, Heddwen L (advisor), Brooks, Heddwen L. (committeemember), Lynch, Ronald M. (committeemember), McDermott, Kimberly M. (committeemember), Wright, Stephen H. (committeemember).

Subjects/Keywords: mTOR Signaling Pathway; Primary Cilia; Physiological Sciences; Lithium-induced Nephropathy

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Gao, Y. (2014). Lithium-Induced Nephropathy: The Role Of mTOR Signaling, Primary Cilia And Hedgehog Pathway . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/347188

Chicago Manual of Style (16^th Edition):

Gao, Yang. “Lithium-Induced Nephropathy: The Role Of mTOR Signaling, Primary Cilia And Hedgehog Pathway .” 2014. Doctoral Dissertation, University of Arizona. Accessed January 28, 2021. http://hdl.handle.net/10150/347188.

MLA Handbook (7^th Edition):

Gao, Yang. “Lithium-Induced Nephropathy: The Role Of mTOR Signaling, Primary Cilia And Hedgehog Pathway .” 2014. Web. 28 Jan 2021.

Vancouver:

Gao Y. Lithium-Induced Nephropathy: The Role Of mTOR Signaling, Primary Cilia And Hedgehog Pathway . [Internet] [Doctoral dissertation]. University of Arizona; 2014. [cited 2021 Jan 28]. Available from: http://hdl.handle.net/10150/347188.

Council of Science Editors:

Gao Y. Lithium-Induced Nephropathy: The Role Of mTOR Signaling, Primary Cilia And Hedgehog Pathway . [Doctoral Dissertation]. University of Arizona; 2014. Available from: http://hdl.handle.net/10150/347188

Clemson University

29. Natarajan, Ojas. Investigation of Molecular Mechanisms Involved in Retardation of Immunosenescence in Caenorhabditis elegans by Royal Jelly.

Degree: PhD, Biological Sciences, 2018, Clemson University

URL: https://tigerprints.clemson.edu/all_dissertations/2555

► With recent advances in medicine, life expectancy has been steadily increasing. This increasing geriatric populous encounter various age-associated diseases including decline in immunity called… (more)

Subjects/Keywords: Aing; C. elegans; Immunity; immunosenescence; S. aureus; signaling pathway

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Natarajan, O. (2018). Investigation of Molecular Mechanisms Involved in Retardation of Immunosenescence in Caenorhabditis elegans by Royal Jelly. (Doctoral Dissertation). Clemson University. Retrieved from https://tigerprints.clemson.edu/all_dissertations/2555

Chicago Manual of Style (16^th Edition):

Natarajan, Ojas. “Investigation of Molecular Mechanisms Involved in Retardation of Immunosenescence in Caenorhabditis elegans by Royal Jelly.” 2018. Doctoral Dissertation, Clemson University. Accessed January 28, 2021. https://tigerprints.clemson.edu/all_dissertations/2555.

MLA Handbook (7^th Edition):

Natarajan, Ojas. “Investigation of Molecular Mechanisms Involved in Retardation of Immunosenescence in Caenorhabditis elegans by Royal Jelly.” 2018. Web. 28 Jan 2021.

Vancouver:

Natarajan O. Investigation of Molecular Mechanisms Involved in Retardation of Immunosenescence in Caenorhabditis elegans by Royal Jelly. [Internet] [Doctoral dissertation]. Clemson University; 2018. [cited 2021 Jan 28]. Available from: https://tigerprints.clemson.edu/all_dissertations/2555.

Council of Science Editors:

Natarajan O. Investigation of Molecular Mechanisms Involved in Retardation of Immunosenescence in Caenorhabditis elegans by Royal Jelly. [Doctoral Dissertation]. Clemson University; 2018. Available from: https://tigerprints.clemson.edu/all_dissertations/2555

Clemson University

30. Wang, Xiaoxia. Studies of Molecular Mechanisms of Royal Jelly Mediated Healthspan Promotion in Caenorhabditis Elegans.

Degree: PhD, Biological Sciences, 2016, Clemson University

URL: https://tigerprints.clemson.edu/all_dissertations/1652

► Numerous studies have demonstrated that many nutraceuticals have potential capacity to mitigate the symptoms of aging and age-related disorders. We found that Royal Jelly (RJ/eRJ)… (more)

▼ Numerous studies have demonstrated that many nutraceuticals have potential capacity to mitigate the symptoms of aging and age-related disorders. We found that Royal Jelly (RJ/eRJ) consumption could extend C. elegans lifespan and increase stress tolerance in an IIS/DAF-16 dependent manner. In consideration that the transactivity of DAF-16 is tightly controlled by its co-factors, our further results indicated that SIR-2.1, 14-3-3, and HCF-1 could interact with each other to fine-tune the activity of DAF-16. Additionally, these co-factors were also required in RJ/eRJ mediated stress tolerance. Given that aging is characterized with progressively declined physiological functions, it is intriguing to investigate whether RJ/eRJ supplementation could slow down the development of neurodegenerative diseases. Strikingly, our results showed that RJ/eRJ supplementation delayed the Î²-amyloid (AÎ²)-toxicity induced body paralysis in C. elegans AD model. The genetic analysis indicated that the RJ/eRJ mediated AÎ² toxicity alleviation required Insulin/IGF Signaling (IIS) pathway and DAF-16, rather than HSF-1 and SKN-1. Further research found that RJ/eRJ relied on DAF-16 to significantly improve the protein solubility in aged worms, which implied that RJ/eRJ supplementation promoted proteostasis and reduced proteotoxicity in AD worms. Additionally, RJ/eRJ also increased the solubility of AÎ² species. In considering that RJ/eRJ supplementation slowed down the AÎ²-induced paralysis in C. elegans, it is possible that RJ/eRJ mediated protection against AÎ² toxicity might be dependent on increasing the solubility of AÎ² species. Overall, our findings revealed that the anti-aging function of RJ/eRJ supplementation and underscored the relationship between the improved proteostasis and the prevention of neurodegenerative disorders. Advisors/Committee Members: Dr.Yuqing Dong, Committee Chair, Dr.Min Cao, Committee Co-Chair, Dr.William Baldwin, Dr.Charles Rice.

Subjects/Keywords: aging; Alzheimer's Disease; C. elegans; Insulin Signaling Pathway; Proteostasis; Royal Jelly

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Wang, X. (2016). Studies of Molecular Mechanisms of Royal Jelly Mediated Healthspan Promotion in Caenorhabditis Elegans. (Doctoral Dissertation). Clemson University. Retrieved from https://tigerprints.clemson.edu/all_dissertations/1652

Chicago Manual of Style (16^th Edition):

Wang, Xiaoxia. “Studies of Molecular Mechanisms of Royal Jelly Mediated Healthspan Promotion in Caenorhabditis Elegans.” 2016. Doctoral Dissertation, Clemson University. Accessed January 28, 2021. https://tigerprints.clemson.edu/all_dissertations/1652.

MLA Handbook (7^th Edition):

Wang, Xiaoxia. “Studies of Molecular Mechanisms of Royal Jelly Mediated Healthspan Promotion in Caenorhabditis Elegans.” 2016. Web. 28 Jan 2021.

Vancouver:

Wang X. Studies of Molecular Mechanisms of Royal Jelly Mediated Healthspan Promotion in Caenorhabditis Elegans. [Internet] [Doctoral dissertation]. Clemson University; 2016. [cited 2021 Jan 28]. Available from: https://tigerprints.clemson.edu/all_dissertations/1652.

Council of Science Editors:

Wang X. Studies of Molecular Mechanisms of Royal Jelly Mediated Healthspan Promotion in Caenorhabditis Elegans. [Doctoral Dissertation]. Clemson University; 2016. Available from: https://tigerprints.clemson.edu/all_dissertations/1652

Open Access Theses and Dissertations