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You searched for subject:(Mitogen Activated Protein Kinases metabolism 60). Showing records 1 – 30 of 30681 total matches.

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1. Jiang, Shaoning. Molecular mechanisms of hepatic insulin resistance following injury.

Degree: PhD, 2010, University of Alabama – Birmingham

Insulin resistance commonly occurs following injuries or critical illness independent of previous diabetic status. The development of insulin resistance and hyperglycemia is associated with increased… (more)

Subjects/Keywords: Adenoviridae – metabolism<; br>; Adenoviridae Infections – metabolism<; br>; Diabetes Mellitus, Type 2 – physiopathology<; br>; Glucose – metabolism<; br>; I-kappa B Kinase – physiology <; br>; Insulin – metabolism<; br>; JNK Mitogen-Activated Protein Kinases – physiology <; br>; Liver

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

APA (6th Edition):

Jiang, S. (2010). Molecular mechanisms of hepatic insulin resistance following injury. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1374

Chicago Manual of Style (16th Edition):

Jiang, Shaoning. “Molecular mechanisms of hepatic insulin resistance following injury.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed October 21, 2019. http://contentdm.mhsl.uab.edu/u?/etd,1374.

MLA Handbook (7th Edition):

Jiang, Shaoning. “Molecular mechanisms of hepatic insulin resistance following injury.” 2010. Web. 21 Oct 2019.

Vancouver:

Jiang S. Molecular mechanisms of hepatic insulin resistance following injury. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2019 Oct 21]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1374.

Council of Science Editors:

Jiang S. Molecular mechanisms of hepatic insulin resistance following injury. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1374

2. Yu, Jei-Hwa. MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1.

Degree: PhD, 2008, University of Alabama – Birmingham

Papillomaviruses (PV) are prevalent pathogens that infect human or animal squamous epithelia. Its genome is a double strand circular DNA of approximately 7.9 kb. It… (more)

Subjects/Keywords: DNA Helicases  – metabolism <; br>; DNA-Binding Proteins  – metabolism <; br>; Human papillomavirus 11  – physiology <; br>; Mitogen-Activated Protein Kinases  – metabolism <; br>; Nuclear Localization Signals  – metabolism <; br>; Replication Origin <; br>; Viral Proteins  – metabolism

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APA (6th Edition):

Yu, J. (2008). MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,213

Chicago Manual of Style (16th Edition):

Yu, Jei-Hwa. “MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed October 21, 2019. http://contentdm.mhsl.uab.edu/u?/etd,213.

MLA Handbook (7th Edition):

Yu, Jei-Hwa. “MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1.” 2008. Web. 21 Oct 2019.

Vancouver:

Yu J. MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2019 Oct 21]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,213.

Council of Science Editors:

Yu J. MAPKs regulate nuclear import of human papillomavirus type 11 replicative helicase E1. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,213

3. Zheng, Ying. A CK2-dependent mechanism for activation of the JAK-STAT signaling pathway: implications for cancer biology.

Degree: PhD, 2010, University of Alabama – Birmingham

Janus Kinase (JAK)-Signal Transducer and Activator of Transcription (STAT) signaling is involved in regulation of cell survival, proliferation and differentiation. JAK tyrosine kinases can be… (more)

Subjects/Keywords: Casein Kinase II  – metabolism<; br>; Hematologic Neoplasms  – metabolism<; br>; JNK Mitogen-Activated Protein Kinases  – metabolism<; br>; Polycythemia Vera  – metabolism<; br>; STAT Transcription Factors  – metabolism<; br>; Signal Transduction  – physiology

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APA (6th Edition):

Zheng, Y. (2010). A CK2-dependent mechanism for activation of the JAK-STAT signaling pathway: implications for cancer biology. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1168

Chicago Manual of Style (16th Edition):

Zheng, Ying. “A CK2-dependent mechanism for activation of the JAK-STAT signaling pathway: implications for cancer biology.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed October 21, 2019. http://contentdm.mhsl.uab.edu/u?/etd,1168.

MLA Handbook (7th Edition):

Zheng, Ying. “A CK2-dependent mechanism for activation of the JAK-STAT signaling pathway: implications for cancer biology.” 2010. Web. 21 Oct 2019.

Vancouver:

Zheng Y. A CK2-dependent mechanism for activation of the JAK-STAT signaling pathway: implications for cancer biology. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2019 Oct 21]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1168.

Council of Science Editors:

Zheng Y. A CK2-dependent mechanism for activation of the JAK-STAT signaling pathway: implications for cancer biology. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1168

4. Yang, Youfeng. The Role Of Map Kinase Cascade In Msp Signaling Response.

Degree: PhD, 2010, University of Alabama – Birmingham

The MSP domain is an evolutionarily conserved immunoglobulin-like structure of about 120 amino acids (Miller et al., 2001). A P56S missense mutation in the MSP… (more)

Subjects/Keywords: Caenorhabditis elegans – metabolism.<; br>; Helminth Proteins – physiology.<; br>; MAP Kinase Signaling System – physiology.<; br>; Mitogen-Activated Protein Kinases – metabolism.<; br>; Oocytes – physiology<; br>; Reactive Oxygen Species – metabolism<; br>; Signal Transduction – physiology

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APA (6th Edition):

Yang, Y. (2010). The Role Of Map Kinase Cascade In Msp Signaling Response. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1399

Chicago Manual of Style (16th Edition):

Yang, Youfeng. “The Role Of Map Kinase Cascade In Msp Signaling Response.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed October 21, 2019. http://contentdm.mhsl.uab.edu/u?/etd,1399.

MLA Handbook (7th Edition):

Yang, Youfeng. “The Role Of Map Kinase Cascade In Msp Signaling Response.” 2010. Web. 21 Oct 2019.

Vancouver:

Yang Y. The Role Of Map Kinase Cascade In Msp Signaling Response. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2019 Oct 21]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1399.

Council of Science Editors:

Yang Y. The Role Of Map Kinase Cascade In Msp Signaling Response. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1399


University of Hong Kong

5. Chiu, Tsz-ling. Role of mitogen-activated protein kinases in vascular relaxation in porcine coronary arteries.

Degree: Master of Medical Sciences, 2014, University of Hong Kong

 Background: Regulation of vascular tone is complex. Various complementary signaling pathways causing contraction and relaxation of vascular smooth muscle take place to ensure proper blood… (more)

Subjects/Keywords: Vascular smooth muscle; Mitogen-activated protein kinases

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APA (6th Edition):

Chiu, T. (2014). Role of mitogen-activated protein kinases in vascular relaxation in porcine coronary arteries. (Masters Thesis). University of Hong Kong. Retrieved from Chiu, T. [趙芷菱]. (2014). Role of mitogen-activated protein kinases in vascular relaxation in porcine coronary arteries. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5303896 ; http://dx.doi.org/10.5353/th_b5303896 ; http://hdl.handle.net/10722/206497

Chicago Manual of Style (16th Edition):

Chiu, Tsz-ling. “Role of mitogen-activated protein kinases in vascular relaxation in porcine coronary arteries.” 2014. Masters Thesis, University of Hong Kong. Accessed October 21, 2019. Chiu, T. [趙芷菱]. (2014). Role of mitogen-activated protein kinases in vascular relaxation in porcine coronary arteries. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5303896 ; http://dx.doi.org/10.5353/th_b5303896 ; http://hdl.handle.net/10722/206497.

MLA Handbook (7th Edition):

Chiu, Tsz-ling. “Role of mitogen-activated protein kinases in vascular relaxation in porcine coronary arteries.” 2014. Web. 21 Oct 2019.

Vancouver:

Chiu T. Role of mitogen-activated protein kinases in vascular relaxation in porcine coronary arteries. [Internet] [Masters thesis]. University of Hong Kong; 2014. [cited 2019 Oct 21]. Available from: Chiu, T. [趙芷菱]. (2014). Role of mitogen-activated protein kinases in vascular relaxation in porcine coronary arteries. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5303896 ; http://dx.doi.org/10.5353/th_b5303896 ; http://hdl.handle.net/10722/206497.

Council of Science Editors:

Chiu T. Role of mitogen-activated protein kinases in vascular relaxation in porcine coronary arteries. [Masters Thesis]. University of Hong Kong; 2014. Available from: Chiu, T. [趙芷菱]. (2014). Role of mitogen-activated protein kinases in vascular relaxation in porcine coronary arteries. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5303896 ; http://dx.doi.org/10.5353/th_b5303896 ; http://hdl.handle.net/10722/206497


Michigan State University

6. Pizzimenti, Natalie Maria. Mitogen activated protein kinase signaling in mouse skeletal muscle.

Degree: 2014, Michigan State University

Thesis M.S. Michigan State University. Physiology - Master of Science 2014.

AMP activated protein kinase (AMPK) and p38 mitogen activated protein kinases (MAPKs) are activated(more)

Subjects/Keywords: Physiology; Mitochondria – Formation; Protein kinases; Mitogen-activated protein kinases

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APA (6th Edition):

Pizzimenti, N. M. (2014). Mitogen activated protein kinase signaling in mouse skeletal muscle. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:2416

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

Chicago Manual of Style (16th Edition):

Pizzimenti, Natalie Maria. “Mitogen activated protein kinase signaling in mouse skeletal muscle.” 2014. Thesis, Michigan State University. Accessed October 21, 2019. http://etd.lib.msu.edu/islandora/object/etd:2416.

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

MLA Handbook (7th Edition):

Pizzimenti, Natalie Maria. “Mitogen activated protein kinase signaling in mouse skeletal muscle.” 2014. Web. 21 Oct 2019.

Vancouver:

Pizzimenti NM. Mitogen activated protein kinase signaling in mouse skeletal muscle. [Internet] [Thesis]. Michigan State University; 2014. [cited 2019 Oct 21]. Available from: http://etd.lib.msu.edu/islandora/object/etd:2416.

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

Council of Science Editors:

Pizzimenti NM. Mitogen activated protein kinase signaling in mouse skeletal muscle. [Thesis]. Michigan State University; 2014. Available from: http://etd.lib.msu.edu/islandora/object/etd:2416

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


University of Texas Southwestern Medical Center

7. Taylor, Clinton A., IV. Regulation and Dysregulation via Docking Interactions in WNK and ERK1/2 MAPK Signaling.

Degree: 2016, University of Texas Southwestern Medical Center

Protein-protein interactions are essential for nearly every cellular process. Within signaling pathways, such interactions carry out numerous functions such as defining substrate specificity, inhibition of… (more)

Subjects/Keywords: Mitogen-Activated Protein Kinase Kinases; Protein-Serine-Threonine Kinases; Signal Transduction; Transcription Factors

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APA (6th Edition):

Taylor, Clinton A., I. (2016). Regulation and Dysregulation via Docking Interactions in WNK and ERK1/2 MAPK Signaling. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/6152

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

Chicago Manual of Style (16th Edition):

Taylor, Clinton A., IV. “Regulation and Dysregulation via Docking Interactions in WNK and ERK1/2 MAPK Signaling.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed October 21, 2019. http://hdl.handle.net/2152.5/6152.

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

MLA Handbook (7th Edition):

Taylor, Clinton A., IV. “Regulation and Dysregulation via Docking Interactions in WNK and ERK1/2 MAPK Signaling.” 2016. Web. 21 Oct 2019.

Vancouver:

Taylor, Clinton A. I. Regulation and Dysregulation via Docking Interactions in WNK and ERK1/2 MAPK Signaling. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/2152.5/6152.

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

Council of Science Editors:

Taylor, Clinton A. I. Regulation and Dysregulation via Docking Interactions in WNK and ERK1/2 MAPK Signaling. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/6152

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


University of Oulu

8. Rysä, J. (Jaana). Gene expression profiling in experimental models of cardiac load.

Degree: 2008, University of Oulu

 Abstract Cardiac hypertrophy provides an adaptive mechanism to maintain cardiac output in response to increased workload, and although initially beneficial, hypertrophy eventually leads to heart… (more)

Subjects/Keywords: DNA microarrays; diastolic heart failure; hypertrophy; mitogen-activated protein kinases; stretch

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APA (6th Edition):

Rysä, J. (. (2008). Gene expression profiling in experimental models of cardiac load. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:9789514287664

Chicago Manual of Style (16th Edition):

Rysä, J (Jaana). “Gene expression profiling in experimental models of cardiac load.” 2008. Doctoral Dissertation, University of Oulu. Accessed October 21, 2019. http://urn.fi/urn:isbn:9789514287664.

MLA Handbook (7th Edition):

Rysä, J (Jaana). “Gene expression profiling in experimental models of cardiac load.” 2008. Web. 21 Oct 2019.

Vancouver:

Rysä J(. Gene expression profiling in experimental models of cardiac load. [Internet] [Doctoral dissertation]. University of Oulu; 2008. [cited 2019 Oct 21]. Available from: http://urn.fi/urn:isbn:9789514287664.

Council of Science Editors:

Rysä J(. Gene expression profiling in experimental models of cardiac load. [Doctoral Dissertation]. University of Oulu; 2008. Available from: http://urn.fi/urn:isbn:9789514287664


University of Hong Kong

9. Zhang, Pingde. TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway.

Degree: PhD, 2011, University of Hong Kong

 Ovarian cancer is the most lethal gynecological malignancy. Most of ovarian cancer patients relapse and subsequently die due to the development of resistance to chemotherapy.… (more)

Subjects/Keywords: JNK mitogen-activated protein kinases.; Ovaries - Cancer.; Cisplatin.; p53 antioncogene.

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APA (6th Edition):

Zhang, P. (2011). TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway. (Doctoral Dissertation). University of Hong Kong. Retrieved from Zhang, P. [张萍德]. (2011). TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775294 ; http://dx.doi.org/10.5353/th_b4775294 ; http://hdl.handle.net/10722/174474

Chicago Manual of Style (16th Edition):

Zhang, Pingde. “TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway.” 2011. Doctoral Dissertation, University of Hong Kong. Accessed October 21, 2019. Zhang, P. [张萍德]. (2011). TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775294 ; http://dx.doi.org/10.5353/th_b4775294 ; http://hdl.handle.net/10722/174474.

MLA Handbook (7th Edition):

Zhang, Pingde. “TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway.” 2011. Web. 21 Oct 2019.

Vancouver:

Zhang P. TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway. [Internet] [Doctoral dissertation]. University of Hong Kong; 2011. [cited 2019 Oct 21]. Available from: Zhang, P. [张萍德]. (2011). TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775294 ; http://dx.doi.org/10.5353/th_b4775294 ; http://hdl.handle.net/10722/174474.

Council of Science Editors:

Zhang P. TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway. [Doctoral Dissertation]. University of Hong Kong; 2011. Available from: Zhang, P. [张萍德]. (2011). TAp73α enhances the cellular sensitivity to cisplatin in ovarian cancer cells via the JNK signaling pathway. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775294 ; http://dx.doi.org/10.5353/th_b4775294 ; http://hdl.handle.net/10722/174474


University of Texas Southwestern Medical Center

10. An, Zhenyi. The Regulation of Autophagy and Its Role in Mitotic Exit.

Degree: 2014, University of Texas Southwestern Medical Center

 Autophagy is an evolutionarily conserved pathway in which cells enclose cytoplasmic contents in double membrane vesicles and deliver them to the lysosome for degradation. Autophagy… (more)

Subjects/Keywords: Apoptosis Regulatory Proteins; Autophagy; Mitogen-Activated Protein Kinases; Phosphorylation

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APA (6th Edition):

An, Z. (2014). The Regulation of Autophagy and Its Role in Mitotic Exit. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/3582

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

Chicago Manual of Style (16th Edition):

An, Zhenyi. “The Regulation of Autophagy and Its Role in Mitotic Exit.” 2014. Thesis, University of Texas Southwestern Medical Center. Accessed October 21, 2019. http://hdl.handle.net/2152.5/3582.

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

MLA Handbook (7th Edition):

An, Zhenyi. “The Regulation of Autophagy and Its Role in Mitotic Exit.” 2014. Web. 21 Oct 2019.

Vancouver:

An Z. The Regulation of Autophagy and Its Role in Mitotic Exit. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2014. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/2152.5/3582.

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

Council of Science Editors:

An Z. The Regulation of Autophagy and Its Role in Mitotic Exit. [Thesis]. University of Texas Southwestern Medical Center; 2014. Available from: http://hdl.handle.net/2152.5/3582

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


University of Georgia

11. Sun, Bin. Inhibition of calcium-independent phospholipase A2 induces prostate cancer cell cytostasis.

Degree: PhD, Toxicology, 2010, University of Georgia

 The goal of this work was to identify mechanisms by which inhibition of calcium-independent phospholipase A2 (iPLA2) induces cytostasis in human LNCaP (p53 wild-type and… (more)

Subjects/Keywords: Phospholipase A2; Phospholipids; p53; Mitogen Activated Protein Kinases; Reactive species; Phospholipid Profiles

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APA (6th Edition):

Sun, B. (2010). Inhibition of calcium-independent phospholipase A2 induces prostate cancer cell cytostasis. (Doctoral Dissertation). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/sun_bin_201008_phd

Chicago Manual of Style (16th Edition):

Sun, Bin. “Inhibition of calcium-independent phospholipase A2 induces prostate cancer cell cytostasis.” 2010. Doctoral Dissertation, University of Georgia. Accessed October 21, 2019. http://purl.galileo.usg.edu/uga_etd/sun_bin_201008_phd.

MLA Handbook (7th Edition):

Sun, Bin. “Inhibition of calcium-independent phospholipase A2 induces prostate cancer cell cytostasis.” 2010. Web. 21 Oct 2019.

Vancouver:

Sun B. Inhibition of calcium-independent phospholipase A2 induces prostate cancer cell cytostasis. [Internet] [Doctoral dissertation]. University of Georgia; 2010. [cited 2019 Oct 21]. Available from: http://purl.galileo.usg.edu/uga_etd/sun_bin_201008_phd.

Council of Science Editors:

Sun B. Inhibition of calcium-independent phospholipase A2 induces prostate cancer cell cytostasis. [Doctoral Dissertation]. University of Georgia; 2010. Available from: http://purl.galileo.usg.edu/uga_etd/sun_bin_201008_phd

12. Karagiannidis, Ioannis. In Vivo μελέτη της συμβολής της φωσφορυλίωσης των MAP κινασών στην αποπτωτική διαδικασία της σήψης.

Degree: 2016, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

The impact of a potential autophagy (LC3a/b) deregulation in hyper and in hypo stages during sepsis-induced kidney injury and the temporal profile of phosphorylated extracellular… (more)

Subjects/Keywords: Απόπτωση (προγραμματισμένος κυτταρικός θάνατος); Αυτοφαγία; Πειραματικά μοντέλα σήψης; Mitogen – Activated Protein Kinases (MAPKs)

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APA (6th Edition):

Karagiannidis, I. (2016). In Vivo μελέτη της συμβολής της φωσφορυλίωσης των MAP κινασών στην αποπτωτική διαδικασία της σήψης. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/37872

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

Chicago Manual of Style (16th Edition):

Karagiannidis, Ioannis. “In Vivo μελέτη της συμβολής της φωσφορυλίωσης των MAP κινασών στην αποπτωτική διαδικασία της σήψης.” 2016. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed October 21, 2019. http://hdl.handle.net/10442/hedi/37872.

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

MLA Handbook (7th Edition):

Karagiannidis, Ioannis. “In Vivo μελέτη της συμβολής της φωσφορυλίωσης των MAP κινασών στην αποπτωτική διαδικασία της σήψης.” 2016. Web. 21 Oct 2019.

Vancouver:

Karagiannidis I. In Vivo μελέτη της συμβολής της φωσφορυλίωσης των MAP κινασών στην αποπτωτική διαδικασία της σήψης. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2016. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/10442/hedi/37872.

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

Council of Science Editors:

Karagiannidis I. In Vivo μελέτη της συμβολής της φωσφορυλίωσης των MAP κινασών στην αποπτωτική διαδικασία της σήψης. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2016. Available from: http://hdl.handle.net/10442/hedi/37872

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


Columbia University

13. Lyashenko, Eugenia. Cell Memory in the Mitogen-Activated Protein Kinase Signaling Pathway.

Degree: 2015, Columbia University

 Cells process information from their environment, such as the stimuli to grow, divide, or die, via cell signaling. Deregulated processing of extracellular stimuli can lead… (more)

Subjects/Keywords: Mitogen-activated protein kinases; Weber-Fechner law; Cellular control mechanisms; Bioinformatics; Biology

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APA (6th Edition):

Lyashenko, E. (2015). Cell Memory in the Mitogen-Activated Protein Kinase Signaling Pathway. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8RF5SVZ

Chicago Manual of Style (16th Edition):

Lyashenko, Eugenia. “Cell Memory in the Mitogen-Activated Protein Kinase Signaling Pathway.” 2015. Doctoral Dissertation, Columbia University. Accessed October 21, 2019. https://doi.org/10.7916/D8RF5SVZ.

MLA Handbook (7th Edition):

Lyashenko, Eugenia. “Cell Memory in the Mitogen-Activated Protein Kinase Signaling Pathway.” 2015. Web. 21 Oct 2019.

Vancouver:

Lyashenko E. Cell Memory in the Mitogen-Activated Protein Kinase Signaling Pathway. [Internet] [Doctoral dissertation]. Columbia University; 2015. [cited 2019 Oct 21]. Available from: https://doi.org/10.7916/D8RF5SVZ.

Council of Science Editors:

Lyashenko E. Cell Memory in the Mitogen-Activated Protein Kinase Signaling Pathway. [Doctoral Dissertation]. Columbia University; 2015. Available from: https://doi.org/10.7916/D8RF5SVZ


Rutgers University

14. Gokina, Pradeepa, 1981-. The role of MAPKs in CNS demyelination.

Degree: Biology, 2013, Rutgers University

Subjects/Keywords: Mitogen-activated protein kinases; Demyelination; Oligodendroglia

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APA (6th Edition):

Gokina, Pradeepa, 1. (2013). The role of MAPKs in CNS demyelination. (Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/41478/

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

Chicago Manual of Style (16th Edition):

Gokina, Pradeepa, 1981-. “The role of MAPKs in CNS demyelination.” 2013. Thesis, Rutgers University. Accessed October 21, 2019. https://rucore.libraries.rutgers.edu/rutgers-lib/41478/.

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

MLA Handbook (7th Edition):

Gokina, Pradeepa, 1981-. “The role of MAPKs in CNS demyelination.” 2013. Web. 21 Oct 2019.

Vancouver:

Gokina, Pradeepa 1. The role of MAPKs in CNS demyelination. [Internet] [Thesis]. Rutgers University; 2013. [cited 2019 Oct 21]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/41478/.

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

Council of Science Editors:

Gokina, Pradeepa 1. The role of MAPKs in CNS demyelination. [Thesis]. Rutgers University; 2013. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/41478/

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


McGill University

15. Houri, Nadia. Study of ERK12 MAP kinases activation by the bradykinin type 2 receptor : characterization of beta-arrestin scaffolding function in the temporal regulation of ERK12 activation induced by the B2R.

Degree: MS, Division of Experimental Medicine., 2007, McGill University

 G protein-coupled receptors (GPCRs) comprise the largest family of transmembrane receptors. The beta-arrestins, adaptor proteins involved in GPCR desensitization, may also act as scaffolds for… (more)

Subjects/Keywords: Extracellular Signal-Regulated MAP Kinases  – metabolism.; Mitogen-Activated Protein Kinase 1  – metabolism.; Receptor, Bradykinin B2  – metabolism.

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APA (6th Edition):

Houri, N. (2007). Study of ERK12 MAP kinases activation by the bradykinin type 2 receptor : characterization of beta-arrestin scaffolding function in the temporal regulation of ERK12 activation induced by the B2R. (Masters Thesis). McGill University. Retrieved from http://digitool.library.mcgill.ca/thesisfile112637.pdf

Chicago Manual of Style (16th Edition):

Houri, Nadia. “Study of ERK12 MAP kinases activation by the bradykinin type 2 receptor : characterization of beta-arrestin scaffolding function in the temporal regulation of ERK12 activation induced by the B2R.” 2007. Masters Thesis, McGill University. Accessed October 21, 2019. http://digitool.library.mcgill.ca/thesisfile112637.pdf.

MLA Handbook (7th Edition):

Houri, Nadia. “Study of ERK12 MAP kinases activation by the bradykinin type 2 receptor : characterization of beta-arrestin scaffolding function in the temporal regulation of ERK12 activation induced by the B2R.” 2007. Web. 21 Oct 2019.

Vancouver:

Houri N. Study of ERK12 MAP kinases activation by the bradykinin type 2 receptor : characterization of beta-arrestin scaffolding function in the temporal regulation of ERK12 activation induced by the B2R. [Internet] [Masters thesis]. McGill University; 2007. [cited 2019 Oct 21]. Available from: http://digitool.library.mcgill.ca/thesisfile112637.pdf.

Council of Science Editors:

Houri N. Study of ERK12 MAP kinases activation by the bradykinin type 2 receptor : characterization of beta-arrestin scaffolding function in the temporal regulation of ERK12 activation induced by the B2R. [Masters Thesis]. McGill University; 2007. Available from: http://digitool.library.mcgill.ca/thesisfile112637.pdf


University of Missouri – Columbia

16. Orsborn, April Marie, 1978-. Analysis of interactions between the germline RNA helicases (GLHs) and their regulators KGB-1 and CSN-5 in Caenorhabditis elegans.

Degree: PhD, 2006, University of Missouri – Columbia

 The Caenorhabditis elegans germline RNA helicases (GLHs) are constitutive components of P granules, non-membranous aggregates of protein and RNA that segregate with the nematode germline.… (more)

Subjects/Keywords: Cytoplasmic Granules; JNK Mitogen-Activated Protein Kinases  – metabolism; Germ Cells  – enzymology; Caenorhabditis elegans Proteins  – metabolism; DEAD-box RNA Helicases  – metabolism

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APA (6th Edition):

Orsborn, April Marie, 1. (2006). Analysis of interactions between the germline RNA helicases (GLHs) and their regulators KGB-1 and CSN-5 in Caenorhabditis elegans. (Doctoral Dissertation). University of Missouri – Columbia. Retrieved from https://doi.org/10.32469/10355/4499

Chicago Manual of Style (16th Edition):

Orsborn, April Marie, 1978-. “Analysis of interactions between the germline RNA helicases (GLHs) and their regulators KGB-1 and CSN-5 in Caenorhabditis elegans.” 2006. Doctoral Dissertation, University of Missouri – Columbia. Accessed October 21, 2019. https://doi.org/10.32469/10355/4499.

MLA Handbook (7th Edition):

Orsborn, April Marie, 1978-. “Analysis of interactions between the germline RNA helicases (GLHs) and their regulators KGB-1 and CSN-5 in Caenorhabditis elegans.” 2006. Web. 21 Oct 2019.

Vancouver:

Orsborn, April Marie 1. Analysis of interactions between the germline RNA helicases (GLHs) and their regulators KGB-1 and CSN-5 in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. University of Missouri – Columbia; 2006. [cited 2019 Oct 21]. Available from: https://doi.org/10.32469/10355/4499.

Council of Science Editors:

Orsborn, April Marie 1. Analysis of interactions between the germline RNA helicases (GLHs) and their regulators KGB-1 and CSN-5 in Caenorhabditis elegans. [Doctoral Dissertation]. University of Missouri – Columbia; 2006. Available from: https://doi.org/10.32469/10355/4499


Johannes Gutenberg Universität Mainz

17. Küppers, Monika. Molekulare Mechanismen der Kontaktinhibition: Identifizierung neuer Tumorsuppressorgene.

Degree: 2008, Johannes Gutenberg Universität Mainz

Die Zellen eines Organismus unterliegen ständig den Einflüssen wachstumsfördernder und –hemmender Signale. Die korrekte Verarbeitung dieser Signale ist essentiell für die Aufrechterhaltung der Gewebehomöostase. Wachstumsfördernde… (more)

Subjects/Keywords: Kontaktinhibition, Zellzyklus, Mitogen-aktivierte Protein Kinasen (MAPK), differentielle Genexpression; contact-inhibition, cell cycle, mitogen-activated protein kinases (MAPK), differential gene expression; Natural sciences and mathematics

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APA (6th Edition):

Küppers, M. (2008). Molekulare Mechanismen der Kontaktinhibition: Identifizierung neuer Tumorsuppressorgene. (Doctoral Dissertation). Johannes Gutenberg Universität Mainz. Retrieved from http://ubm.opus.hbz-nrw.de/volltexte/2008/1722/

Chicago Manual of Style (16th Edition):

Küppers, Monika. “Molekulare Mechanismen der Kontaktinhibition: Identifizierung neuer Tumorsuppressorgene.” 2008. Doctoral Dissertation, Johannes Gutenberg Universität Mainz. Accessed October 21, 2019. http://ubm.opus.hbz-nrw.de/volltexte/2008/1722/.

MLA Handbook (7th Edition):

Küppers, Monika. “Molekulare Mechanismen der Kontaktinhibition: Identifizierung neuer Tumorsuppressorgene.” 2008. Web. 21 Oct 2019.

Vancouver:

Küppers M. Molekulare Mechanismen der Kontaktinhibition: Identifizierung neuer Tumorsuppressorgene. [Internet] [Doctoral dissertation]. Johannes Gutenberg Universität Mainz; 2008. [cited 2019 Oct 21]. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2008/1722/.

Council of Science Editors:

Küppers M. Molekulare Mechanismen der Kontaktinhibition: Identifizierung neuer Tumorsuppressorgene. [Doctoral Dissertation]. Johannes Gutenberg Universität Mainz; 2008. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2008/1722/


University of Western Australia

18. Arulpragasam, Ajanthy. The role of 14-3-3 proteins in calcium-sensing receptor cell signalling and expression.

Degree: PhD, 2010, University of Western Australia

[Truncated abstract] The calcium-sensing receptor (CaR), belonging to class C of G protein-coupled receptors (GPCRs), is highly expressed in tissues that govern the CaR’s primary… (more)

Subjects/Keywords: G proteins; Calcium; Cell receptors; Cellular signal transduction; Mitogen-activated protein kinases; Cytology; 14-3-3 proteins; Signalling; Calcium-sensing receptor

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APA (6th Edition):

Arulpragasam, A. (2010). The role of 14-3-3 proteins in calcium-sensing receptor cell signalling and expression. (Doctoral Dissertation). University of Western Australia. Retrieved from http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=30648&local_base=GEN01-INS01

Chicago Manual of Style (16th Edition):

Arulpragasam, Ajanthy. “The role of 14-3-3 proteins in calcium-sensing receptor cell signalling and expression.” 2010. Doctoral Dissertation, University of Western Australia. Accessed October 21, 2019. http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=30648&local_base=GEN01-INS01.

MLA Handbook (7th Edition):

Arulpragasam, Ajanthy. “The role of 14-3-3 proteins in calcium-sensing receptor cell signalling and expression.” 2010. Web. 21 Oct 2019.

Vancouver:

Arulpragasam A. The role of 14-3-3 proteins in calcium-sensing receptor cell signalling and expression. [Internet] [Doctoral dissertation]. University of Western Australia; 2010. [cited 2019 Oct 21]. Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=30648&local_base=GEN01-INS01.

Council of Science Editors:

Arulpragasam A. The role of 14-3-3 proteins in calcium-sensing receptor cell signalling and expression. [Doctoral Dissertation]. University of Western Australia; 2010. Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=30648&local_base=GEN01-INS01


University of Hong Kong

19. Lam, King-yin, Andy. Differential regulation of FOXM1 isoforms by RaF/MEK/ERK signaling.

Degree: M. Phil., 2010, University of Hong Kong

published_or_final_version

Biochemistry

Master

Master of Philosophy

Advisors/Committee Members: Shiu, SYW, Yao, KM.

Subjects/Keywords: Transcription factors.; Cellular signal transduction.; Mitogen-activated protein kinases.

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APA (6th Edition):

Lam, King-yin, A. (2010). Differential regulation of FOXM1 isoforms by RaF/MEK/ERK signaling. (Masters Thesis). University of Hong Kong. Retrieved from Lam, K. A. [林敬賢]. (2010). Differential regulation of FOXM1 isoforms by RaF/MEK/ERK signaling. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4425101 ; http://dx.doi.org/10.5353/th_b4425101 ; http://hdl.handle.net/10722/65109

Chicago Manual of Style (16th Edition):

Lam, King-yin, Andy. “Differential regulation of FOXM1 isoforms by RaF/MEK/ERK signaling.” 2010. Masters Thesis, University of Hong Kong. Accessed October 21, 2019. Lam, K. A. [林敬賢]. (2010). Differential regulation of FOXM1 isoforms by RaF/MEK/ERK signaling. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4425101 ; http://dx.doi.org/10.5353/th_b4425101 ; http://hdl.handle.net/10722/65109.

MLA Handbook (7th Edition):

Lam, King-yin, Andy. “Differential regulation of FOXM1 isoforms by RaF/MEK/ERK signaling.” 2010. Web. 21 Oct 2019.

Vancouver:

Lam, King-yin A. Differential regulation of FOXM1 isoforms by RaF/MEK/ERK signaling. [Internet] [Masters thesis]. University of Hong Kong; 2010. [cited 2019 Oct 21]. Available from: Lam, K. A. [林敬賢]. (2010). Differential regulation of FOXM1 isoforms by RaF/MEK/ERK signaling. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4425101 ; http://dx.doi.org/10.5353/th_b4425101 ; http://hdl.handle.net/10722/65109.

Council of Science Editors:

Lam, King-yin A. Differential regulation of FOXM1 isoforms by RaF/MEK/ERK signaling. [Masters Thesis]. University of Hong Kong; 2010. Available from: Lam, K. A. [林敬賢]. (2010). Differential regulation of FOXM1 isoforms by RaF/MEK/ERK signaling. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4425101 ; http://dx.doi.org/10.5353/th_b4425101 ; http://hdl.handle.net/10722/65109


University of North Carolina – Greensboro

20. Eanes, Lauren A. Analysis of molecular target(s) of naringenin in MCF-7 breast cancer cells.

Degree: 2014, University of North Carolina – Greensboro

 Estrogen receptor (ER) antagonists such as tamoxifen have been used successfully to treat ER+ breast cancers for more than 30 years. Tamoxifen targets the ER… (more)

Subjects/Keywords: Breast – Cancer – Treatment; Tamoxifen; Drug resistance in cancer cells; Estrogen – Receptors – Pathophysiology; Mitogen-activated protein kinases

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APA (6th Edition):

Eanes, L. A. (2014). Analysis of molecular target(s) of naringenin in MCF-7 breast cancer cells. (Masters Thesis). University of North Carolina – Greensboro. Retrieved from http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16160

Chicago Manual of Style (16th Edition):

Eanes, Lauren A. “Analysis of molecular target(s) of naringenin in MCF-7 breast cancer cells.” 2014. Masters Thesis, University of North Carolina – Greensboro. Accessed October 21, 2019. http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16160.

MLA Handbook (7th Edition):

Eanes, Lauren A. “Analysis of molecular target(s) of naringenin in MCF-7 breast cancer cells.” 2014. Web. 21 Oct 2019.

Vancouver:

Eanes LA. Analysis of molecular target(s) of naringenin in MCF-7 breast cancer cells. [Internet] [Masters thesis]. University of North Carolina – Greensboro; 2014. [cited 2019 Oct 21]. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16160.

Council of Science Editors:

Eanes LA. Analysis of molecular target(s) of naringenin in MCF-7 breast cancer cells. [Masters Thesis]. University of North Carolina – Greensboro; 2014. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=16160


University of Missouri – Columbia

21. Larue, Clayton T., 1977-. Regulation of plant development in Arabidopsis.

Degree: PhD, 2008, University of Missouri – Columbia

 [ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] The development of a complex organism, such as a plant, requires the function of multiple… (more)

Subjects/Keywords: Arabidopsis  – Development; Abscission (Botany); Mitogen-activated protein kinases

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APA (6th Edition):

Larue, Clayton T., 1. (2008). Regulation of plant development in Arabidopsis. (Doctoral Dissertation). University of Missouri – Columbia. Retrieved from https://doi.org/10.32469/10355/6051

Chicago Manual of Style (16th Edition):

Larue, Clayton T., 1977-. “Regulation of plant development in Arabidopsis.” 2008. Doctoral Dissertation, University of Missouri – Columbia. Accessed October 21, 2019. https://doi.org/10.32469/10355/6051.

MLA Handbook (7th Edition):

Larue, Clayton T., 1977-. “Regulation of plant development in Arabidopsis.” 2008. Web. 21 Oct 2019.

Vancouver:

Larue, Clayton T. 1. Regulation of plant development in Arabidopsis. [Internet] [Doctoral dissertation]. University of Missouri – Columbia; 2008. [cited 2019 Oct 21]. Available from: https://doi.org/10.32469/10355/6051.

Council of Science Editors:

Larue, Clayton T. 1. Regulation of plant development in Arabidopsis. [Doctoral Dissertation]. University of Missouri – Columbia; 2008. Available from: https://doi.org/10.32469/10355/6051


University of Texas Southwestern Medical Center

22. Lo, Miao-Chia. The Study of Wnt Signaling Effector POP-1/TCF in C. Elegans Early Embryos.

Degree: 2005, University of Texas Southwestern Medical Center

 In C. elegans embryos, the combined Wnt/MAPK pathway polarizes the founder cell of mesendoderm, EMS blastomere, such that EMS produces two daughters with distinct developmental… (more)

Subjects/Keywords: Caenorhabditis elegans; DNA-Binding Proteins; Mitogen-Activated Protein Kinases

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APA (6th Edition):

Lo, M. (2005). The Study of Wnt Signaling Effector POP-1/TCF in C. Elegans Early Embryos. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/566

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

Chicago Manual of Style (16th Edition):

Lo, Miao-Chia. “The Study of Wnt Signaling Effector POP-1/TCF in C. Elegans Early Embryos.” 2005. Thesis, University of Texas Southwestern Medical Center. Accessed October 21, 2019. http://hdl.handle.net/2152.5/566.

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

MLA Handbook (7th Edition):

Lo, Miao-Chia. “The Study of Wnt Signaling Effector POP-1/TCF in C. Elegans Early Embryos.” 2005. Web. 21 Oct 2019.

Vancouver:

Lo M. The Study of Wnt Signaling Effector POP-1/TCF in C. Elegans Early Embryos. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2005. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/2152.5/566.

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

Council of Science Editors:

Lo M. The Study of Wnt Signaling Effector POP-1/TCF in C. Elegans Early Embryos. [Thesis]. University of Texas Southwestern Medical Center; 2005. Available from: http://hdl.handle.net/2152.5/566

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


Freie Universität Berlin

23. Grobe, Theresa. Mechanisms of cell activation by Chlamydia trachomatis Serovar K.

Degree: 2014, Freie Universität Berlin

 Chlamydia trachomatis is the most common cause of sexually transmitted disease. They typically induce asymptomatic lower genital tract infections, such as cervicitis, endometritis and salpingitis.… (more)

Subjects/Keywords: chlamydia trachomatis; mitogen-activated protein kinases; nuclear factor-kappa B; interleukin-8; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

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APA (6th Edition):

Grobe, T. (2014). Mechanisms of cell activation by Chlamydia trachomatis Serovar K. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-11204

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

Chicago Manual of Style (16th Edition):

Grobe, Theresa. “Mechanisms of cell activation by Chlamydia trachomatis Serovar K.” 2014. Thesis, Freie Universität Berlin. Accessed October 21, 2019. http://dx.doi.org/10.17169/refubium-11204.

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

MLA Handbook (7th Edition):

Grobe, Theresa. “Mechanisms of cell activation by Chlamydia trachomatis Serovar K.” 2014. Web. 21 Oct 2019.

Vancouver:

Grobe T. Mechanisms of cell activation by Chlamydia trachomatis Serovar K. [Internet] [Thesis]. Freie Universität Berlin; 2014. [cited 2019 Oct 21]. Available from: http://dx.doi.org/10.17169/refubium-11204.

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

Council of Science Editors:

Grobe T. Mechanisms of cell activation by Chlamydia trachomatis Serovar K. [Thesis]. Freie Universität Berlin; 2014. Available from: http://dx.doi.org/10.17169/refubium-11204

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


Michigan State University

24. Gopallawa, Indiwari. Angiotensin 1-7/Mas promotes alveolar epithelial cell survival through upregulation of map kinase phosphatase-2.

Degree: 2015, Michigan State University

Thesis Ph. D. Michigan State University. Biochemistry and Molecular Biology 2015.

Apoptosis is now known to be an important regulator of maintaining normal organ homeostasis.… (more)

Subjects/Keywords: Mitogen-activated protein kinases; Phosphatases; Angiotensin converting enzyme; Angiotensin II – Antagonists; Angiotensins; Apoptosis; Epithelial cells; Cellular biology; Molecular biology; Biochemistry

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APA (6th Edition):

Gopallawa, I. (2015). Angiotensin 1-7/Mas promotes alveolar epithelial cell survival through upregulation of map kinase phosphatase-2. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:3683

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

Chicago Manual of Style (16th Edition):

Gopallawa, Indiwari. “Angiotensin 1-7/Mas promotes alveolar epithelial cell survival through upregulation of map kinase phosphatase-2.” 2015. Thesis, Michigan State University. Accessed October 21, 2019. http://etd.lib.msu.edu/islandora/object/etd:3683.

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

MLA Handbook (7th Edition):

Gopallawa, Indiwari. “Angiotensin 1-7/Mas promotes alveolar epithelial cell survival through upregulation of map kinase phosphatase-2.” 2015. Web. 21 Oct 2019.

Vancouver:

Gopallawa I. Angiotensin 1-7/Mas promotes alveolar epithelial cell survival through upregulation of map kinase phosphatase-2. [Internet] [Thesis]. Michigan State University; 2015. [cited 2019 Oct 21]. Available from: http://etd.lib.msu.edu/islandora/object/etd:3683.

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

Council of Science Editors:

Gopallawa I. Angiotensin 1-7/Mas promotes alveolar epithelial cell survival through upregulation of map kinase phosphatase-2. [Thesis]. Michigan State University; 2015. Available from: http://etd.lib.msu.edu/islandora/object/etd:3683

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


University of Texas Southwestern Medical Center

25. Juang, Yu-Chi. Structural Analysis of STE20-Related Proline-Alanine-Rich Kinase (SPAK).

Degree: 2009, University of Texas Southwestern Medical Center

 Ste20-related proline-alanine-rich kinase (SPAK) is a kinase that regulates ion cotransporters including KCC, NKCC1, NKCC2 and NCC. Recently, SPAK was identified as a target regulated… (more)

Subjects/Keywords: Mitogen-Activated Protein Kinases; Transcription Factors; Protein-Serine-Threonine Kinases

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APA (6th Edition):

Juang, Y. (2009). Structural Analysis of STE20-Related Proline-Alanine-Rich Kinase (SPAK). (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/634

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

Chicago Manual of Style (16th Edition):

Juang, Yu-Chi. “Structural Analysis of STE20-Related Proline-Alanine-Rich Kinase (SPAK).” 2009. Thesis, University of Texas Southwestern Medical Center. Accessed October 21, 2019. http://hdl.handle.net/2152.5/634.

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

MLA Handbook (7th Edition):

Juang, Yu-Chi. “Structural Analysis of STE20-Related Proline-Alanine-Rich Kinase (SPAK).” 2009. Web. 21 Oct 2019.

Vancouver:

Juang Y. Structural Analysis of STE20-Related Proline-Alanine-Rich Kinase (SPAK). [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2009. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/2152.5/634.

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

Council of Science Editors:

Juang Y. Structural Analysis of STE20-Related Proline-Alanine-Rich Kinase (SPAK). [Thesis]. University of Texas Southwestern Medical Center; 2009. Available from: http://hdl.handle.net/2152.5/634

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


University of Texas Southwestern Medical Center

26. Karra, Aroon Saikumar. Nuclear Behaviors of ERK1/2 Signaling.

Degree: 2017, University of Texas Southwestern Medical Center

 The rat sarcoma (Ras)- rapidly accelerated fibrosarcoma (Raf)- mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK) kinase (MEK)- ERK pathway is essential for proper development and… (more)

Subjects/Keywords: Mitogen-Activated Protein Kinase 1; Oligonucleotides

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APA (6th Edition):

Karra, A. S. (2017). Nuclear Behaviors of ERK1/2 Signaling. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/6621

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

Chicago Manual of Style (16th Edition):

Karra, Aroon Saikumar. “Nuclear Behaviors of ERK1/2 Signaling.” 2017. Thesis, University of Texas Southwestern Medical Center. Accessed October 21, 2019. http://hdl.handle.net/2152.5/6621.

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

MLA Handbook (7th Edition):

Karra, Aroon Saikumar. “Nuclear Behaviors of ERK1/2 Signaling.” 2017. Web. 21 Oct 2019.

Vancouver:

Karra AS. Nuclear Behaviors of ERK1/2 Signaling. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2017. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/2152.5/6621.

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

Council of Science Editors:

Karra AS. Nuclear Behaviors of ERK1/2 Signaling. [Thesis]. University of Texas Southwestern Medical Center; 2017. Available from: http://hdl.handle.net/2152.5/6621

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


Université de Montréal

27. Torabi, Mohammad Ali. Effects of deoxynivalenol and deepoxy-deoxynivalenol on bovine ovarian theca cell function .

Degree: 2017, Université de Montréal

 La mycotoxine déoxynivalénol (DON) et son métabolite déépoxy-déoxynivalenol (DOM-1) ont des effets significatifs sur la modification de la fonction des cellules thècales de l’ovaire bovin.… (more)

Subjects/Keywords: Phosphoprotéome; Les cellules de la thèque; Déoxynivalénol; Déépoxy-déoxynivalenol; Protéines kinases activées par des mitogènes; La prolifération; Phosphoproteome; Theca cells; Deoxynivalenol; Deepoxy-deoxynivalenol; Mitogen-activated protein kinases; Proliferation

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APA (6th Edition):

Torabi, M. A. (2017). Effects of deoxynivalenol and deepoxy-deoxynivalenol on bovine ovarian theca cell function . (Thesis). Université de Montréal. Retrieved from http://hdl.handle.net/1866/19167

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

Chicago Manual of Style (16th Edition):

Torabi, Mohammad Ali. “Effects of deoxynivalenol and deepoxy-deoxynivalenol on bovine ovarian theca cell function .” 2017. Thesis, Université de Montréal. Accessed October 21, 2019. http://hdl.handle.net/1866/19167.

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

MLA Handbook (7th Edition):

Torabi, Mohammad Ali. “Effects of deoxynivalenol and deepoxy-deoxynivalenol on bovine ovarian theca cell function .” 2017. Web. 21 Oct 2019.

Vancouver:

Torabi MA. Effects of deoxynivalenol and deepoxy-deoxynivalenol on bovine ovarian theca cell function . [Internet] [Thesis]. Université de Montréal; 2017. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/1866/19167.

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

Council of Science Editors:

Torabi MA. Effects of deoxynivalenol and deepoxy-deoxynivalenol on bovine ovarian theca cell function . [Thesis]. Université de Montréal; 2017. Available from: http://hdl.handle.net/1866/19167

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

28. Dolan, Philip J. The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau.

Degree: PhD, 2010, University of Alabama – Birmingham

Alzheimer Disease (AD) is pathologically characterized by the appearance of senile plaques composed of β-amyloid (Aβ) and neurofibrillary tangles composed of the microtubule-associated protein tau.… (more)

Subjects/Keywords: Alzheimer Disease  – enzymology<; br>; Autophagy<; br>; Caspases  – metabolism<; br>; Protein Kinases  – metabolism<; br>; Signal Transduction<; br>; tau Proteins  – physiology

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APA (6th Edition):

Dolan, P. J. (2010). The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1090

Chicago Manual of Style (16th Edition):

Dolan, Philip J. “The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed October 21, 2019. http://contentdm.mhsl.uab.edu/u?/etd,1090.

MLA Handbook (7th Edition):

Dolan, Philip J. “The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau.” 2010. Web. 21 Oct 2019.

Vancouver:

Dolan PJ. The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2019 Oct 21]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1090.

Council of Science Editors:

Dolan PJ. The role of post-translational modifications and valosin-containing protein in the turnover and stability of the microtubule-associated protein tau. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1090


University of Hong Kong

29. 鄭軍偉.; Cheng, Kwan-wai. Regulation of equilibrative nucleoside transporter-1 by protein kinaseC and mitogen-activating protein kinase.

Degree: Master of Medical Sciences, 2005, University of Hong Kong

published_or_final_version

Medical Sciences

Master

Master of Medical Sciences

Subjects/Keywords: Nucleosides.; Mitogen-activated protein kinases.; Genetic regulation.; Protein kinase C.

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APA (6th Edition):

鄭軍偉.; Cheng, K. (2005). Regulation of equilibrative nucleoside transporter-1 by protein kinaseC and mitogen-activating protein kinase. (Masters Thesis). University of Hong Kong. Retrieved from Cheng, K. [鄭軍偉]. (2005). Regulation of equilibrative nucleoside transporter-1 by protein kinase C and mitogen-activating protein kinase. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4500998 ; http://dx.doi.org/10.5353/th_b4500998 ; http://hdl.handle.net/10722/131551

Chicago Manual of Style (16th Edition):

鄭軍偉.; Cheng, Kwan-wai. “Regulation of equilibrative nucleoside transporter-1 by protein kinaseC and mitogen-activating protein kinase.” 2005. Masters Thesis, University of Hong Kong. Accessed October 21, 2019. Cheng, K. [鄭軍偉]. (2005). Regulation of equilibrative nucleoside transporter-1 by protein kinase C and mitogen-activating protein kinase. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4500998 ; http://dx.doi.org/10.5353/th_b4500998 ; http://hdl.handle.net/10722/131551.

MLA Handbook (7th Edition):

鄭軍偉.; Cheng, Kwan-wai. “Regulation of equilibrative nucleoside transporter-1 by protein kinaseC and mitogen-activating protein kinase.” 2005. Web. 21 Oct 2019.

Vancouver:

鄭軍偉.; Cheng K. Regulation of equilibrative nucleoside transporter-1 by protein kinaseC and mitogen-activating protein kinase. [Internet] [Masters thesis]. University of Hong Kong; 2005. [cited 2019 Oct 21]. Available from: Cheng, K. [鄭軍偉]. (2005). Regulation of equilibrative nucleoside transporter-1 by protein kinase C and mitogen-activating protein kinase. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4500998 ; http://dx.doi.org/10.5353/th_b4500998 ; http://hdl.handle.net/10722/131551.

Council of Science Editors:

鄭軍偉.; Cheng K. Regulation of equilibrative nucleoside transporter-1 by protein kinaseC and mitogen-activating protein kinase. [Masters Thesis]. University of Hong Kong; 2005. Available from: Cheng, K. [鄭軍偉]. (2005). Regulation of equilibrative nucleoside transporter-1 by protein kinase C and mitogen-activating protein kinase. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4500998 ; http://dx.doi.org/10.5353/th_b4500998 ; http://hdl.handle.net/10722/131551

30. Varela-Nieto, Isabel. Insulin receptor substrate 2 (IRS2)-deficient mice show sensorineural hearing loss that is delayed by concomitant protein tyrosine phosphatase 1B (PTP1B) loss of function.

Degree: 2018, Feinstein Institute for Medical Research

Subjects/Keywords: Cochlea; Mitogen-Activated Protein Kinases; Protein Tyrosine Phosphatase; Insulin Receptor Substrate Proteins; Medicina

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APA (6th Edition):

Varela-Nieto, I. (2018). Insulin receptor substrate 2 (IRS2)-deficient mice show sensorineural hearing loss that is delayed by concomitant protein tyrosine phosphatase 1B (PTP1B) loss of function. (Thesis). Feinstein Institute for Medical Research. Retrieved from http://hdl.handle.net/10486/663875

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

Chicago Manual of Style (16th Edition):

Varela-Nieto, Isabel. “Insulin receptor substrate 2 (IRS2)-deficient mice show sensorineural hearing loss that is delayed by concomitant protein tyrosine phosphatase 1B (PTP1B) loss of function.” 2018. Thesis, Feinstein Institute for Medical Research. Accessed October 21, 2019. http://hdl.handle.net/10486/663875.

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

MLA Handbook (7th Edition):

Varela-Nieto, Isabel. “Insulin receptor substrate 2 (IRS2)-deficient mice show sensorineural hearing loss that is delayed by concomitant protein tyrosine phosphatase 1B (PTP1B) loss of function.” 2018. Web. 21 Oct 2019.

Vancouver:

Varela-Nieto I. Insulin receptor substrate 2 (IRS2)-deficient mice show sensorineural hearing loss that is delayed by concomitant protein tyrosine phosphatase 1B (PTP1B) loss of function. [Internet] [Thesis]. Feinstein Institute for Medical Research; 2018. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/10486/663875.

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

Council of Science Editors:

Varela-Nieto I. Insulin receptor substrate 2 (IRS2)-deficient mice show sensorineural hearing loss that is delayed by concomitant protein tyrosine phosphatase 1B (PTP1B) loss of function. [Thesis]. Feinstein Institute for Medical Research; 2018. Available from: http://hdl.handle.net/10486/663875

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

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