subject:(Protein kinases)

University of Utah

1. Tsai, I-Chun. Regulation of casein kinase I [epsilon] in non-canonical Wnt signaling;.

Degree: PhD, Oncological Sciences;, 2007, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1449/rec/1088

► Casein kinase I epsilon (CKI?) and casein kinase I delta (CKI?) are members of the CKI serine/threonine protein kinase family. These two highly-related kinases are… (more)

▼ Casein kinase I epsilon (CKI?) and casein kinase I delta (CKI?) are members of the CKI serine/threonine protein kinase family. These two highly-related kinases are ubiquitously expressed in mammalian tissues and are implicated in multiple cellular processes, including Wnt signaling transduction, circadian rhythms and Hedgehog pathway. Due to the ability to induce axis duplication and to activate the TCF-dependent reporter, CKI? and CKI? were first reported as positive regulators of the Wnt?-catenin pathway. Biochemical studies in our laboratory demonstrated that CKI? could destabilize the ?-catenin destruction complex, leading to the accumulation of ?-catenin. However, CKI?; is not only involved in the Wnt/?-catenin pathway but is also required for the convergent extension (CE) movements during Xenopus development. CE comprises the morphological polarization and cell migration, regulating the formation of the body axis in a ?-catenin independent manner. Downstream of Wnt, Frizzled (Fz) receptors and Dishevelled (Dvl/Dsh) protein, CE movements can be stimulated by the activation of small GTPases, including Rho and Rac, which facilitate cytoskeleton reorganization and activate the JNK pathway. Although CKI?; activity has been shown to be important for the regulation of CE movements, the molecular mechanism by which CKI?; regulates CE movements has not been addressed yet. In order to find additional roles of CKI?; in the Wnt signaling pathway, my study focuses on understanding how CKI?; regulates CE movements and the ?-catenin-independent Wnt pathway. The characterization of CKI? and CKI? mutants demonstrates that CKI?/? participate in the control of convergent extension (CE) movements through a ?-catenin independent mechanism. Further investigation of CKI?; function uncovered a novel mechanism of CKI?, in which CKI?; activates Rap1, a monomeric GTP binding protein, through regulating the activity of a GAP (GTPase activating protein) of Rap1, E6TP1. Taken together, this dissertation extends the knowledge of CKI?/? in mediating Wnt/PCP (Planer Cell Polarity) signaling. Since the regulation of cell polarity is highly related to the regulation of cell migration and cancer metastasis, results from these studies not only deepen our understanding the CKI?;/? function in embryonic development but also may be applied for understanding of the progression of cancer development in the future.

Subjects/Keywords: Protein Kinases; Biochemistry

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APA (6^th Edition):

Tsai, I. (2007). Regulation of casein kinase I [epsilon] in non-canonical Wnt signaling;. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1449/rec/1088

Chicago Manual of Style (16^th Edition):

Tsai, I-Chun. “Regulation of casein kinase I [epsilon] in non-canonical Wnt signaling;.” 2007. Doctoral Dissertation, University of Utah. Accessed February 28, 2020. http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1449/rec/1088.

MLA Handbook (7^th Edition):

Tsai, I-Chun. “Regulation of casein kinase I [epsilon] in non-canonical Wnt signaling;.” 2007. Web. 28 Feb 2020.

Vancouver:

Tsai I. Regulation of casein kinase I [epsilon] in non-canonical Wnt signaling;. [Internet] [Doctoral dissertation]. University of Utah; 2007. [cited 2020 Feb 28]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1449/rec/1088.

Council of Science Editors:

Tsai I. Regulation of casein kinase I [epsilon] in non-canonical Wnt signaling;. [Doctoral Dissertation]. University of Utah; 2007. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1449/rec/1088

Columbia University

2. Taveras, Carmen D. Role of Aurora B-mediated phosphorylation during mitosis and interphase.

Degree: 2017, Columbia University

URL: https://doi.org/10.7916/D8QC08VV

► Accurate chromosome segregation requires a spindle apparatus composed of microtubules that arise from the spindle to attach to the kinetochore, a protein complex assembled at… (more)

▼ Accurate chromosome segregation requires a spindle apparatus composed of microtubules that arise from the spindle to attach to the kinetochore, a protein complex assembled at the centromere of each chromosome. Failure to segregate chromosomes accurately may lead to lethal early developmental defects and tumorigenesis. To achieve proper kinetochore binding to microtubules, mammalian cells have evolved elaborate mechanisms to correct attachment errors and stabilize correct ones. Current models suggest that tension between kinetochore pairs (inter-kinetochore stretch) and tension at the kinetochore (intra-kinetochore stretch) produces a spatial separation of Aurora B kinase from kinetochore-associated and microtubule-binding substrates, subsequently reducing their phosphorylations and increasing their microtubule affinity. However, the tension-based models do not explain how the initial microtubule binding at unattached kinetochores occurs, where there is no tension and kinetochore-associated substrates are highly phosphorylated and, hence unable to bind to microtubules. Therefore, there must be a mechanism that explains how the phosphorylation of kinetochore substrates by Aurora B is reduced in the absence of tension. In the first part of this thesis, I examine the structural features of the coiled-coil domain of the kinetochore-associated kinesin motor protein, CENP-E. Using Single-Molecule High-Resolution Colocalization (SHREC) microscopy analysis of kinetochore-associated CENP-E, I show that CENP-E undergoes structural rearrangements prior to and after tension generation at the kinetochore. Chemical inhibition of the motor motility or genetic perturbations of the coiled-coil domain of CENP-E increases Aurora B-mediated Ndc80 phosphorylation in a tension-independent manner. Importantly, metaphase chromosome misalignment caused by inhibition of CENP-E can be rescued by chemical inhibition of Aurora B kinase. Therefore, CENP-E regulates the initial kinetochore binding to microtubules and the stabilization of kinetochore-microtubule attachments. Formin-dependent actin assembly is known to play a role in multiple processes, including cytokinesis, filopodia formation, cell polarity, and cell adhesion. Thus, formin malfunction is directly linked to various pathologies, including defects in cell migration and tumor suppression. Although the role of formins in actin polymerization has been well described, the mechanistic processes that regulate the actin assembly function of formins remain poorly understood, especially the interplay among the various sub-families of formins and how they are spatiotemporally regulated. In the second part of this thesis, I show that Aurora B-mediated phosphorylation of the formin, mDia3 regulates actin assembly. Previous studies identified two Aurora B phosphorylation sites in the FH2 domain of mDia3. To this end, phosphomimetic and non-phosphorylatable mutants of a constitutively active form of mDia3 were designed to test whether phosphorylation by Aurora B regulates actin…

Subjects/Keywords: Cytology; Protein kinases

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APA (6^th Edition):

Taveras, C. D. (2017). Role of Aurora B-mediated phosphorylation during mitosis and interphase. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8QC08VV

Chicago Manual of Style (16^th Edition):

Taveras, Carmen D. “Role of Aurora B-mediated phosphorylation during mitosis and interphase.” 2017. Doctoral Dissertation, Columbia University. Accessed February 28, 2020. https://doi.org/10.7916/D8QC08VV.

MLA Handbook (7^th Edition):

Taveras, Carmen D. “Role of Aurora B-mediated phosphorylation during mitosis and interphase.” 2017. Web. 28 Feb 2020.

Vancouver:

Taveras CD. Role of Aurora B-mediated phosphorylation during mitosis and interphase. [Internet] [Doctoral dissertation]. Columbia University; 2017. [cited 2020 Feb 28]. Available from: https://doi.org/10.7916/D8QC08VV.

Council of Science Editors:

Taveras CD. Role of Aurora B-mediated phosphorylation during mitosis and interphase. [Doctoral Dissertation]. Columbia University; 2017. Available from: https://doi.org/10.7916/D8QC08VV

Rutgers University

3. Fellmeth, Jessica, 1983-. Analysis of human Aurora C Kinase variants in oocyte meiosis.

Degree: PhD, Microbiology and Molecular Genetics, 2015, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/48487/

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The birth of a healthy child is often a priority for couples, yet many couples will unfortunately suffer from infertility. Aneuploidy is the leading genetic… (more)

Subjects/Keywords: Protein kinases; Ovum

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APA (6^th Edition):

Fellmeth, Jessica, 1. (2015). Analysis of human Aurora C Kinase variants in oocyte meiosis. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/48487/

Chicago Manual of Style (16^th Edition):

Fellmeth, Jessica, 1983-. “Analysis of human Aurora C Kinase variants in oocyte meiosis.” 2015. Doctoral Dissertation, Rutgers University. Accessed February 28, 2020. https://rucore.libraries.rutgers.edu/rutgers-lib/48487/.

MLA Handbook (7^th Edition):

Fellmeth, Jessica, 1983-. “Analysis of human Aurora C Kinase variants in oocyte meiosis.” 2015. Web. 28 Feb 2020.

Vancouver:

Fellmeth, Jessica 1. Analysis of human Aurora C Kinase variants in oocyte meiosis. [Internet] [Doctoral dissertation]. Rutgers University; 2015. [cited 2020 Feb 28]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/48487/.

Council of Science Editors:

Fellmeth, Jessica 1. Analysis of human Aurora C Kinase variants in oocyte meiosis. [Doctoral Dissertation]. Rutgers University; 2015. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/48487/

Hong Kong University of Science and Technology

4. Wang, Xi. Stk24 promotes myogenic differentiation via multiple mechanisms.

Degree: 2011, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-7914 ; https://doi.org/10.14711/thesis-b1155425 ; http://repository.ust.hk/ir/bitstream/1783.1-7914/1/th_redirect.html

► Through an RNAi-based screening for kinases involved in myogenic differentiation, weidentified Stk24/MST3, a member of the mammalian Ste20 family, as a key regulator. Knockdown of… (more)

Subjects/Keywords: Myogenesis ; Protein kinases

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APA (6^th Edition):

Wang, X. (2011). Stk24 promotes myogenic differentiation via multiple mechanisms. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-7914 ; https://doi.org/10.14711/thesis-b1155425 ; http://repository.ust.hk/ir/bitstream/1783.1-7914/1/th_redirect.html

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):

Wang, Xi. “Stk24 promotes myogenic differentiation via multiple mechanisms.” 2011. Thesis, Hong Kong University of Science and Technology. Accessed February 28, 2020. http://repository.ust.hk/ir/Record/1783.1-7914 ; https://doi.org/10.14711/thesis-b1155425 ; http://repository.ust.hk/ir/bitstream/1783.1-7914/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Wang, Xi. “Stk24 promotes myogenic differentiation via multiple mechanisms.” 2011. Web. 28 Feb 2020.

Vancouver:

Wang X. Stk24 promotes myogenic differentiation via multiple mechanisms. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2011. [cited 2020 Feb 28]. Available from: http://repository.ust.hk/ir/Record/1783.1-7914 ; https://doi.org/10.14711/thesis-b1155425 ; http://repository.ust.hk/ir/bitstream/1783.1-7914/1/th_redirect.html.

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

Council of Science Editors:

Wang X. Stk24 promotes myogenic differentiation via multiple mechanisms. [Thesis]. Hong Kong University of Science and Technology; 2011. Available from: http://repository.ust.hk/ir/Record/1783.1-7914 ; https://doi.org/10.14711/thesis-b1155425 ; http://repository.ust.hk/ir/bitstream/1783.1-7914/1/th_redirect.html

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

Hong Kong University of Science and Technology

5. Zhang, Peng. S-nitrosylation of cyclin-dependent kinase 5 and its activator p35 in neuronal morphogenesis and synaptic function.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-86315 ; https://doi.org/10.14711/thesis-b1266266 ; http://repository.ust.hk/ir/bitstream/1783.1-86315/1/th_redirect.html

► Cyclin-dependent kinase 5 (Cdk5), a proline-directed serine/threonine kinase, plays important roles in various neuronal functions including neuronal migration, neurite outgrowth, synapse development, and plasticity. The… (more)

▼ Cyclin-dependent kinase 5 (Cdk5), a proline-directed serine/threonine kinase, plays important roles in various neuronal functions including neuronal migration, neurite outgrowth, synapse development, and plasticity. The dysfunction of Cdk5 activity is associated with neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Therefore, the precise regulation of Cdk5 activity is important for proper neuronal development and functioning. Unlike other cyclin-dependent kinase family members, which are regulated by cyclins, Cdk5 is activated through its association with the neuronal specific activators, p35 and p39. However, whether and how Cdk5 activity is regulated in neurons by other molecular mechanisms remain unclear. This study revealed Cdk5 and its activator p35 can undergo post-translational modification by S-nitrosylation, which involves a reaction in which a nitrogen monoxide group is attached to the thiol side chain of the cysteine residue(s) of a protein. Cdk5 S-nitrosylation occurs at Cys83, which is one of the critical amino acids within the ATP-binding pocket of the kinase. Upon S-nitrosylation, Cdk5 exhibits reduced kinase activity, whereas the mutation of Cys83 to alanine on Cdk5 renders the kinase refractory to such inhibition. Meanwhile, p35 S-nitrosylation occurs at Cys92; this modification promotes its proteasome-dependent degradation, consequently resulting in reduced Cdk5 activity. Importantly, S-nitrosylated Cdk5 and p35 can be detected in vivo. While the S-nitrosylation of Cdk5 and p35 was detected in wild-type mouse brain lysate, this specific S-nitrosylation was absent in neuronal nitric oxide synthase-knockout (nNOS) mice. More importantly, Cdk5/p35 S-nitrosylation negatively regulates the activity of Cdk5 in vivo as revealed by enhanced Cdk5 activity in nNOS-knockout mouse brains. Furthermore, Cdk5/p35 S-nitrosylation is implicated in the regulation of neuronal morphogenesis and synaptic plasticity. Blockade of Cdk5 S-nitrosylation in cultured hippocampal neurons enhanced dendritic growth and branching, indicating that Cdk5 S-nitrosylation is a novel mechanism in the regulation of dendritic growth during development. Moreover, Cdk5/p35 S-nitrosylation was found to be involved in the regulation of synaptic function. Cdk5 hyperactivation contributed to synaptic failure upon NO production blockade. Notably, Cdk5/p35 overexpression and silencing phenocopied and reversed these synaptic deficits, respectively, upon pharmacological inhibition or genetic depletion of nNOS. More importantly, blocking p35 S-nitrosylation reduced dendritic spine density and the percentage of mature spines in cultured hippocampal neurons as well as the surface expression of GluA1 in 293T cells. This suggests that p35 S-nitrosylation is critical for the regulation of synaptic function. The present rules collectively demonstrate a novel mechanism in the regulation of the multi-faceted kinase Cdk5 in many neuronal functions including dendritic morphogenesis and synaptic plasticity.

Subjects/Keywords: Cyclin-dependent kinases ; Protein kinases ; Neurotransmitters ; Morphogenesis

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APA (6^th Edition):

Zhang, P. (2013). S-nitrosylation of cyclin-dependent kinase 5 and its activator p35 in neuronal morphogenesis and synaptic function. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-86315 ; https://doi.org/10.14711/thesis-b1266266 ; http://repository.ust.hk/ir/bitstream/1783.1-86315/1/th_redirect.html

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, Peng. “S-nitrosylation of cyclin-dependent kinase 5 and its activator p35 in neuronal morphogenesis and synaptic function.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed February 28, 2020. http://repository.ust.hk/ir/Record/1783.1-86315 ; https://doi.org/10.14711/thesis-b1266266 ; http://repository.ust.hk/ir/bitstream/1783.1-86315/1/th_redirect.html.

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, Peng. “S-nitrosylation of cyclin-dependent kinase 5 and its activator p35 in neuronal morphogenesis and synaptic function.” 2013. Web. 28 Feb 2020.

Vancouver:

Zhang P. S-nitrosylation of cyclin-dependent kinase 5 and its activator p35 in neuronal morphogenesis and synaptic function. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2020 Feb 28]. Available from: http://repository.ust.hk/ir/Record/1783.1-86315 ; https://doi.org/10.14711/thesis-b1266266 ; http://repository.ust.hk/ir/bitstream/1783.1-86315/1/th_redirect.html.

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

Council of Science Editors:

Zhang P. S-nitrosylation of cyclin-dependent kinase 5 and its activator p35 in neuronal morphogenesis and synaptic function. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-86315 ; https://doi.org/10.14711/thesis-b1266266 ; http://repository.ust.hk/ir/bitstream/1783.1-86315/1/th_redirect.html

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

Indian Institute of Science

6. Reddy, Mamatha M. Manganese-Dependent Serine/Threonine/Tyrosine Kinase From Arabidopsis Thaliana : Role Of Serine And Threonine Residues In The Regulation Of Kinase Activity.

Degree: 2006, Indian Institute of Science

URL: http://hdl.handle.net/2005/365

► Protein phosphorylation is an important post-translational modification of proteins, which can either activate or inhibit the function of a given protein. The enzymes, protein kinases… (more)

Subjects/Keywords: Protein Kinases; Carrier Proteins; Arabidopsis Thaliana; Protein Tyrosine Kinases; Plant Protein Kinases; Protein Kinases - Regulation; Plant Signaling; Kinase Activity; Plant Biochemistry

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APA (6^th Edition):

Reddy, M. M. (2006). Manganese-Dependent Serine/Threonine/Tyrosine Kinase From Arabidopsis Thaliana : Role Of Serine And Threonine Residues In The Regulation Of Kinase Activity. (Thesis). Indian Institute of Science. Retrieved from http://hdl.handle.net/2005/365

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):

Reddy, Mamatha M. “Manganese-Dependent Serine/Threonine/Tyrosine Kinase From Arabidopsis Thaliana : Role Of Serine And Threonine Residues In The Regulation Of Kinase Activity.” 2006. Thesis, Indian Institute of Science. Accessed February 28, 2020. http://hdl.handle.net/2005/365.

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

MLA Handbook (7^th Edition):

Reddy, Mamatha M. “Manganese-Dependent Serine/Threonine/Tyrosine Kinase From Arabidopsis Thaliana : Role Of Serine And Threonine Residues In The Regulation Of Kinase Activity.” 2006. Web. 28 Feb 2020.

Vancouver:

Reddy MM. Manganese-Dependent Serine/Threonine/Tyrosine Kinase From Arabidopsis Thaliana : Role Of Serine And Threonine Residues In The Regulation Of Kinase Activity. [Internet] [Thesis]. Indian Institute of Science; 2006. [cited 2020 Feb 28]. Available from: http://hdl.handle.net/2005/365.

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

Council of Science Editors:

Reddy MM. Manganese-Dependent Serine/Threonine/Tyrosine Kinase From Arabidopsis Thaliana : Role Of Serine And Threonine Residues In The Regulation Of Kinase Activity. [Thesis]. Indian Institute of Science; 2006. Available from: http://hdl.handle.net/2005/365

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

University of Hong Kong

7. Liu, Ling. Regulation of post-translational modifications of the protein kinase LKB1: molecular mechanisms and physiologicalimplications.

Degree: PhD, 2011, University of Hong Kong

URL: Liu, L. [刘凌]. (2011). Regulation of post-translational modifications of the protein kinase LKB1 : molecular mechanisms and physiological implications. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4766083 ; http://dx.doi.org/10.5353/th_b4766083 ; http://hdl.handle.net/10722/174451

► Background and objectives: Endothelial dysfunction and cancer are two of the important aspects of obesity-related medical complications, the prevalence of which is reaching an epidemic… (more)

▼ Background and objectives: Endothelial dysfunction and cancer are two of the important aspects of obesity-related medical complications, the prevalence of which is reaching an epidemic level worldwide. The protein kinase LKB1 has been shown to play opposite roles in these two metabolic diseases by promoting cellular senescence and inhibiting cell proliferation through regulating a series of its downstream targets. However, the molecular mechanisms wherebyLKB1 itself is regulated by its upstream molecules remains poorly understood. The major objectives of this study are to identify novel upstream regulators of LKB1 and to investigate how these upstream regulators modulate the subcellular localization and physiological functions of LKB1 by post-translational modifications. Key findings: 1. Our proteomic analysis demonstrated that LKB1 was modified by both acetylation and phosphorylation. The acetylation sites of mouseLKB1 include Lys48, Lys64and Lys312. The phosphorylation sites of mouseLKB1 include: Ser31, Thr32,Tyr36, Ser69, Thr71, Ser334and Thr336. 2. In both human embryonic kidney 293 (HEK293)cells and primary porcine aortic endothelial cells (PAECs), the nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase SirT1 attenuated the acetylation levels of LKB1,which consequently resulted in enhancedLKB1ubiquitination, thereby leading to the proteasome-mediated degradation of LKB1. 3. In primary PAECs, overexpression of SirT1 protected cells from cell cycle arrest and cellular senescence, whereas overexpression of LKB1 exhibited the opposite effects.SirT1 antagonizedLKB1-induced G1 phase arrest and cellular senescence by promoting the deacetylation and protein degradation of LKB1. 4. The in vitro phosphorylation assay and mass spectrometry analysis demonstrated that LKB1 could be phosphorylated by the Akt kinase at Ser334which was critical for the interaction between LKB1 and 14-3-3. The enhanced association between LKB1 and 14-3-3 subsequently attenuated the interaction between LKB1 and Ste20 related adaptor α(STRADα), which further promoted the nuclear accumulation of LKB1. 5. The cell proliferation and cell cycle distribution analysis of the stably-transfected MDA-MB-231 breast cancer cells demonstrated that overexpression of the LKB1 mutant S334D, which mimicked Ser334 phosphorylation and localized exclusively in the nucleus, completely lost its anti-tumor activities. On the other hand, the S334A mutation enhanced the tumor suppressive functions of LKB1. 6. Nude mice inoculated with the LKB1 S334A stably-transfected MDA-MB-231 cells exhibited delayed tumor onset, decreased tumor growth rate and tumor weight. By contrast, inoculation of nude mice with the MDA-MB-231 cells overexpressing LKB1 S334D mutation showed the opposite effects on these parameters. Conclusions: These results collectively suggest that the deacetylase SirT1 and the protein kinase Aktare the two important upstream regulators of LKB1. SirT1 prevents LKB1-induced cellular senescence and protect endothelial ageing by promoting… Advisors/Committee Members: Wang, Y, Xu, A.

Subjects/Keywords: Protein kinases.; Post-translational modification.

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APA (6^th Edition):

Liu, L. (2011). Regulation of post-translational modifications of the protein kinase LKB1: molecular mechanisms and physiologicalimplications. (Doctoral Dissertation). University of Hong Kong. Retrieved from Liu, L. [刘凌]. (2011). Regulation of post-translational modifications of the protein kinase LKB1 : molecular mechanisms and physiological implications. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4766083 ; http://dx.doi.org/10.5353/th_b4766083 ; http://hdl.handle.net/10722/174451

Chicago Manual of Style (16^th Edition):

Liu, Ling. “Regulation of post-translational modifications of the protein kinase LKB1: molecular mechanisms and physiologicalimplications.” 2011. Doctoral Dissertation, University of Hong Kong. Accessed February 28, 2020. Liu, L. [刘凌]. (2011). Regulation of post-translational modifications of the protein kinase LKB1 : molecular mechanisms and physiological implications. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4766083 ; http://dx.doi.org/10.5353/th_b4766083 ; http://hdl.handle.net/10722/174451.

MLA Handbook (7^th Edition):

Liu, Ling. “Regulation of post-translational modifications of the protein kinase LKB1: molecular mechanisms and physiologicalimplications.” 2011. Web. 28 Feb 2020.

Vancouver:

Liu L. Regulation of post-translational modifications of the protein kinase LKB1: molecular mechanisms and physiologicalimplications. [Internet] [Doctoral dissertation]. University of Hong Kong; 2011. [cited 2020 Feb 28]. Available from: Liu, L. [刘凌]. (2011). Regulation of post-translational modifications of the protein kinase LKB1 : molecular mechanisms and physiological implications. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4766083 ; http://dx.doi.org/10.5353/th_b4766083 ; http://hdl.handle.net/10722/174451.

Council of Science Editors:

Liu L. Regulation of post-translational modifications of the protein kinase LKB1: molecular mechanisms and physiologicalimplications. [Doctoral Dissertation]. University of Hong Kong; 2011. Available from: Liu, L. [刘凌]. (2011). Regulation of post-translational modifications of the protein kinase LKB1 : molecular mechanisms and physiological implications. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4766083 ; http://dx.doi.org/10.5353/th_b4766083 ; http://hdl.handle.net/10722/174451

University of Hong Kong

8. 刘沁; Liu, Qin. Characterization of Per2 and SIRT1 : age-related tissue distribution changes.

Degree: Master of Medical Sciences, 2017, University of Hong Kong

URL: http://hdl.handle.net/10722/251348

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The circadian clock supports and governs many body physiological processes. Period2 (PER2) is a key molecule regulating the circadian clock and acts as a repressor… (more)

Subjects/Keywords: Circadian rhythms; Protein kinases; Sirtuins

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APA (6^th Edition):

刘沁; Liu, Q. (2017). Characterization of Per2 and SIRT1 : age-related tissue distribution changes. (Masters Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/251348

Chicago Manual of Style (16^th Edition):

刘沁; Liu, Qin. “Characterization of Per2 and SIRT1 : age-related tissue distribution changes.” 2017. Masters Thesis, University of Hong Kong. Accessed February 28, 2020. http://hdl.handle.net/10722/251348.

MLA Handbook (7^th Edition):

刘沁; Liu, Qin. “Characterization of Per2 and SIRT1 : age-related tissue distribution changes.” 2017. Web. 28 Feb 2020.

Vancouver:

刘沁; Liu Q. Characterization of Per2 and SIRT1 : age-related tissue distribution changes. [Internet] [Masters thesis]. University of Hong Kong; 2017. [cited 2020 Feb 28]. Available from: http://hdl.handle.net/10722/251348.

Council of Science Editors:

刘沁; Liu Q. Characterization of Per2 and SIRT1 : age-related tissue distribution changes. [Masters Thesis]. University of Hong Kong; 2017. Available from: http://hdl.handle.net/10722/251348

University of Hong Kong

9. 關冠麒; Kwan, Kwun-ki. The role of PAK4 in extracellular matrix degradation.

Degree: M. Phil., 2014, University of Hong Kong

URL: Kwan, K. [關冠麒]. (2014). The role of PAK4 in extracellular matrix degradation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387945. ; http://dx.doi.org/10.5353/th_b5387945 ; http://hdl.handle.net/10722/251376

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Extracellular Matrix (ECM) Degradation is an essential process for cancer cell invasion from the tumor to blood stream. A membrane structure called invadopodia is thought… (more)

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Extracellular Matrix (ECM) Degradation is an essential process for cancer cell invasion from the tumor to blood stream. A membrane structure called invadopodia is thought to be responsible to this process. p21-activated kinase 4 (PAK4), which is a serine/threonine protein kinase, has been found to be overexpressed in various cancers. PAK4 has been shown to participate in cell survival and cytoskeleton dynamics, so as to promote the proliferation and migration of cancer cells. Overexpression of PAK4 can also promote podosomes formation, a homolog of invadopodia in macrophages. This research aims to investigate the role of PAK4 in the ECM degrading properties of hepatocellular carcinoma (HCC). Here, a panel of HCC cell lines was tested by ECM degradation assay. Among all the cell lines tested, only Hep3Band HLE cells possessed invadopodia to degrade the gelatin matrix. However, a new gelatin degradation pattern, characterized by large patches around cell peripheral, namely around-cell-peripheral degradation (ACPD), was observed in two HCC cell lines, SMMC-7721 (SMMC) and MHCC-97L. PAK4 overexpression in SMMC was shown to promote ACPD and it showed a faster recovery of the degradation after removal of MMPs inhibitor. Quantitative real-time PCR analysis showed PAK4 overexpression promoted transcription of MMP-2 and MMP-9, which are gelatin-degrading MMPs. In addition, the secretion of active dimeric form of MMP-9 was upregulated, as shown by gelatin zymography, suggesting that MMP activity is required for ACPD. Also, I found that PAK4 enhanced the induction of MMP-9 under the treatment of TNF-α, an NFκB pathway activator. Immunofluorescence staining experiments showed that overexpression of wild type and dominant active (DA, S445N)PAK4, but not its dominant negative form(DN, K350/351M),could significantly induce the nuclear translocation of NFκB, even without treatment of TNF-α. The ectopic expression of PAK4 DN in SMMC blocked the nuclear translocation of NFκB induced by TNF-α. Taken together, these results suggested that PAK4 can promote the translocation of NFκB in both TNF-α dependent and independent pathway. The effect of PAK4 on NFκB translocation was further confirmed by subcellular fractionation experiment. In summary, our data suggest PAK4 induces MMP-9 transcription by activation of NFκB pathway, to promote ACPD activity in SMMC cells.

published_or_final_version

Anatomy

Master

Master of Philosophy

Subjects/Keywords: Extracellular matrix; Protein kinases

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APA (6^th Edition):

關冠麒; Kwan, K. (2014). The role of PAK4 in extracellular matrix degradation. (Masters Thesis). University of Hong Kong. Retrieved from Kwan, K. [關冠麒]. (2014). The role of PAK4 in extracellular matrix degradation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387945. ; http://dx.doi.org/10.5353/th_b5387945 ; http://hdl.handle.net/10722/251376

Chicago Manual of Style (16^th Edition):

關冠麒; Kwan, Kwun-ki. “The role of PAK4 in extracellular matrix degradation.” 2014. Masters Thesis, University of Hong Kong. Accessed February 28, 2020. Kwan, K. [關冠麒]. (2014). The role of PAK4 in extracellular matrix degradation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387945. ; http://dx.doi.org/10.5353/th_b5387945 ; http://hdl.handle.net/10722/251376.

MLA Handbook (7^th Edition):

關冠麒; Kwan, Kwun-ki. “The role of PAK4 in extracellular matrix degradation.” 2014. Web. 28 Feb 2020.

Vancouver:

關冠麒; Kwan K. The role of PAK4 in extracellular matrix degradation. [Internet] [Masters thesis]. University of Hong Kong; 2014. [cited 2020 Feb 28]. Available from: Kwan, K. [關冠麒]. (2014). The role of PAK4 in extracellular matrix degradation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387945. ; http://dx.doi.org/10.5353/th_b5387945 ; http://hdl.handle.net/10722/251376.

Council of Science Editors:

關冠麒; Kwan K. The role of PAK4 in extracellular matrix degradation. [Masters Thesis]. University of Hong Kong; 2014. Available from: Kwan, K. [關冠麒]. (2014). The role of PAK4 in extracellular matrix degradation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387945. ; http://dx.doi.org/10.5353/th_b5387945 ; http://hdl.handle.net/10722/251376

University of Hong Kong

10. Tsang, Kwong-shing. FBI-1 and AMPK in choriocarcinoma cells.

Degree: Master of Medical Sciences, 2015, University of Hong Kong

URL: Tsang, K. [曾廣成]. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659705 ; http://hdl.handle.net/10722/221489

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Choriocarcinoma is a rare and highly aggressive tumorwhich belongs to the gestational trophoblastic diseases (GTD). It can be originated from either gestational or non-gestational origins.… (more)

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Choriocarcinoma is a rare and highly aggressive tumorwhich belongs to the gestational trophoblastic diseases (GTD). It can be originated from either gestational or non-gestational origins. Choriocarcinoma is characterized by biphasic pattern and is composed of a mixed population of mononuclear cytotrophoblasts and multinucleated syncytotrophoblasts. Because of its low prevalence, information on the biology of choriocarcinoma is still insufficient. FBI-1 is an oncogenic transcription factor that is found to be overexpressed in various cancers. In our previous study, overexpression of FBI-1 in gestational choriocarcinoma cell lines,JEG-3 and JAR, were found. FBI-1 affects cell survival through regulating apoptosis and modulating cell motility in choriocarcinoma cells. However, the underlying mechanisms on how FBI-1affectscellular functions is largely unknown. AMPK is a master regulator in metabolic pathways and helps cells to maintain energy homeostasis in response to stressful conditions. Dysregulation on AMPK upsets the balance in metabolism that may play a role in the pathogenesis of cancers. Besides, AMPK is strongly associated with Warburg effect which is considered as a hallmark of cancer. In this study, we aim to investigate the relation between FBI-1 and AMPK in choriocarcinoma. Normal trophoblast cell lines HTR-8/SVneo and TEV-1as well as choriocarcinoma cell lines JAR, BeWo and JEG-3 were used. Levels of mRNA and protein expressions were evaluated by qRT-PCR and western blot respectively. In choriocarcinoma cell lines, relative lower levels of both AMPKα1 andα2 mRNA and protein were demonstrated when compared with the normal trophoblast cells lines. After knock down of FBI-1 in choriocarcinoma cell lines,JEG-3 and JAR, the expression of AMPK α1 but not theα2 subunit was suppressed. The expressions of a panel of glycolysis-related genes, including hexokinase II (HK2), phosphoglycerate kinase 1 (PGK1), lactate dehydrogenase A (LDHA), pyruvate kinase muscle isozymeM2 (PKM2), aldolase C (ALDOC) and glucose transporter 1(GLUT1), were examined in this study. It was found that the expressions of most of these genes were unaffected. ALDOC mRNA and HK2 protein expression was found to decrease in choriocarcinoma cells with FBI-1 knockdown, suggesting that glycolytic pathway was affected by FBI-1. These results tend to indicate that AMPK may cooperate with FBI-1 in choriocarcinoma cells to gain survival advantages through modulation of glycolysis although further study is needed.

published_or_final_version

Pathology

Master

Master of Medical Sciences

Subjects/Keywords: Protein kinases; Transcription factors; Choriocarcinoma

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APA (6^th Edition):

Tsang, K. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Masters Thesis). University of Hong Kong. Retrieved from Tsang, K. [曾廣成]. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659705 ; http://hdl.handle.net/10722/221489

Chicago Manual of Style (16^th Edition):

Tsang, Kwong-shing. “FBI-1 and AMPK in choriocarcinoma cells.” 2015. Masters Thesis, University of Hong Kong. Accessed February 28, 2020. Tsang, K. [曾廣成]. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659705 ; http://hdl.handle.net/10722/221489.

MLA Handbook (7^th Edition):

Tsang, Kwong-shing. “FBI-1 and AMPK in choriocarcinoma cells.” 2015. Web. 28 Feb 2020.

Vancouver:

Tsang K. FBI-1 and AMPK in choriocarcinoma cells. [Internet] [Masters thesis]. University of Hong Kong; 2015. [cited 2020 Feb 28]. Available from: Tsang, K. [曾廣成]. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659705 ; http://hdl.handle.net/10722/221489.

Council of Science Editors:

Tsang K. FBI-1 and AMPK in choriocarcinoma cells. [Masters Thesis]. University of Hong Kong; 2015. Available from: Tsang, K. [曾廣成]. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659705 ; http://hdl.handle.net/10722/221489

University of Hong Kong

11. 金冀琴; Jin, Jiqin. The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury.

Degree: PhD, 2014, University of Hong Kong

URL: Jin, J. [金冀琴]. (2014). The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387951 ; http://dx.doi.org/10.5353/th_b5387951 ; http://hdl.handle.net/10722/222197

► Background: Myocardial ischaemia and reperfusion (I/R) injury, a major global public health problem, is associated with significant morbidity and mortality. Diabetic hearts are more sensitive… (more)

▼ Background: Myocardial ischaemia and reperfusion (I/R) injury, a major global public health problem, is associated with significant morbidity and mortality. Diabetic hearts are more sensitive to I/R and consequently are associated with greater morbidity and mortality, while a number of cardioprotective interventions such as ischaemia preconditioning and ischaemia post-conditioning are partly lost or are completely abolished in diabetes. Objectives: I investigated the role of protein kinase C beta 2 (PKC β2) in diabetes induced heart sensitization after I/R and explored the underlying mechanism. Also, I investigated whether remifentanil preconditioning (RPC) ameliorates myocardial infarct size in diabetic rats. Materials and methods: Diabetic rats model was established with streptozotocin (STZ) while ruboxistaurin (RBX), CGP-53353 (CGP), and siRNA of PKC β2 were induced in diabetic rats or high glucose-exposed H9C2 cells to investigate the relationship between PKC β2 and myocardial I/R injury with following indexes including cardiac function, myocardial infarct size, cell apoptosis, concentrations of Creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), and mitochondrial membrane potential. The siRNA of caveolin (Cav-3) and Akt were used in H9C2 cells to detect the mechanism of PKC β2 induced aggravating myocardial I/R injury. Both in diabetic rats and high glucose-exposed H9C2 cells, cardiac protective ability of RPC were measured. The naloxone and caveolin (Cav-3) siRNA were used in RPC to detect the mechanism of RPC. The proteins expression of PKCβ2, Cav-3, Akt, and cleaved caspase 3 were measured by western blot. Results: The expression of PKC β2 was significantly up regulated in diabetes after acute myocardial I/R. In diabetic rats, RBX markedly reduced myocardial infarct size and apoptotic cells. RBX also restored left ventricular functions and decreased concentrations of CK-MB and LDH after I/R. In high glucose-exposed H9C2 cells, both CGP and PKC β2 siRNA decreased apoptotic cells and impaired mitochondrion after hypoxia and reoxygenation (H/R). Cav-3 siRNA or Akt siRNA aggravated cell apoptosis and mitochondrial injury after H/R. Proteins expression of Cav-3 and Akt were increased after RBX treatment in diabetic I/R model. Furthermore, RPC attenuated myocardial infarct size and restored cardiac systolic ability in non-diabetic rats. RPC decreased apoptotic cardiomyocytes and attenuated mitochondrial injury in cultured cardiomyocytes. Activation of Akt and Bcl-2 were involved in RPC. Naloxone and Cav-3 siRNA blocked the cardioprotection of RPC against myocardial I/R injury. RPC failed to ameliorate myocardial infarct size in diabetic rats and did not decrease high glucose-exposed H9C2 cell apoptosis after H/R. Conclusions: The high expression of PKC β2 contributed to diabetic hearts being more sensitive to I/R. RBX ameliorates myocardial I/R injury by attenuating post-reperfusion myocardial infarct size and cardiac dysfunction. The plausible mechanism underlying the RBX-induced…

Subjects/Keywords: Ischemia; Protein kinases; Reperfusion injury

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APA (6^th Edition):

金冀琴; Jin, J. (2014). The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury. (Doctoral Dissertation). University of Hong Kong. Retrieved from Jin, J. [金冀琴]. (2014). The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387951 ; http://dx.doi.org/10.5353/th_b5387951 ; http://hdl.handle.net/10722/222197

Chicago Manual of Style (16^th Edition):

金冀琴; Jin, Jiqin. “The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury.” 2014. Doctoral Dissertation, University of Hong Kong. Accessed February 28, 2020. Jin, J. [金冀琴]. (2014). The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387951 ; http://dx.doi.org/10.5353/th_b5387951 ; http://hdl.handle.net/10722/222197.

MLA Handbook (7^th Edition):

金冀琴; Jin, Jiqin. “The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury.” 2014. Web. 28 Feb 2020.

Vancouver:

金冀琴; Jin J. The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury. [Internet] [Doctoral dissertation]. University of Hong Kong; 2014. [cited 2020 Feb 28]. Available from: Jin, J. [金冀琴]. (2014). The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387951 ; http://dx.doi.org/10.5353/th_b5387951 ; http://hdl.handle.net/10722/222197.

Council of Science Editors:

金冀琴; Jin J. The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury. [Doctoral Dissertation]. University of Hong Kong; 2014. Available from: Jin, J. [金冀琴]. (2014). The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387951 ; http://dx.doi.org/10.5353/th_b5387951 ; http://hdl.handle.net/10722/222197

University of Hong Kong

12. 潘竣熺; Poon, Chun-hei. Investigating the roles of protein kinase R (PKR) to modulate the effects of systemic inflammation on the brain.

Degree: PhD, 2015, University of Hong Kong

URL: Poon, C. [潘竣熺]. (2015). Investigating the roles of protein kinase R (PKR) to modulate the effects of systemic inflammation on the brain. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387956 ; http://dx.doi.org/10.5353/th_b5387956 ; http://hdl.handle.net/10722/222276

► Systemic inflammation induces neuroinflammation and alters neural activity and functions, ultimately leading to sickness behavior (fever, anorexia, motor impairments, decreased exploratory activity, and depressed mood).… (more)

▼ Systemic inflammation induces neuroinflammation and alters neural activity and functions, ultimately leading to sickness behavior (fever, anorexia, motor impairments, decreased exploratory activity, and depressed mood). While these changes collectively help the body to recover from infections and injuries, increasing lines of evidence have indicated that their dysregulation may be involved in depression and delirium. Therefore, a more thorough understanding about their regulation will be beneficial. The aims of this study are to investigate the roles of protein kinase R (PKR), an immune-regulatory kinase that has also been implicated to modulate neurons, in systemic inflammation-induced neuroinflammation, sickness behavior, and neuronal responses. Three-month old female wild type (WT) and PKR knockout (-/-) mice were subcutaneously injected with live Escherichia coli (E. coli) or phosphate buffered saline (PBS). Central and peripheral inflammation were assessed by determining the mRNA expression levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in the brain (hypothalamus and hippocampus) and the liver. Additionally, the percentage of neutrophils was quantified from blood smears as another indicator of systemic inflammation. Moreover, sickness behavior was monitored by recording the changes in rectal temperature and food consumption, and by several behavioral tasks (burrowing, open field test, object investigation test, social interaction test, and forced swimming test). Finally, neuronal responses to systemic inflammation were studied in terms of neural activity changes at the paraventricular nucleus (PVN), i.e. indirectly by immunohistochemical staining for c-fos (a neural activity marker), and also in terms of protein level changes of several synaptic proteins, i.e. postsynaptic density 95 (PSD95), NMDA receptor 2B (NMDAR2B), and NMDA receptor 1 (NMDAR1), in the hypothalamus and hippocampus. My data indicate that E. coli induced inflammatory changes in the brain and at the periphery in both genotypes of mice. Loss of PKR effectively attenuated the inflammatory changes at the periphery, whereas it slightly inhibited the neuroinflammatory responses in the hypothalamus, and it had no effect on those in the hippocampus. Unexpectedly, the decrease of systemic inflammation in PKR -/- mice was not associated with reduced sickness behavior. Instead PKR -/- mice displayed exacerbated sickness behavior when compared WT mice. Regarding the neuronal response changes to systemic inflammation, E. coli increased the number of c-fos immunopositive cells at the PVN of WT mice, but this was not observed in PKR -/- mice. Although E. coli did not affect the expression of NMDAR1 and PSD95 (hypothalamus and hippocampus) and NMDAR2B (hypothalamus) in both genotypes, it lowered NMDAR2B expression in the hippocampus of PKR -/- mice but not in WT mice. Taken together, these findings suggest that (1) deficiency of PKR could…

Subjects/Keywords: Inflammation; Brain - Immunology; Protein kinases

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APA (6^th Edition):

潘竣熺; Poon, C. (2015). Investigating the roles of protein kinase R (PKR) to modulate the effects of systemic inflammation on the brain. (Doctoral Dissertation). University of Hong Kong. Retrieved from Poon, C. [潘竣熺]. (2015). Investigating the roles of protein kinase R (PKR) to modulate the effects of systemic inflammation on the brain. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387956 ; http://dx.doi.org/10.5353/th_b5387956 ; http://hdl.handle.net/10722/222276

Chicago Manual of Style (16^th Edition):

潘竣熺; Poon, Chun-hei. “Investigating the roles of protein kinase R (PKR) to modulate the effects of systemic inflammation on the brain.” 2015. Doctoral Dissertation, University of Hong Kong. Accessed February 28, 2020. Poon, C. [潘竣熺]. (2015). Investigating the roles of protein kinase R (PKR) to modulate the effects of systemic inflammation on the brain. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387956 ; http://dx.doi.org/10.5353/th_b5387956 ; http://hdl.handle.net/10722/222276.

MLA Handbook (7^th Edition):

潘竣熺; Poon, Chun-hei. “Investigating the roles of protein kinase R (PKR) to modulate the effects of systemic inflammation on the brain.” 2015. Web. 28 Feb 2020.

Vancouver:

潘竣熺; Poon C. Investigating the roles of protein kinase R (PKR) to modulate the effects of systemic inflammation on the brain. [Internet] [Doctoral dissertation]. University of Hong Kong; 2015. [cited 2020 Feb 28]. Available from: Poon, C. [潘竣熺]. (2015). Investigating the roles of protein kinase R (PKR) to modulate the effects of systemic inflammation on the brain. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387956 ; http://dx.doi.org/10.5353/th_b5387956 ; http://hdl.handle.net/10722/222276.

Council of Science Editors:

潘竣熺; Poon C. Investigating the roles of protein kinase R (PKR) to modulate the effects of systemic inflammation on the brain. [Doctoral Dissertation]. University of Hong Kong; 2015. Available from: Poon, C. [潘竣熺]. (2015). Investigating the roles of protein kinase R (PKR) to modulate the effects of systemic inflammation on the brain. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387956 ; http://dx.doi.org/10.5353/th_b5387956 ; http://hdl.handle.net/10722/222276

University of Hong Kong

13. Gao, Weiwei. Salt-inducible kinases function as a host restriction to human T-cell leukemia virus type 1 transcription.

Degree: Master of Medical Sciences, 2012, University of Hong Kong

URL: Gao, W. [高蔚为]. (2012). Salt-inducible kinases function as a host restriction to human T-cell leukemia virus type 1 transcription. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4818309 ; http://dx.doi.org/10.5353/th_b4818309 ; http://hdl.handle.net/10722/173861

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Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HTLV-1 Tax is… (more)

Subjects/Keywords: HTLV-I (Virus); Protein kinases.

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APA (6^th Edition):

Gao, W. (2012). Salt-inducible kinases function as a host restriction to human T-cell leukemia virus type 1 transcription. (Masters Thesis). University of Hong Kong. Retrieved from Gao, W. [高蔚为]. (2012). Salt-inducible kinases function as a host restriction to human T-cell leukemia virus type 1 transcription. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4818309 ; http://dx.doi.org/10.5353/th_b4818309 ; http://hdl.handle.net/10722/173861

Chicago Manual of Style (16^th Edition):

Gao, Weiwei. “Salt-inducible kinases function as a host restriction to human T-cell leukemia virus type 1 transcription.” 2012. Masters Thesis, University of Hong Kong. Accessed February 28, 2020. Gao, W. [高蔚为]. (2012). Salt-inducible kinases function as a host restriction to human T-cell leukemia virus type 1 transcription. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4818309 ; http://dx.doi.org/10.5353/th_b4818309 ; http://hdl.handle.net/10722/173861.

MLA Handbook (7^th Edition):

Gao, Weiwei. “Salt-inducible kinases function as a host restriction to human T-cell leukemia virus type 1 transcription.” 2012. Web. 28 Feb 2020.

Vancouver:

Gao W. Salt-inducible kinases function as a host restriction to human T-cell leukemia virus type 1 transcription. [Internet] [Masters thesis]. University of Hong Kong; 2012. [cited 2020 Feb 28]. Available from: Gao, W. [高蔚为]. (2012). Salt-inducible kinases function as a host restriction to human T-cell leukemia virus type 1 transcription. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4818309 ; http://dx.doi.org/10.5353/th_b4818309 ; http://hdl.handle.net/10722/173861.

Council of Science Editors:

Gao W. Salt-inducible kinases function as a host restriction to human T-cell leukemia virus type 1 transcription. [Masters Thesis]. University of Hong Kong; 2012. Available from: Gao, W. [高蔚为]. (2012). Salt-inducible kinases function as a host restriction to human T-cell leukemia virus type 1 transcription. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4818309 ; http://dx.doi.org/10.5353/th_b4818309 ; http://hdl.handle.net/10722/173861

University of Hong Kong

14. Chu, Chun-ho, Terence. Dysregulated PAK4 and chemosensitivity in ovarian cancer: an in vitro study.

Degree: Master of Medical Sciences, 2012, University of Hong Kong

URL: Chu, C. T. [朱雋皞]. (2012). Dysregulated PAK4 and chemosensitivity in ovarian cancer : an in vitro study. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4827399 ; http://dx.doi.org/10.5353/th_b4827399 ; http://hdl.handle.net/10722/173867

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Ovarian cancer is regarded as the most lethal gynecological malignancy around the world. Despite the advancing medical improvements in both surgery and chemotherapy, the mortality… (more)

Subjects/Keywords: Ovaries - Cancer.; Protein kinases.

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APA (6^th Edition):

Chu, Chun-ho, T. (2012). Dysregulated PAK4 and chemosensitivity in ovarian cancer: an in vitro study. (Masters Thesis). University of Hong Kong. Retrieved from Chu, C. T. [朱雋皞]. (2012). Dysregulated PAK4 and chemosensitivity in ovarian cancer : an in vitro study. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4827399 ; http://dx.doi.org/10.5353/th_b4827399 ; http://hdl.handle.net/10722/173867

Chicago Manual of Style (16^th Edition):

Chu, Chun-ho, Terence. “Dysregulated PAK4 and chemosensitivity in ovarian cancer: an in vitro study.” 2012. Masters Thesis, University of Hong Kong. Accessed February 28, 2020. Chu, C. T. [朱雋皞]. (2012). Dysregulated PAK4 and chemosensitivity in ovarian cancer : an in vitro study. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4827399 ; http://dx.doi.org/10.5353/th_b4827399 ; http://hdl.handle.net/10722/173867.

MLA Handbook (7^th Edition):

Chu, Chun-ho, Terence. “Dysregulated PAK4 and chemosensitivity in ovarian cancer: an in vitro study.” 2012. Web. 28 Feb 2020.

Vancouver:

Chu, Chun-ho T. Dysregulated PAK4 and chemosensitivity in ovarian cancer: an in vitro study. [Internet] [Masters thesis]. University of Hong Kong; 2012. [cited 2020 Feb 28]. Available from: Chu, C. T. [朱雋皞]. (2012). Dysregulated PAK4 and chemosensitivity in ovarian cancer : an in vitro study. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4827399 ; http://dx.doi.org/10.5353/th_b4827399 ; http://hdl.handle.net/10722/173867.

Council of Science Editors:

Chu, Chun-ho T. Dysregulated PAK4 and chemosensitivity in ovarian cancer: an in vitro study. [Masters Thesis]. University of Hong Kong; 2012. Available from: Chu, C. T. [朱雋皞]. (2012). Dysregulated PAK4 and chemosensitivity in ovarian cancer : an in vitro study. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4827399 ; http://dx.doi.org/10.5353/th_b4827399 ; http://hdl.handle.net/10722/173867

Ryerson University

15. Martin, Zechariah. mTor controls lysosome function by modulating the RAB7 GTPASE.

Degree: 2017, Ryerson University

URL: https://digital.library.ryerson.ca/islandora/object/RULA%3A7189

► Mammalian target of rapamycin (mTOR) is a protein kinase that integrates signals including stress and nutrient availability, to modulate the metabolic state of the cell.… (more)

▼ Mammalian target of rapamycin (mTOR) is a protein kinase that integrates signals including stress and nutrient availability, to modulate the metabolic state of the cell. Interestingly, mTOR complex 1 (mTORC1) is specifically found on lysosomes where it regulates lysosome function, trafficking and morphology. However, little is known about how mTOR interfaces with lysosomal regulators, like the Rab7 GTPase, the canonical mediator of lysosome function, including biogenesis and trafficking to lysosomes to control processes such as antigen presentation and cell signaling. Rab7 can exist in two states. GDP-bound Rab7 is inactive but can be converted to GTP-bound Rab7, the catalytically active form of Rab7. Guanine nucleotide exchange factors (GEFs) are responsible for this conversion. Conversely, GTP-hydrolysis activating proteins (GAPs) facilitate Rab7 GTP hydrolysis, resulting in the conversion of GTP to GDP, rendering Rab7 inactive. We hypothesized that mTOR and Rab7 are functionally linked. Here we show that mTOR negatively controls Rab7. mTOR inhibition through the use of torin, EBSS (an amino acid deprived media) and A-769662 (an AMPK activator), increased levels of both total and active Rab7 (Rab7-GTP) on the lysosomal membrane. This was observed through fractionation, fluorescence microscopy and biochemical pull-down assays. This negative regulation is specific to mTOR, acting through TBC1D15, a Rab7 GAP. mTOR inhibition resulted in a significant reduction in levels of TBC1D15 via ubiquitination, which can be restored upon inhibition of the proteasome. Additionally, mTOR inhibition increased lysosomal proteolytic activity, and enhanced trafficking of material toward the lysosome. Our work suggests that under starvation conditions, trafficking to the lysosome is accelerated, re-establishing nutrient homeostasis. This research could provide a novel link between membrane regulation (Rab7) and metabolic stress sensors (mTOR), allowing insight into the pathogenesis of several metabolic diseases, including certain forms of cancer.

Subjects/Keywords: Lysosomes; Rapamycin; Protein kinases

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

APA (6^th Edition):

Martin, Z. (2017). mTor controls lysosome function by modulating the RAB7 GTPASE. (Thesis). Ryerson University. Retrieved from https://digital.library.ryerson.ca/islandora/object/RULA%3A7189

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):

Martin, Zechariah. “mTor controls lysosome function by modulating the RAB7 GTPASE.” 2017. Thesis, Ryerson University. Accessed February 28, 2020. https://digital.library.ryerson.ca/islandora/object/RULA%3A7189.

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

MLA Handbook (7^th Edition):

Martin, Zechariah. “mTor controls lysosome function by modulating the RAB7 GTPASE.” 2017. Web. 28 Feb 2020.

Vancouver:

Martin Z. mTor controls lysosome function by modulating the RAB7 GTPASE. [Internet] [Thesis]. Ryerson University; 2017. [cited 2020 Feb 28]. Available from: https://digital.library.ryerson.ca/islandora/object/RULA%3A7189.

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

Council of Science Editors:

Martin Z. mTor controls lysosome function by modulating the RAB7 GTPASE. [Thesis]. Ryerson University; 2017. Available from: https://digital.library.ryerson.ca/islandora/object/RULA%3A7189

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

Queens University

16. Zheng, Jimin. Structural and Functional Studies of Escherichia coli Kinases and Phosphatases .

Degree: Biochemistry, 2010, Queens University

URL: http://hdl.handle.net/1974/5908

► Phosphorylation/dephosphorylation is likely the most crucial chemical reaction taking place in all living organisms. It is the basis for the regulatory control of many diverse… (more)

▼ Phosphorylation/dephosphorylation is likely the most crucial chemical reaction taking place in all living organisms. It is the basis for the regulatory control of many diverse biological events triggered by extracellular effectors. Moreover, it is a ubiquitous element of intracellular signal transduction pathways that regulates a wide range of processes. While protein phosphorylation has been extensively characterized in eukaryotes, far less is known about its emerging counterparts in prokaryotes. This study involved determination of the crystal structures and functional characterization of two protein kinases, YihE and AceK (also a protein phosphatase), and two nucleotide pyrophosphatases, YjjX and YhdE. X-ray crystallographic structure determination combined with bioinformatics analyses, mutageneses and biochemical experiments, both in vitro and in vivo, were utilized for the functional characterization of each protein. YihE was found to be a previously unknown kinase component of a new type of bacterial phospho-relay mechanism, thus adding kinase activity as another response to the Cpx sensing system that functions to maintain cellular homeostasis. AceK, which possesses both kinase and phosphatase activities, modifies isocitrate dehydrogenase (ICDH) to regulate the flux of isocitrate into the glyoxylate cycle. The structures of Acek alone and in complex with its substrate, ICDH, provided us with information to explain the mechanisms underlying its bifunctionality and its molecular switch. Through structural comparison and, particularly, functional characterization, we revealed that YjjX is a novel ITPase/XTPase responsible for the removal of non-canonical nucleotides from the cell during oxidative stress in Escherichia coli. YhdE, identified as a novel dTTPase, was observed to retard cell growth and form a filamentous phenotype when overexpressed in the cell, suggesting that YhdE is involved in the control of cell growth and division by regulating the cell nucleotide pool for DNA synthesis. In summary, this research has made a substantial ii contribution to the investigation of bacterial phosphorylation and dephophorylation systems that respond to various environmental conditions.

Subjects/Keywords: Protein structure; Prokaryotic Kinases Phosphatases

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APA (6^th Edition):

Zheng, J. (2010). Structural and Functional Studies of Escherichia coli Kinases and Phosphatases . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/5908

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):

Zheng, Jimin. “Structural and Functional Studies of Escherichia coli Kinases and Phosphatases .” 2010. Thesis, Queens University. Accessed February 28, 2020. http://hdl.handle.net/1974/5908.

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

MLA Handbook (7^th Edition):

Zheng, Jimin. “Structural and Functional Studies of Escherichia coli Kinases and Phosphatases .” 2010. Web. 28 Feb 2020.

Vancouver:

Zheng J. Structural and Functional Studies of Escherichia coli Kinases and Phosphatases . [Internet] [Thesis]. Queens University; 2010. [cited 2020 Feb 28]. Available from: http://hdl.handle.net/1974/5908.

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

Council of Science Editors:

Zheng J. Structural and Functional Studies of Escherichia coli Kinases and Phosphatases . [Thesis]. Queens University; 2010. Available from: http://hdl.handle.net/1974/5908

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

Rutgers University

17. Rane, Chetan K., 1989-. PAK4 as a drug target in breast cancer therapy.

Degree: PhD, Pharmacology, Cellular and Molecular, 2017, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/54913/

►

PAK4, belonging to Group II PAKs, is an important signaling protein with key roles in regulating cell growth, cell survival and cell morphology. PAK4 protein… (more)

▼

PAK4, belonging to Group II PAKs, is an important signaling protein with key roles in regulating cell growth, cell survival and cell morphology. PAK4 protein levels are higher in several subtypes of breast cancer cells and PAK4 gene is amplified in basal like breast cancer. PAK4 overexpression in a mouse mammary epithelial cell line (iMMEC) results in oncogenic transformation of these cells, while siRNA mediated PAK4 down regulation in a human triple negative breast cancer cell line, MDA-MB-231, resulted in significant inhibition of its tumorigenic potential. These results point to a central role for PAK4 in mammary tumorigenesis. PAK4 expression pattern makes it an attractive drug target, however, it is important to note that PAK4 has both kinase-dependent and – independent functions in regulating tumor formation. Hence, blocking its kinase activity alone is insufficient in blocking its tumorigenic potential. Our lab collaborated with Karyopharm Therapeutics to investigate a novel PAK4 inhibitor, KPT-9274. I observed that treatment with KPT-9274 and KPT-8752 (isoform of KPT-9274) inhibited the cell growth, cell survival and cell motility of breast cancer cell lines, with this effect most significantly observed in triple negative breast cancer cell lines. I observed that treatment with KPT inhibitors inhibited PAK4 protein levels along with PAK4 associated downstream signaling pathways in triple negative breast cancer cell lines. Most importantly, I observed that KPT- 9274 significantly inhibited tumor growth in mouse xenograft models of 3 human triple negative breast cancer cell lines. KPT-9274 was capable of reducing steady state PAK4 protein levels in vivo, without significantly affecting PAK1 protein levels, indicating that KPT-9274 exhibits in vivo PAK4 specificity. This study shows that PAK4 can serve as a novel drug target in triple negative breast cancer therapy and KPT-9274 can have clinical benefits for the triple negative breast cancer population. Next, I analyzed RNA-seq data of samples collected from non-transformed WT iMMECs and iMMECs overexpressing PAK4, that form tumors in mice. Sequencing analysis identified several genes previously unknown to be regulated by PAK4. Using q-PCR, I was able to validate the RNAseq data, further suggesting that RNA-seq is a promising and reproducible tool to study PAK4 induced transcriptional changes. This study reveals the PAK4 transcriptome profile in mammary tumor forming cells, and can provide translational utility in other types of cancers as well. Delineating the varied effectors of PAK4 signaling cascade will help uncover novel biomarkers for cancer, with some serving as potential therapeutic targets.

Advisors/Committee Members: Kong, Tony (chair), Liu, Fang (co-chair), Minden, Audrey (internal member), Cai, Li (outside member), School of Graduate Studies.

Subjects/Keywords: Breast – Cancer – Treatment; Protein kinases

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

APA (6^th Edition):

Rane, Chetan K., 1. (2017). PAK4 as a drug target in breast cancer therapy. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/54913/

Chicago Manual of Style (16^th Edition):

Rane, Chetan K., 1989-. “PAK4 as a drug target in breast cancer therapy.” 2017. Doctoral Dissertation, Rutgers University. Accessed February 28, 2020. https://rucore.libraries.rutgers.edu/rutgers-lib/54913/.

MLA Handbook (7^th Edition):

Rane, Chetan K., 1989-. “PAK4 as a drug target in breast cancer therapy.” 2017. Web. 28 Feb 2020.

Vancouver:

Rane, Chetan K. 1. PAK4 as a drug target in breast cancer therapy. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2020 Feb 28]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/54913/.

Council of Science Editors:

Rane, Chetan K. 1. PAK4 as a drug target in breast cancer therapy. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/54913/

Hong Kong University of Science and Technology

18. He, Jing. A preliminary study of PICK1's role in mitochondrial function and Parkinson's disease.

Degree: 2011, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-62386 ; https://doi.org/10.14711/thesis-b1155680 ; http://repository.ust.hk/ir/bitstream/1783.1-62386/1/th_redirect.html

► Parkinson’s disease (PD) is a prevalent neurodegenerative disorder that is characterized by bradykinesia, rigidity, resting tremor and postural instability. The death of dopaminergic neurons in… (more)

Subjects/Keywords: Protein kinases ; Mitochondria ; Parkinson's disease

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

APA (6^th Edition):

He, J. (2011). A preliminary study of PICK1's role in mitochondrial function and Parkinson's disease. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-62386 ; https://doi.org/10.14711/thesis-b1155680 ; http://repository.ust.hk/ir/bitstream/1783.1-62386/1/th_redirect.html

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):

He, Jing. “A preliminary study of PICK1's role in mitochondrial function and Parkinson's disease.” 2011. Thesis, Hong Kong University of Science and Technology. Accessed February 28, 2020. http://repository.ust.hk/ir/Record/1783.1-62386 ; https://doi.org/10.14711/thesis-b1155680 ; http://repository.ust.hk/ir/bitstream/1783.1-62386/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

He, Jing. “A preliminary study of PICK1's role in mitochondrial function and Parkinson's disease.” 2011. Web. 28 Feb 2020.

Vancouver:

He J. A preliminary study of PICK1's role in mitochondrial function and Parkinson's disease. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2011. [cited 2020 Feb 28]. Available from: http://repository.ust.hk/ir/Record/1783.1-62386 ; https://doi.org/10.14711/thesis-b1155680 ; http://repository.ust.hk/ir/bitstream/1783.1-62386/1/th_redirect.html.

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

Council of Science Editors:

He J. A preliminary study of PICK1's role in mitochondrial function and Parkinson's disease. [Thesis]. Hong Kong University of Science and Technology; 2011. Available from: http://repository.ust.hk/ir/Record/1783.1-62386 ; https://doi.org/10.14711/thesis-b1155680 ; http://repository.ust.hk/ir/bitstream/1783.1-62386/1/th_redirect.html

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

Hong Kong University of Science and Technology

19. Tang, Jing. Functional characterization of Cdk5-dependent Mst3 phosphorylation and Mst3 activity in regulating cortical development.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-86316 ; https://doi.org/10.14711/thesis-b1266307 ; http://repository.ust.hk/ir/bitstream/1783.1-86316/1/th_redirect.html

► The cerebral cortex is the outermost layered structure of the cerebrum in humans and some other vertebrates. It serves as the organization center of the… (more)

▼ The cerebral cortex is the outermost layered structure of the cerebrum in humans and some other vertebrates. It serves as the organization center of the brain and is involved in memory, attention, thought, language, movement, and emotion. In humans, the cerebral cortex comprises 6 layers, 2 to 4 mm thick and contains between 10 and 14 billion neurons. The radial migration of newborn neurons is critical for cerebral cortex lamination. Proper neuronal migration requires the precise and rapid reorganization of the actin and microtubule cytoskeleton. However, the signaling mechanisms underlying these processes are not well understood. The present study reveals that Mst3, a serine/threonine kinase highly expressed in the developing mouse brain, is essential for neuronal migration and final neuronal positioning in the developing mouse neocortex. Mst3 silencing by in utero electroporation perturbs the multipolar–bipolar transition of migrating neurons and significantly retards radial migration. The dendritic arborization as well as the upper cortical neurons excitability is also impaired in Mst3 knockdown neurons. The kinase activity of Mst3 is essential for its functions in neuronal morphogenesis and migration, and is regulated via Ser79 phosphorylation by a serine/threonine kinase, cyclin-dependent kinase 5 (Cdk5). Interestingly, Mst3 regulates neuronal migration by modulating the activity of RhoA, a Rho GTPase critical for actin cytoskeletal reorganization. The present results show that Mst3 phosphorylates RhoA at Ser26, thereby negatively regulating the GTPase activity of RhoA. Importantly, RhoA knockdown restores normal neuronal migration in Mst3-knockdown cortices. These findings collectively indicate that Cdk5/Mst3 signaling pathway regulates neuronal migration via RhoA-dependent actin dynamics. The convergence of various kinase signaling pathways toward cytoskeletal organization and remodeling during neuronal migration indicates that corticogenesis is precisely regulated by a complex and coordinated signaling system.

Subjects/Keywords: Cerebral cortex ; Protein kinases

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APA (6^th Edition):

Tang, J. (2013). Functional characterization of Cdk5-dependent Mst3 phosphorylation and Mst3 activity in regulating cortical development. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-86316 ; https://doi.org/10.14711/thesis-b1266307 ; http://repository.ust.hk/ir/bitstream/1783.1-86316/1/th_redirect.html

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):

Tang, Jing. “Functional characterization of Cdk5-dependent Mst3 phosphorylation and Mst3 activity in regulating cortical development.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed February 28, 2020. http://repository.ust.hk/ir/Record/1783.1-86316 ; https://doi.org/10.14711/thesis-b1266307 ; http://repository.ust.hk/ir/bitstream/1783.1-86316/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Tang, Jing. “Functional characterization of Cdk5-dependent Mst3 phosphorylation and Mst3 activity in regulating cortical development.” 2013. Web. 28 Feb 2020.

Vancouver:

Tang J. Functional characterization of Cdk5-dependent Mst3 phosphorylation and Mst3 activity in regulating cortical development. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2020 Feb 28]. Available from: http://repository.ust.hk/ir/Record/1783.1-86316 ; https://doi.org/10.14711/thesis-b1266307 ; http://repository.ust.hk/ir/bitstream/1783.1-86316/1/th_redirect.html.

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

Council of Science Editors:

Tang J. Functional characterization of Cdk5-dependent Mst3 phosphorylation and Mst3 activity in regulating cortical development. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-86316 ; https://doi.org/10.14711/thesis-b1266307 ; http://repository.ust.hk/ir/bitstream/1783.1-86316/1/th_redirect.html

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

Hong Kong University of Science and Technology

20. Sun, Xulun. Identification and functional characterization of NME7-binding proteins.

Degree: 2014, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-87471 ; https://doi.org/10.14711/thesis-b1334235 ; http://repository.ust.hk/ir/bitstream/1783.1-87471/1/th_redirect.html

► In proliferating cells, centrosomes organize the microtubule network and this function depends on the γ-tubulin ring complex (γTuRC). While in quiescent cells, the mother centriole… (more)

▼ In proliferating cells, centrosomes organize the microtubule network and this function depends on the γ-tubulin ring complex (γTuRC). While in quiescent cells, the mother centriole of the centrosome organizes the formation of primary cilia, which are microtubule-based organelles present in most vertebrate cells. Cilia are involved in many essential signaling pathways and plays important roles in helping cells sense extracellular environment. The previous study of our laboratory identified that NME7 (non-metastatic cells 7) is a novel γTuRC component, which promotes γTuRC-mediated microtubule nucleation through its kinase action. NME7 is a member of the nucleoside-diphosphate kinase (NDPK) family. nme7 knockout mice exhibit cilia-related defects, including situs inversus and hydrocephalus. Moreover, we found that NME7 localizes to cilia and is essential for ciliary growth. Considering the NME7’s important role in the events such as microtubule nucleation and ciliogenesis, I identify NME7-binding proteins by mass spectrometry, characterize their interactions with NME7, and uncover the function of these interactions. One of the identified proteins has been reported to block primary cilia assembly in proliferating cells. I found that NME7 and the binding partner have interaction with each other, and the binding protein can also be a competitor for the binding of γTuRC to NME7. Interestingly, the protein level of the binding protein significantly decreased in NME7-depleted cells. I further investigated how NME7 knockdown affects the expression of the binding protein. Protein stability analysis showed that NME7 depletion decreases protein stability of the binding protein. Furthermore, depletion of the binding protein or NME7 resulted in cilia formation in proliferating cells. These results suggest that NME7 may block ciliogenesis in proliferating cells by stabilization of the binding protein. In summary, I provided a series of potential NME7-binding partners which might be essential for the regulation and functional study of NME7.

Subjects/Keywords: Microtubules ; Protein kinases ; Ciliata

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APA (6^th Edition):

Sun, X. (2014). Identification and functional characterization of NME7-binding proteins. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-87471 ; https://doi.org/10.14711/thesis-b1334235 ; http://repository.ust.hk/ir/bitstream/1783.1-87471/1/th_redirect.html

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, Xulun. “Identification and functional characterization of NME7-binding proteins.” 2014. Thesis, Hong Kong University of Science and Technology. Accessed February 28, 2020. http://repository.ust.hk/ir/Record/1783.1-87471 ; https://doi.org/10.14711/thesis-b1334235 ; http://repository.ust.hk/ir/bitstream/1783.1-87471/1/th_redirect.html.

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, Xulun. “Identification and functional characterization of NME7-binding proteins.” 2014. Web. 28 Feb 2020.

Vancouver:

Sun X. Identification and functional characterization of NME7-binding proteins. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2014. [cited 2020 Feb 28]. Available from: http://repository.ust.hk/ir/Record/1783.1-87471 ; https://doi.org/10.14711/thesis-b1334235 ; http://repository.ust.hk/ir/bitstream/1783.1-87471/1/th_redirect.html.

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

Council of Science Editors:

Sun X. Identification and functional characterization of NME7-binding proteins. [Thesis]. Hong Kong University of Science and Technology; 2014. Available from: http://repository.ust.hk/ir/Record/1783.1-87471 ; https://doi.org/10.14711/thesis-b1334235 ; http://repository.ust.hk/ir/bitstream/1783.1-87471/1/th_redirect.html

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

Hong Kong University of Science and Technology

21. Mao, Zhuo. PICK1 and ICA69's roles in insulin granule biogenesis and Zn²⁺ homeostasis.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-76070 ; https://doi.org/10.14711/thesis-b1213285 ; http://repository.ust.hk/ir/bitstream/1783.1-76070/1/th_redirect.html

► Diabetes mellitus is a chronic metabolic disease characterized by elevated blood glucose that results from defects in insulin secretion and/or action. Until now, the cellular… (more)

Subjects/Keywords: Protein kinases ; Insulin ; Somatomedin ; Homeostasis

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APA (6^th Edition):

Mao, Z. (2013). PICK1 and ICA69's roles in insulin granule biogenesis and Zn²⁺ homeostasis. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-76070 ; https://doi.org/10.14711/thesis-b1213285 ; http://repository.ust.hk/ir/bitstream/1783.1-76070/1/th_redirect.html

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):

Mao, Zhuo. “PICK1 and ICA69's roles in insulin granule biogenesis and Zn²⁺ homeostasis.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed February 28, 2020. http://repository.ust.hk/ir/Record/1783.1-76070 ; https://doi.org/10.14711/thesis-b1213285 ; http://repository.ust.hk/ir/bitstream/1783.1-76070/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Mao, Zhuo. “PICK1 and ICA69's roles in insulin granule biogenesis and Zn²⁺ homeostasis.” 2013. Web. 28 Feb 2020.

Vancouver:

Mao Z. PICK1 and ICA69's roles in insulin granule biogenesis and Zn²⁺ homeostasis. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2020 Feb 28]. Available from: http://repository.ust.hk/ir/Record/1783.1-76070 ; https://doi.org/10.14711/thesis-b1213285 ; http://repository.ust.hk/ir/bitstream/1783.1-76070/1/th_redirect.html.

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

Council of Science Editors:

Mao Z. PICK1 and ICA69's roles in insulin granule biogenesis and Zn²⁺ homeostasis. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-76070 ; https://doi.org/10.14711/thesis-b1213285 ; http://repository.ust.hk/ir/bitstream/1783.1-76070/1/th_redirect.html

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

King Abdullah University of Science and Technology

22. Diaz Galicia, Miriam Escarlet. Engineering of kinase-based protein interacting devices: active expression of tyrosine kinase domains.

Degree: 2018, King Abdullah University of Science and Technology

URL: http://hdl.handle.net/10754/627877

► Protein-protein interactions modulate cellular processes in health and disease. However, tracing weak or rare associations or dissociations of proteins is not a trivial task. Kinases… (more)

Subjects/Keywords: Kinases; Synthetic Biology; Protein-Protein Interaction

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APA (6^th Edition):

Diaz Galicia, M. E. (2018). Engineering of kinase-based protein interacting devices: active expression of tyrosine kinase domains. (Thesis). King Abdullah University of Science and Technology. Retrieved from http://hdl.handle.net/10754/627877

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):

Diaz Galicia, Miriam Escarlet. “Engineering of kinase-based protein interacting devices: active expression of tyrosine kinase domains.” 2018. Thesis, King Abdullah University of Science and Technology. Accessed February 28, 2020. http://hdl.handle.net/10754/627877.

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

MLA Handbook (7^th Edition):

Diaz Galicia, Miriam Escarlet. “Engineering of kinase-based protein interacting devices: active expression of tyrosine kinase domains.” 2018. Web. 28 Feb 2020.

Vancouver:

Diaz Galicia ME. Engineering of kinase-based protein interacting devices: active expression of tyrosine kinase domains. [Internet] [Thesis]. King Abdullah University of Science and Technology; 2018. [cited 2020 Feb 28]. Available from: http://hdl.handle.net/10754/627877.

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

Council of Science Editors:

Diaz Galicia ME. Engineering of kinase-based protein interacting devices: active expression of tyrosine kinase domains. [Thesis]. King Abdullah University of Science and Technology; 2018. Available from: http://hdl.handle.net/10754/627877

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

University of California – San Francisco

23. Won, Angela P. The Role of Protein-Protein Interactions in Shaping MAP Kinase Kinase Identity.

Degree: Biochemistry and Molecular Biology, 2010, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/6st633p1

► Eukaryotic cells process information through discrete signaling pathways that must maintain high signal fidelity to ensure proper response to environmental stimuli. Often, the signaling proteins… (more)

▼ Eukaryotic cells process information through discrete signaling pathways that must maintain high signal fidelity to ensure proper response to environmental stimuli. Often, the signaling proteins in these pathways use shared interaction elements, both catalytic domains and protein-protein interactions. These elements help define network connectivity and guide information flow. Within the yeast Saccharomyces cerevisae, four distinct mitogen activated protein kinase kinases (MAPKKs) share closely related catalytic domains yet act in separate critical pathways. How have these four related kinases diverged to take on four distinct functional roles? Within this thesis, I explore the relative contributions of modular interaction domains and motifs versus catalytic specificity in defining a kinases' identity. We probe kinase identity by asking whether we can use recruitment interactions to force other MAPKK catalytic domains to play the functional role of the mating MAPKK, Ste7. We find that two alternative MAPKK's, the osmoresponse MAPKK Pbs2 and the hypotonic response MAPKK Mkk2, can be forced to functionally replace the mating MAPKK Ste7, but only if the proper ensemble of recruitment interactions are overlaid on their catalytic domains. Further, we find that these alternative kinases do not exhibit cross-pathway activity and are restricted towards one identity. These results indicate recruitment interactions can play a dominant role in defining functional identity within a family, and is consistent with a model in which new kinase functions can arise through recombination of existing catalytic domains with new interaction modules. However, these recruitment interactions cannot be used in a "plug and play" method to alter any kinase's specificity. We find that addition of Ste7 recruitment interactions does not convert the identity of the hypotonic shock MAPKK, Mkk1. Further, subtle differences are observed in the temporal activity and level of flux of the converted alternative kinases. Altogether, these results indicate that although recruitment interactions can be utilized as a powerful tool to alter functional identity, evolution may have always insured pathway fidelity in some instances through the intrinsic contributions of kinase catalytic domains.

Subjects/Keywords: Biology, Molecular; MAP kinases; protein-protein interactions

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

APA (6^th Edition):

Won, A. P. (2010). The Role of Protein-Protein Interactions in Shaping MAP Kinase Kinase Identity. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/6st633p1

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):

Won, Angela P. “The Role of Protein-Protein Interactions in Shaping MAP Kinase Kinase Identity.” 2010. Thesis, University of California – San Francisco. Accessed February 28, 2020. http://www.escholarship.org/uc/item/6st633p1.

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

MLA Handbook (7^th Edition):

Won, Angela P. “The Role of Protein-Protein Interactions in Shaping MAP Kinase Kinase Identity.” 2010. Web. 28 Feb 2020.

Vancouver:

Won AP. The Role of Protein-Protein Interactions in Shaping MAP Kinase Kinase Identity. [Internet] [Thesis]. University of California – San Francisco; 2010. [cited 2020 Feb 28]. Available from: http://www.escholarship.org/uc/item/6st633p1.

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

Council of Science Editors:

Won AP. The Role of Protein-Protein Interactions in Shaping MAP Kinase Kinase Identity. [Thesis]. University of California – San Francisco; 2010. Available from: http://www.escholarship.org/uc/item/6st633p1

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

24. Moon, Thomas Matthew. Autoinhibition and Chloride Sensing in the WNK1 Kinase.

Degree: 2012, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/1001

► Protein kinases control diverse cellular pathways and have are the subject of intensive study regarding how they maintain specificity toward sub- strates. The research presented… (more)

▼ Protein kinases control diverse cellular pathways and have are the subject of intensive study regarding how they maintain specificity toward sub- strates. The research presented here focuses on a 230kDa serine/threonine protein kinase known as WNK1 (with no lysine {k}). The protein was first cloned by Melanie Cobb's laboratory, and its isoforms have been associated with a monogenic form of hypertension as well as with breast and prostate cancer. Recent data have also shown that WNK1 is necessary for maintaining spindle polarity in mitosis and plays a role in post-mitotic abscission. The function of WNK1 is most commonly associated with the regulation of CCCs via the activation of the WNK1 substrates OSR/SPAK. Prior investigation of the system has demonstrated that CCCs are activated by increasing con- centrations of extracellular salt and by intracellular phosphorylation from the OSR/SPAK kinases. Due to it ubiquity in mammalian cell types, a question has arisen as to how the pathway responds to changes in osmolarity. Further, because of the involvement of WNK1 in a diverse set of cellular mechanisms, how is WNK1 activity and substrate specificity controlled? An autoinhibitory domain of WNK1 was characterized by the Cobb Lab regarding its ability to inhibit the kinase in cis and in trans. In this study, we find that the solution structure of the autoinhibitory domain retains a conserved RFXV binding site from the PASK/FRAY homology 2 (PF2) domain present in OSR/SPAK. Titration data shows that incubation with a 5-mer and a 20-mer peptide derived from the WNK1 kinase domain displays extensive chemical shift perturbation as assessed by 1H,15N-HSQC. Expression of this autoinhibitory domain in cis with the WNK1 kinase domain followed by size-exclusion chromatography shows substantial confor- mational changes when dialized from high to low salt. A measurement of the activity of the WNK1 kinase domain in the presence of increasing amounts of sodium chloride indicate an IC50 of 130mM. Further biophysical investigation using differential scanning fluorimetry with the kinase domain shows that the domain undergoes substantial increases in domain stabilization as the concen- tration of salt is increased. Continued analysis of this phenomena has pointed toward evidence of anion sensing by the WNK1 kinase domain. Other protein kinases studied in our lab do not exhibit this salt sensitivity. To determine the binding site of chloride in the WNK1 kinase domain, the inactive WNK1 kinase was cocrystallized in the presence of sodium bro- mide. A dataset was collected using the bromine anomalous edge (0.92 ̊A). The anomalous difference fourier map was calculated and a 5.2 σ peak was observed at the N-terminus of the 3.10 helix present in the DLG motif of the activation loop. To corroborate these data, the structure of the inactive kinase domain previously crystallized in sodium chloride was re-refined. A similar binding site corroborated by a 2mFo − DFc peak of 5.5 σ was observed in subunit A near the N-terminus of the 3.10 helix. When… Advisors/Committee Members: Goldsmith, Elizabeth J..

Subjects/Keywords: Protein-Serine-Threonine Kinases; Crystallography, X-Ray; Protein Kinases Inhibitors

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

APA (6^th Edition):

Moon, T. M. (2012). Autoinhibition and Chloride Sensing in the WNK1 Kinase. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1001

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):

Moon, Thomas Matthew. “Autoinhibition and Chloride Sensing in the WNK1 Kinase.” 2012. Thesis, University of Texas Southwestern Medical Center. Accessed February 28, 2020. http://hdl.handle.net/2152.5/1001.

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

MLA Handbook (7^th Edition):

Moon, Thomas Matthew. “Autoinhibition and Chloride Sensing in the WNK1 Kinase.” 2012. Web. 28 Feb 2020.

Vancouver:

Moon TM. Autoinhibition and Chloride Sensing in the WNK1 Kinase. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2012. [cited 2020 Feb 28]. Available from: http://hdl.handle.net/2152.5/1001.

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

Council of Science Editors:

Moon TM. Autoinhibition and Chloride Sensing in the WNK1 Kinase. [Thesis]. University of Texas Southwestern Medical Center; 2012. Available from: http://hdl.handle.net/2152.5/1001

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

Michigan State University

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

Degree: 2014, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:2416

►

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 (6^th 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 (16^th Edition):

Pizzimenti, Natalie Maria. “Mitogen activated protein kinase signaling in mouse skeletal muscle.” 2014. Thesis, Michigan State University. Accessed February 28, 2020. 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 (7^th Edition):

Pizzimenti, Natalie Maria. “Mitogen activated protein kinase signaling in mouse skeletal muscle.” 2014. Web. 28 Feb 2020.

Vancouver:

Pizzimenti NM. Mitogen activated protein kinase signaling in mouse skeletal muscle. [Internet] [Thesis]. Michigan State University; 2014. [cited 2020 Feb 28]. 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

Indian Institute of Science

26. Rakshambikai, R. Structural and Evolutionary Analyses of Signalling Proteins with Special Reference to Protein Kinases.

Degree: 2014, Indian Institute of Science

URL: http://hdl.handle.net/2005/3188

► Cellular response to environmental changes involves a wide repertoire of complex signalling systems often resulting in up and down regulation of various genes. These mechanisms… (more)

Subjects/Keywords: Cellular Signal Transduction; Kinase Network; Protein Kinases; Signalling Proteins; Protein Signalling; Protein Kinase Phosphorylates; Rogue Kinases; Hybrid Kinases; Takifugu Kinases; Zebrafish Kinases; PIM Kinases; Takifugu Rubripes; Rogue Kinase; Molecular Biophysics

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APA (6^th Edition):

Rakshambikai, R. (2014). Structural and Evolutionary Analyses of Signalling Proteins with Special Reference to Protein Kinases. (Thesis). Indian Institute of Science. Retrieved from http://hdl.handle.net/2005/3188

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):

Rakshambikai, R. “Structural and Evolutionary Analyses of Signalling Proteins with Special Reference to Protein Kinases.” 2014. Thesis, Indian Institute of Science. Accessed February 28, 2020. http://hdl.handle.net/2005/3188.

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

MLA Handbook (7^th Edition):

Rakshambikai, R. “Structural and Evolutionary Analyses of Signalling Proteins with Special Reference to Protein Kinases.” 2014. Web. 28 Feb 2020.

Vancouver:

Rakshambikai R. Structural and Evolutionary Analyses of Signalling Proteins with Special Reference to Protein Kinases. [Internet] [Thesis]. Indian Institute of Science; 2014. [cited 2020 Feb 28]. Available from: http://hdl.handle.net/2005/3188.

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

Council of Science Editors:

Rakshambikai R. Structural and Evolutionary Analyses of Signalling Proteins with Special Reference to Protein Kinases. [Thesis]. Indian Institute of Science; 2014. Available from: http://hdl.handle.net/2005/3188

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

Hong Kong University of Science and Technology

27. Wang, Chihao. Biochemical and structural characterization of interactions within par complex.

Degree: 2012, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-7817 ; https://doi.org/10.14711/thesis-b1207876 ; http://repository.ust.hk/ir/bitstream/1783.1-7817/1/th_redirect.html

► Cell polarity refers to asymmetric organization of cell structure and differential distribution of cellular materials. It is implicated in a variety of processes including early… (more)

▼ Cell polarity refers to asymmetric organization of cell structure and differential distribution of cellular materials. It is implicated in a variety of processes including early patterning of organisms, development of organs, stem cell self-renew, junction formation in epithelial cells, cell migration and axonal specification in neurons. In multicellular organisms, the Par complex which is composed of scaffold proteins PAR3 and PAR6 (PARtitioning-defective 3 and 6) and the serine/threonine protein kinase aPKC (atypical Protein Kinase C) is involved in all known cell polarity events. This protein complex is thought to receive upstream polarization signals, amplify and relay them downstream to induce cellular responses including cytoskeleton rearrangements and protein localization changes. aPKC is the only enzyme in the Par complex, thus it is a good candidate to amplify polarity signals and to transduce them to downstream. However, neither the substrate specificity nor the regulation mechanism is clear for the enzyme. The catalytic domain of aPKC has been reported to bind to and phosphorylate the aPKC binding domain of PAR3. To study these questions, biochemical studies were carried out to map the minimal aPKC binding region of PAR3 and to identify the phosphorylation site(s) of the kinase. The complex structure of aPKC catalytic domain-PAR3 peptide was solved by X-ray crystallography. The structure, together with biochemistry studies, reveals a set of substrate recognition sites within the aPKC catalytic domain, and allows the consensus substrate sequence of aPKC to be discerned. An unexpected finding from the structure of the aPKC catalytic domain-PAR3 peptide complex was that the kinase domain assumes an active conformation without the activation loop phosphorylation. This finding suggests that the activity regulation of aPKC originates from a region(s) outside the kinase’s catalytic domain. I further found that the pseudosubstrate sequence of aPKC can directly regulate the kinase activity by inhibiting substrate from binding.

Subjects/Keywords: Protein-protein interactions ; Protein kinase C ; Protein kinases

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APA (6^th Edition):

Wang, C. (2012). Biochemical and structural characterization of interactions within par complex. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-7817 ; https://doi.org/10.14711/thesis-b1207876 ; http://repository.ust.hk/ir/bitstream/1783.1-7817/1/th_redirect.html

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):

Wang, Chihao. “Biochemical and structural characterization of interactions within par complex.” 2012. Thesis, Hong Kong University of Science and Technology. Accessed February 28, 2020. http://repository.ust.hk/ir/Record/1783.1-7817 ; https://doi.org/10.14711/thesis-b1207876 ; http://repository.ust.hk/ir/bitstream/1783.1-7817/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Wang, Chihao. “Biochemical and structural characterization of interactions within par complex.” 2012. Web. 28 Feb 2020.

Vancouver:

Wang C. Biochemical and structural characterization of interactions within par complex. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2012. [cited 2020 Feb 28]. Available from: http://repository.ust.hk/ir/Record/1783.1-7817 ; https://doi.org/10.14711/thesis-b1207876 ; http://repository.ust.hk/ir/bitstream/1783.1-7817/1/th_redirect.html.

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

Council of Science Editors:

Wang C. Biochemical and structural characterization of interactions within par complex. [Thesis]. Hong Kong University of Science and Technology; 2012. Available from: http://repository.ust.hk/ir/Record/1783.1-7817 ; https://doi.org/10.14711/thesis-b1207876 ; http://repository.ust.hk/ir/bitstream/1783.1-7817/1/th_redirect.html

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

Indian Institute of Science

28. Anamika, *. Genome-Wide And Structural Analyses Of Protein Kinase Superfamily.

Degree: 2009, Indian Institute of Science

URL: http://hdl.handle.net/2005/674

► A signal transduction process refers to chain of highly regulated biochemical steps which results in the transfer of signal in response to a stimulus in… (more)

▼ A signal transduction process refers to chain of highly regulated biochemical steps which results in the transfer of signal in response to a stimulus in the extracellular environment to the intracellular compartments such as nucleus. Variety of biomolecules such as proteins and lipids participate in such processes. One of the superfamilies of proteins which actively participate in signaling processes is protein kinase which transfers γ-phosphate from Adenosine Triphosphate (ATP) to the specific hydroxyl group(s) in the protein substrates. Phosphorylation and dephosphorylation events are critical in many signal transduction pathways affecting biological system as a whole. Protein phosphorylation carried out by protein kinases has emerged as pre-eminent mechanism for the regulation of variety of cellular processes such as cell growth, development, differentiation, homeostasis, apoptosis, metabolism, transcription and translation. The current thesis encompasses the investigations carried out by the author, using various bioinformatics tools and methods, to comprehend the structural and functional roles of diverse set of protein kinase subfamilies in various eukaryotic and prokaryotic organisms. The present thesis has been divided into various chapters. Chapter 1 of the thesis provides introduction to the superfamily of protein kinases and covers the relevant literature. The database of Kinases in Genomes (KinG) set-up in the author’s group a few years ago (Krupa et al, 2004a), comprises of a collection of Serine/Threonine/Tyrosine protein kinases recognized using bioinformatics approaches, from the genomic data of various eukaryotes, prokaryotes and viruses (Krupa et al, 2004a). KinG database also provides classification of protein kinases into various groups and subfamilies (Hanks et al, 1988). Information on non-kinase domains which are tethered to the catalytic kinase domains is also available for every kinase in the KinG database. KinG is periodically (annually) updated with rise in the number of genome sequence datasets of various organisms, increase in the number of known protein domain families and refinement or reannotation of genomic datasets (Anamika et al, 2008c). Author describes the work on annual update of KinG database in Chapter 2 of the thesis. Availability of an improved version of the human genomic data has provided an opportunity to re-investigate protein kinase complement of the human genome and enabled an analysis of the splice variants. This analysis is also described in Chapter 2. Chapter 3, Chapter 4 and Chapter 5 report recognition and analysis of repertoire of protein kinases in Chimpanzee, two Plasmodium species (Plasmodium falciparum and Plasmodium yoelii yoelli) and Entamoeba histolytica respectively. A detailed analysis of the non-kinase domains which are tethered to catalytic protein kinase domains in eukaryotic organisms is presented in Chapter 6. Chapter 7 discusses a systematic classification framework developed by the author to classify Serine/Threonine protein kinases in prokaryotic… Advisors/Committee Members: Srinivasan, N.

Subjects/Keywords: Genome Structure; Protein Kinases; Protein Kinases - Phosphorylation; Human Protein Kinases; Eukaryotic Protein Kinases; Prokaryotic Protein kinases; Protein Kinase-Substrate Interaction; Chimpanzee Protein Kinome; Plasmodium Kinome; Entamoeba Histolytica Kinome; King G (Kinases in Genomes); Protein Kinome; Protein Kinase; Biochemical Genetics

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APA (6^th Edition):

Anamika, *. (2009). Genome-Wide And Structural Analyses Of Protein Kinase Superfamily. (Thesis). Indian Institute of Science. Retrieved from http://hdl.handle.net/2005/674

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):

Anamika, *. “Genome-Wide And Structural Analyses Of Protein Kinase Superfamily.” 2009. Thesis, Indian Institute of Science. Accessed February 28, 2020. http://hdl.handle.net/2005/674.

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

MLA Handbook (7^th Edition):

Anamika, *. “Genome-Wide And Structural Analyses Of Protein Kinase Superfamily.” 2009. Web. 28 Feb 2020.

Vancouver:

Anamika *. Genome-Wide And Structural Analyses Of Protein Kinase Superfamily. [Internet] [Thesis]. Indian Institute of Science; 2009. [cited 2020 Feb 28]. Available from: http://hdl.handle.net/2005/674.

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

Council of Science Editors:

Anamika *. Genome-Wide And Structural Analyses Of Protein Kinase Superfamily. [Thesis]. Indian Institute of Science; 2009. Available from: http://hdl.handle.net/2005/674

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

29. Shang, Libin. Mechanistic Studies of Autophagy Initiation in Mammalian Cells.

Degree: 2011, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/886

► Macroautophagy (herein referred to as autophagy) is an evolutionarily conserved self-digestive process cells use to adapt to starvation and other stresses. During autophagy, portions of… (more)

Subjects/Keywords: TOR-Serine-Threonine Kinases; Protein-Serine-Threonine Kinases; Autophagy

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APA (6^th Edition):

Shang, L. (2011). Mechanistic Studies of Autophagy Initiation in Mammalian Cells. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/886

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):

Shang, Libin. “Mechanistic Studies of Autophagy Initiation in Mammalian Cells.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed February 28, 2020. http://hdl.handle.net/2152.5/886.

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

MLA Handbook (7^th Edition):

Shang, Libin. “Mechanistic Studies of Autophagy Initiation in Mammalian Cells.” 2011. Web. 28 Feb 2020.

Vancouver:

Shang L. Mechanistic Studies of Autophagy Initiation in Mammalian Cells. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2020 Feb 28]. Available from: http://hdl.handle.net/2152.5/886.

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

Council of Science Editors:

Shang L. Mechanistic Studies of Autophagy Initiation in Mammalian Cells. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/886

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

Hong Kong University of Science and Technology

30. Cheng, Kai. Identification of Pctaire1 as a p35-interacting protein and a novel substrate for Cdk5.

Degree: 2003, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-1318 ; https://doi.org/10.14711/thesis-b802008 ; http://repository.ust.hk/ir/bitstream/1783.1-1318/1/th_redirect.html

► Cyclin-dependent kinase 5 (Cdk5) is a member of Cdk family. While other members of Cdk family associate with cyclins, Cdk5 interacts with its neuronal specific… (more)

Subjects/Keywords: Cyclin-dependent kinases ; Protein kinases

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APA (6^th Edition):

Cheng, K. (2003). Identification of Pctaire1 as a p35-interacting protein and a novel substrate for Cdk5. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-1318 ; https://doi.org/10.14711/thesis-b802008 ; http://repository.ust.hk/ir/bitstream/1783.1-1318/1/th_redirect.html

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):

Cheng, Kai. “Identification of Pctaire1 as a p35-interacting protein and a novel substrate for Cdk5.” 2003. Thesis, Hong Kong University of Science and Technology. Accessed February 28, 2020. http://repository.ust.hk/ir/Record/1783.1-1318 ; https://doi.org/10.14711/thesis-b802008 ; http://repository.ust.hk/ir/bitstream/1783.1-1318/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Cheng, Kai. “Identification of Pctaire1 as a p35-interacting protein and a novel substrate for Cdk5.” 2003. Web. 28 Feb 2020.

Vancouver:

Cheng K. Identification of Pctaire1 as a p35-interacting protein and a novel substrate for Cdk5. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2003. [cited 2020 Feb 28]. Available from: http://repository.ust.hk/ir/Record/1783.1-1318 ; https://doi.org/10.14711/thesis-b802008 ; http://repository.ust.hk/ir/bitstream/1783.1-1318/1/th_redirect.html.

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

Council of Science Editors:

Cheng K. Identification of Pctaire1 as a p35-interacting protein and a novel substrate for Cdk5. [Thesis]. Hong Kong University of Science and Technology; 2003. Available from: http://repository.ust.hk/ir/Record/1783.1-1318 ; https://doi.org/10.14711/thesis-b802008 ; http://repository.ust.hk/ir/bitstream/1783.1-1318/1/th_redirect.html

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

Open Access Theses and Dissertations