Spelling suggestions: "subject:"proteintyrosine 3kinase"" "subject:"proteintyrosine 6kinase""
81 |
Gene regulation of zebrafish hematopoiesis during embryonic development with special references to survivins and jak2aMa, Chun-hang. January 2009 (has links)
Thesis (Ph. D.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 156-169) Also available in print.
|
82 |
Signalling pathways of M918T RET mutant in multiple endocrine neoplasia type 2BChan, Chin-ho. January 2005 (has links)
Thesis (M. Phil.)--University of Hong Kong, 2005. / Title proper from title frame. Also available in printed format.
|
83 |
Jak2 tyrosine kinase new insights regarding structure, function, and pharmacology /Sandberg, Eric M., January 2004 (has links)
Thesis (Ph.D.)--University of Florida, 2004. / Typescript. Title from title page of source document. Document formatted into pages; contains 118 pages. Includes Vita. Includes bibliographical references.
|
84 |
Regulation of the pro-survival AKT signaling cascade : roles of receptor tyrosine kinases, G proteins, and their crosstalks /Wu, Hoi Ti. January 2006 (has links)
Thesis (Ph.D.)--Hong Kong University of Science and Technology, 2006. / Includes bibliographical references (leaves 174-207). Also available in electronic version.
|
85 |
Regulation of EphA4 expression through the APC-mediated ubiquitin-proteasome pathway /Shen, Ying. January 2007 (has links)
Thesis (M.Phil.)--Hong Kong University of Science and Technology, 2007. / Includes bibliographical references (leaves 81-90). Also available in electronic version.
|
86 |
Intracellular signals underlying the inductive effects of agrin during neuromuscular junction formation : study on the roles of ras and ShcLemaire, Mathieu. January 2000 (has links)
No description available.
|
87 |
The role of proline rich tyrosine kinase 2 (Pyk2) on cisplatin resistance in HCCGeng, Wei, 耿瑋 January 2009 (has links)
published_or_final_version / Surgery / Master / Master of Philosophy
|
88 |
The study of the impact of selected mutations in FMS-like Tyrosine Kinase III (FLT3) and Nucleophosmin (NPM1) - and HIV status on patients with acute Myeloid Leukemia and their response to induction therapy.Naidoo, Horacia. January 2012 (has links)
Acute Myeloid Leukemia (AML), the most common form of acute leukemia in adults, is only curable in approximately 30% of all cases. Despite prognostic risk stratification using sub-typing and cytogenetic analysis to direct therapy, the mortality and relapse rate remains high. AML patients with normal karyotypes are defined as intermediate risk and are the most challenging to treat. Somatic mutations may be the key in refining prognostic stratification and providing useful therapeutic targets. The FMS-like tyrosine kinase 3 (FLT3) and Nucleophosmin (NPM1) genes have common mutated forms that are associated with overall survival and response to therapy. We assessed mutations in the FLT3 and NPM1 genes and their levels of expression in twenty eight AML patients in the presence and absence of HIV and their response to induction therapy. Furthermore, we used a novel technique, High Resolution Melting (HRM) Analysis to detect FLT3 Internal Tandem Duplications (ITD) and NPM1 exon 12 mutations. Five of the patients in this study were HIV positive, three of whom did not survive post-induction therapy. Of the AML patients, 17.9% were positive for the NPM1 mutation and 21% had mutated FLT3. Interestingly, the presence of the FLT3 and NPM1 mutations were coupled with an increase in expression levels of FLT3 and NPM1 from presentation to post-induction respectively and the loss of these mutations were coupled with a decrease in levels of expression from presentation to post-induction. However, an increase/decrease from presentation to post-induction did not necessarily denote the presence/absence of a mutation. Therefore, while mutational status of genes may generally confer mRNA levels, our results showed that there existed no definitive trend between mRNA levels of NPM1 and FLT3 expression and mutational status. We found that the HRM method was definitive for the simpler NPM1 mutation however detection of the FLT3-ITD mutation was challenging. There isn’t a clear distinction between mutated and non-mutated FLT3 due to the formation of hetero-duplexes during analysis, making detection highly subjective and error-prone. Sequencing allowed confirmation of mutated FLT3 and non-mutated FLT3 which were not in all instances in concordance with HRM analysis. The prognostic value in terms of overall survival of NPM1 and FLT3 mutations in this study is indefinite. Furthermore, the analysis of the HIV positive AML patients revealed no clear correlation between NPM1 and FLT3 levels of mRNA expression and mutational status. Also, the small number of HIV positive AML patients did not allow for conclusions to be made regarding HIV status and survival when affected with AML. / Thesis (M.Sc.)-University of KwaZulu-Natal, Pietermaritzburg, 2012.
|
89 |
The world according to mast cells the role of Kit in normal and neoplastic canine mast cells /Lin, Tzu-yin, January 2007 (has links)
Thesis (Ph. D.)--Ohio State University, 2007. / Title from first page of PDF file. Includes bibliographical references (p. 199-227).
|
90 |
Purification and identification of a 100 kDa protein, which is tyrosine-phosphorylated by EGF stimulation in SFME cellMurayama, Kaoru 01 May 1997 (has links)
Serum-free mouse embryo (SFME) cells, which were derived
from 16-day-old Balb/c mouse embryo brain, grow in absence of
serum without losing genomic normality or proliferative
potential, and require epidermal growth factor (EGF) for
normal growth. EGF is a well studied mitogen that binds to a
specific receptor on the cell surface membrane to activate
the proliferative signal transduction pathways. The activated
receptor is a tyrosine specific protein kinase, and tyrosine
phosphorylation is one of the important mediators of EGF
receptor (EGFR) signal transduction.
Using anti-phosphotyrosine Western immunoblotting, we
detected a 100 kDa protein which is tyrosine-phosphorylated
in response to EGF in SFME cells. This protein is
constitutively phosphorylated in an SFME cell line which
expresses the neu oncogene. The neu oncogene encodes an
analog protein of EGFR which does not require a ligand for
activation, and neu-transformed SFME cells are tumorgenic in
mice.This protein, p100 was not a fragment of EGFR, and was
not antigenically related to other signal transduction
phosphoproteins of about 100 kDa. We attempted to purify p100
from neu SFME tumor cells for amino acid sequencing. / Graduation date: 1997
|
Page generated in 0.0758 seconds