Dissertations / Theses: 'Tyrosine‐protein kinase (tyrosine kinase)'

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Gatesman, Ammer Amanda. "PKCalpha direct cSrc activation and podosome formation through the adaptor protein AFAP-110." Morgantown, W. Va. : [West Virginia University Libraries], 2004. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=3762.

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Thesis (Ph. D.)--West Virginia University, 2004
Title from document title page. Document formatted into pages; contains vii, 350 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 322-346).

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Holland, Pamela M. "Identification, interactions, and specificity of a novel MAP kinase kinase, MKK7 /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/9262.

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Bäckesjö, Carl-Magnus. "Molecular biology of Bruton's tyrosine kinase /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-693-6.

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Dikic, Inga. "Signal Transduction by Proline-Rich Tyrosine Kinase Pyk2." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5316-3/.

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Lin, Xiaofeng. "Probing the regulatory mechanisms of protein tyrosine kinases, using C-terminal SRC kinase (CSK) as a model system /." View online ; access limited to URI, 2005. http://0-wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3188064.

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Hardwick, James S. "Regulation of the Lck tyrosine protein kinase by oxidant-induced tyrosine phosphorylation /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1997. http://wwwlib.umi.com/cr/ucsd/fullcit?p9814544.

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7

Benjamin, Audra Ruth. "Lung liquid homeostasis : The involvement of protein kinase A and protein tyrosine kinase." Thesis, St George's, University of London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511892.

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Pursglove, Sharon Elizabeth. "Biophysical analysis of Tec Kinase regulatory regions : implications for the control of Kinase activity." Title page, contents and summary only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09php9863.pdf.

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9

Collins-De, Peyer Laurence. "Screening of a rat thymus and a human hippocampus cDNA library for a novel fyn-related oncogene." Thesis, Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21253870.

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10

Griaud, François. "Proteomic analysis of leukaemogenic protein tyrosine kinase action." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/proteomic-analysis-of-leukaemogenic-protein-tyrosine-kinase-action(ff9d490b-5a94-45fc-a857-4f0826e4a11a).html.

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Introduction: Chronic myeloid leukaemia is a blood cancer which progresses from a chronic phase to an acute blast crisis if untreated. Disease progression and treatment resistance may be precipitated by the mutator action of BCR/ABL protein tyrosine kinase (PTK), but only few protein phosphosites involved in the DNA damage response have been investigated with respect to BCR/ABL action. Aim: The aim of this PhD project was to demonstrate that BCR/ABL PTK expression can affect the response to genotoxic stress signalling at the protein phosphorylation level. Methodology: Etoposide-induced DNA damage response has been studied in control and BCR/ABL PTK-expressing Ba/F3 cells using apoptosis and γH2AX assays. Quantitative phosphoproteomics was performed with iTRAQ peptide labelling to discover putative modulated phosphorylation sites. Absolute quantification (AQUA ) performed with selected reaction monitoring was used to validate discovery phosphoproteomics. The effect of genotoxic stress on the THO complex protein Thoc5/Fmip was studied using western blots. Results: The expression of BCR/ABL PTK induced γH2AX phosphorylation after etoposide exposure. This was associated with the modulation of H2AX tyrosine 142 phosphorylation, MDC1 (serines 595 and 1053) and Hemogen serine 380 phosphorylation among proteins regulated by both BCR/ABL PTK and etoposide. We identified that leukaemogenic PTKs mediate Thoc5/Fmip phosphorylation on tyrosine 225 via Src proto-oncogene and oxidative stress, while ATM and MEK1/2 may control its phosphorylation. Human CD34+ CD38- leukaemic stem cells showed pronounced level of THOC5/FMIP tyrosine phosphorylation. Expression of phosphomutant Thoc5/Fmip Y225F might reduce apoptosis mediated by etoposide and H2O2. Conclusion: BCR/ABL PTK can sustain, create, block and change the intensity of protein phosphorylation related to genotoxic stress. Modulation of H2AX, MDC1, Hemogen and Thoc5/Fmip post-translational modifications by BCR/ABL PTK might promote unfaithful DNA repair, genomic instability, anti-apoptotic signalling or abnormal cell differentiation, resulting in leukaemia progression.

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Vargas-Vallejo, Leonardo. "Subcellular localization and signaling of Bruton's tyrosine kinase (Btk) /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-344-9/.

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Veenstra, Cynthia. "The receptor tyrosine kinase Met and the protein tyrosine phosphatase PTPN2 in breast cancer." Doctoral thesis, Linköpings universitet, Avdelningen för kliniska vetenskaper, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-135047.

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Breast cancer is the most common form of cancer in women worldwide and the second leading cause of cancer death. It is a heterogeneous disease and is subdivided into different subtypes, all with different treatment responses and survival outcomes. Luminal breast cancers are characterised by the expression of oestrogen receptor and generally have a good prognosis. More aggressive tumours are marked by the presence of growth stimulating receptor tyrosine kinase HER2 (HER2-like breast cancer) or the absence of oestrogen receptor, progesterone receptor, and HER2 (triple-negative breast cancer,TNBC). The latter is the most aggressive form and is difficult to treat due to lack of treatment targets. This thesis aimed to explore possible prognostic and predictive biomarkers in different subtypes and study their role in breast cancer. To this aid, breast cancer tumours of pre- and post-menopausal patients enrolled in two cohorts were analysed for gene copy numbers and expression of proteins involved in cell proliferation. Gene copy numbers of receptor tyrosine kinases MET and EGFR, Met’s ligand HGF, and protein tyrosine phosphatase PTPN2 were determined by droplet digital PCR or quantitative PCR in both cohorts. Met, phosphorylated Met (pMet), HGF, and PTPN2 protein expression levels were analysed with immunohistochemical staining in the pre-menopausal cohort. Moreover,the role of the aforementioned proteins was investigated in breast cancer cell lines. Amplification of MET, HGF, and EGFR in breast tissues was found to be low (5-8%). These three genes, all located on chromosome 7, were found to be strongly correlated with eachother and to be associated with shortened distant recurrence-free survival. High protein expression of Met, pMet, and HGF was found in 33%, 53%, and 49% of the breast tumours. MET and EGFR were found to be more often amplified in TNBC disease, correlating with worse survival. Moreover, stromal expression of HGF was associated with shorter survival in TNBC. EGF stimulation in TNBC cell line MDA-MB-468 led to inhibited cell proliferation and migration. Partial knockdown of EGFR caused TNBC cells to proliferate and migrate more upon EGF treatment, mirroring EGFR inhibitor resistance. Knockdown of Met had in part the opposite effects, indicating that Met inhibitors might be useful in the treatment of TNBC. The increase in proliferation and migration upon EGFR depletion could be counteracted with simultaneous knockdown of EGFR and Met, indicating that dual inhibition of these proteins might be a future treatment option in TNBC. Copy loss of PTPN2 was reported in 15% of the cases in both pre- and post-menopausal cohorts. Low cytoplasmic PTPN2 protein expression was found in half of the cases. Loss of PTPN2 gene or protein was associated with a shorter distant recurrence-free survival in Luminal A and HER2-positive tumours, not in TNBC, suggesting a subtype-related prognostic value of PTPN2. Subtype relevance of PTPN2 was further implied by in vitro analyses. Whereas PTPN2 knockdown had no observed effect on TNBC cell lines, knockdown in the Luminal A cell line MCF7 inhibited Met phosphorylation and promoted phosphorylation of Akt, a key regulator of cellular proliferation and survival. The cell growth and survival regulating RAS/MAPK pathway remained unaffected. Knockdown in the HER2-positive cell line SKBR3 led to increased Met phosphorylation and decreased RAS/MAPK-related Erk phosphorylation as well as EGF-mediated transcription factor STAT3 phosphorylation. These results indicate that the role of PTPN2 in breast cancer is subtype-related and needs to be further investigated for future treatment options.

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O'Brien, Richard Mark. "Studies on the insulin receptor tyrosine-specific protein kinase." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252645.

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Che, Azmi Norhaida. "Functional proteomic analysis of leukaemogenic protein tyrosine kinase targets." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/functional-proteomic-analysis-of-leukaemogenic-protein-tyrosine-kinase-targets(a6dc9816-886b-495f-a6e1-f00aec05382f).html.

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Myeloproliferative neoplasms (MPNs) are clonal proliferative disorders associated with JAK2 mutation (e.g JAK2 K539L, JAK2 V617F), MPL mutation (e.g MPL W515L) or product from reciprocal chromosomal translocations in many cases (e.g BCR/ABL). The mutated thrombopoietin receptor MPL W515L found in thrombocytosis and myelofibrosis is constitutively activated leading to a downstream signal transduction cascade activation including the JAK-STAT signalling pathway. MPL W515L induced JAK2 mutation is associated with polycythaemia vera. Using quantitative proteomics I have investigated the effects of the MPL W515L oncogene on the proteome. This was performed to delineate specific features of MPL W515L action with a view to identifying new therapeutic targets for MPN patients. Within the proteins identified as being differentially expressed as a consequence of MPL W515L expression I observed an enrichment of proteins involved in motility. This was associated with a MPL W515L induced increase in chemokinesis. Further investigation into this altered chemokinesis elucidated a pathway from CXCL12/CXCR4/CD45 mediated Src activation through to THOC5 Y225 phosphorylation that had been compromised by MPL W515L. The MPL W515L induced THOC5 phosphorylation was linked to elevated MYC expression. Either chemical inhibition of MYC or gene silencing reduced both the level of THOC5 Y225 phosphorylation and also the increased chemokinesis. Of interest, because of its reported role in both myelofibrosis and motility, the MPL W515L expressing cells were found to demonstrate increased release of transforming growth factor beta (TGFβ). I demonstrated that TGFβ stimulates the phosphorylation of THOC5. Via the expression of Y225F mutants of THOC5 and the chemical inhibition of TGFβ I show a role for this elevated TGFβ in the increased chemokinesis of MPL W515L expressing cells. TGFβ has been reported to upregulate sphingosine-1-phosphate (S1P) which contributes to fibrosis. Having previously published on the differential effects of S1P on the motility of HSC populations I investigated the potential role of S1P in the MPL W515L induced chemokinesis. Inhibition of sphingosine kinase reduced the increase in chemokinesis and THOC5 Y225 phosphorylation in MPL W515L expressing cells. Furthermore I demonstrated that MPL W515L expression led to an increase in the intracellular levels of S1P suggesting a role for S1P in MPN. To further understand the role of THOC5 phosphorylation in the increased chemokinesis I undertook a discovery proteomics screen of MPL W515L cells co-expressing either wild type or Y225F mutant THOC5. Enhancer zester homolog 2 (EZH2) was shown to increase in MPL W515L as compared to MPL W515L mutant THOC5 Y225F expressing and control cells and as such may be linked to the increases in chemokinesis observed. Present work is aimed at clarifying the role of EZH2 in chemokinesis. In conclusion I have identified a novel pathway disrupted in MPN and allow me to start to understand the mechanisms by which the phosphorylation of THOC5 may contribute to leukaemogenic transformation through links to TGFβ, MYC, and S1P biology.

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Cambareri, Antony Charles. "Molecular and cellular studies examining the biological significance of different isoforms of the receptor tyrosine kinase, c-Kit /." Title page, table of contents and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09phc174.pdf.

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Lee, Daniel Cho-En. "Structural and functional studies of bacterial protein tyrosine kinases." Thesis, Kingston, Ont. : [s.n.], 2008. http://hdl.handle.net/1974/1521.

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Lam, Hiu-chor. "Functional characterization of tyrosine phosphatase non-receptor 21, a novel modulator of ErbB4/NRG3." Click to view the E-thesis via HKUTO View the Table of Contents & Abstract, 2010. http://sunzi.lib.hku.hk/hkuto/record/B44229288.

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Lam, Hiu-chor, and 林曉初. "Functional characterization of tyrosine phosphatase non-receptor 21, anovel modulator of ErbB4/NRG3." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44229288.

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19

Sandberg, Eric M. "Jak2 tyrosine kinase new insights regarding structure, function, and pharmacology /." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0006882.

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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.

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Vearing, Christopher John, and chris vearing@med monash edu au. "Structure, function & control of the EphA3 receptor tyrosine kinase." Swinburne University of Technology, 2005. http://adt.lib.swin.edu.au./public/adt-VSWT20051017.094940.

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The implication of the transmembrane signalling Receptor Tyrosine Kinases (RTKs) in cancer has accelerated the pursuit for drugs to target these molecules. In the process our understanding of how these membrane bound molecules are entangled in cell signalling has significantly expanded. There is now evidence that RTKs can facilitate the formation of a lattice-type network of signalling molecules to elicit whole cell responses to external ligand stimuli. Although beginning to be unravelled, knowledge pertaining to the mechanisms of molecular control that initiate these signalling pathways is still in its infancy. In this thesis, a random mutagenesis approach allowed the identification of the crucial interaction surfaces between membrane-bound EphA3 and its preferential binding partner ephrinA5, that are required to induce the formation of higher-order Eph signalling complexes. Modelling and experimental dissection of this co-ordinated receptor aggregation has provided detailed insights into the molecular mechanisms of Eph receptor activation, which in some aspects may also apply to other members of the RTK family. In particular, the importance of certain molecular interfaces in determining preferential and non-preferential Eph/ephrin interactions, suggests their role in the selection of biologically important binding partners. In addition to the assignment of the ephrin-interaction surfaces, the random mutagenesis strategy also identified a continuous conformational epitope as binding site for an anti-EphA3 monoclonal antibody. Fortuitously, antibody binding to this site functionally mimics ephrin stimulation of EphA3 positive cells, and in particular together with divalent ephrinA5, yields synergistically enhanced EphA3 activation. Elucidation of the underlying mechanism has provided opportunities to develop an efficient EphA3 targeting mechanism that is based on increased affinity and accelerated ephrinA5 uptake as consequence of this unique activation mechanism. On a genetic level, novel oligonucleotide analogues known as Peptide Nucleic Acids (PNAs) were analysed for their ability to sterically inhibit EphA3 DNA transcription and suggest a dosedependent downregulation of EphA3 expression, in malignant melanoma cells. Combined, ephrinA5, the anti-EphA3 MAb (IIIA4) and PNA, offer the possibility to investigate the specific machinery involved in Eph receptor expression and signalling for the specific targeting of EphA3 expressing tumour cells.

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Lee, Chun-wai Davy. "RET receptor tyrosine kinase in developing, adult and polycystic kidneys." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23273732.

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Atmosukarto, Ines Irene Caterina. "Biochemical and genetic approach to the characterisation of Tec function in the mouse." Title page, contents and summary only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09pha881.pdf.

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Copy of author's previously published work inserted. Includes bibliographical references (leaves 160-182). Concentrates mainly on the characterisation of the molecular mechanism of action of the tec protein tyrosine kinase using biochemical and genetic approaches.

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Vernersson, Lindahl Emma. "Investigating the function of Anaplastic Lymphoma Kinase." Doctoral thesis, Umeå : Univ, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1956.

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Grabbe, Caroline. "Protein tyrosine kinases and the regulation of signalling and adhesion in Drosophila melanogaster /." Doctoral thesis, Umeå : Umeå University, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-971.

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Yang, Yaoming. "Regulation of protein tyrosine kinase ZAP-70 by serine phosphorylation." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19442.

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The activation of the protein tyrosine kinase (PTK) ZAP-70 is fundamental to T cell receptor (TCR) signal transduction. TCR engagement induces raft-association of ZAP-70 and juxtaposes the cytoplasmic ZAP-70 with the raft-enriched Lck, which phosphorylates and activates ZAP-70. The active ZAP-70, cooperatively with Lck, initiates multiple intracellular pathways eventually leading to T cell activation and IL-2 production. Here, we describe the serine phosphorylation on ZAP-70 on the highly conserved S520DVWS524 motif, and investigate its role in coupling ZAP-70 with TCR signal transduction.

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Puil, Lorri Jane. "Protein-tyrosine kinase signalling pathways in normal hematopoiesis and leukemogenesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ35289.pdf.

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Schuller, Annika Corinna. "Protein recruitment to receptor tyrosine kinase-mediated early signalling complexes." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445051/.

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Receptor tyrosine kinase (RTK) signalling regulates the activation of numerous cellular processes in response to various external stimuli. Spatio-temporal regulation of protein recruitment to activated tyrosine kinase receptors is important for the generation of specific cellular responses to various external stimuli. The involvement of the signalling proteins She, FRS2, Grb2 and Sos and the formation of distinct signalling complexes downstream of three RTKs (TrkA, EGFR, FGFR) was assessed to analyse their role in maintaining signalling specificity. All four signalling proteins played a role in TrkA, EGFR and FGFR signalling, but their recruitment to and involvement in signalling complexes varied depending on the stimulus. The observations indicated that formation of unique multiprotein assemblies provides a mechanism for different receptors to elicit specific signals despite employing the same signalling proteins. Detailed analysis of She recruitment to the FGFR2 revealed co-localisation and co-precipitation with the receptor but no direct interaction. This finding provided additional insight into how the availability of binding sites on different receptors regulates the recruitment of individual proteins to receptor-specific signalling complexes. Secondly, the effects of mutations in the FGFR2 extracellular region on protein recruitment to the receptor and its overall signalling specificity were investigated. Two substitution mutations in the FGFR2, which cause Apert syndrome, result in increased affinity of FGFR2 for FGF. Detailed analysis of the FGFR2 itself and signalling from it in the presence of these mutations indicated that they also result in altered receptor glycosylation, phosphorylation and glycosaminoglycans dependency as well as enhanced Erkl/2 activation. Additionally, recruitment and phosphorylation of She were altered in cells expressing the Apert syndrome mutations. The effects of the mutations on the FGFR2 and the signalling complex formed profoundly altered FGFR2-induced signals and cellular responses. These findings highlight the importance of retaining the integrity of protein recruitment and signalling complex formation to achieve signalling specificity.

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Goodman, K. M. "RET receptor tyrosine kinase architecture, protein interactions and chemical inhibition." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1380777/.

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The RET receptor tyrosine kinase plays a major role in embryonic and adult vertebrate development. Deregulation of RET signalling leads directly to multiple human diseases. Like many receptor tyrosine kinases, the intracellular tyrosine kinase domain of RET is activated by binding of ligand/co-receptor to its ectodomain (ECD). RET is unique among receptor tyrosine kinases, possessing cadherin-like domains (CLD1–4) within its ECD. This thesis describes the architecture of the RET-ECD elucidated using small- angle X-ray scattering (SAXS). These data reveal the interdomain angles and non- linearity of the four CLDs, as well as the location of the membrane-proximal cysteine rich domain (CRD) packed against CLD4. I use this SAXS-derived model of the RET- ECD together with published crystal structures of a RET ligand and co-receptor, to fit into a negative stain electron microscopy 3D reconstruction of a mammalian ligand/co- receptor/RET-ECD ternary complex. The resulting preliminary pseudo-atomic model contains a two-fold symmetrical RET ternary complex with two RET-ECDs wrapped around a core ligand/co-receptor, making extensive contacts from both the N-terminal CLD1–3 region and the membrane-proximal CRD consistent with previous biochemical data and our antibody-epitope mapping. This thesis describes the first view of the RET- ECD and the ligand/co-receptor/RET ternary complex architecture, with important implications for Hirschsprung’s disease and for understanding how ligand-independent RET activation occurs in type 2 multiple endocrine neoplasias.

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Amdjadi, Kambiz. "Characterization of te tyrosine kinase interacting protein of herpesvirus ateles /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3007143.

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Hägebarth, Andrea. "Brk tyrosine kinase signaling in the gastrointestinal tract." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2005. http://dx.doi.org/10.18452/15379.

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Die Tyrosin Kinase Brk stellt den Prototypen nicht N-terminal myristoylierter, Nicht-Rezeptor Tyrosin Kinasen dar. Die Expression dieser Kinase ist auf epitheliale Gewebe beschränkt und wird während der Entwicklung differentiell reguliert. In normalen Geweben ist die Brk Expression auf nichtproliferierende, terminal differenzierte Zellen beschränkt. Um die regulatorische Funktion von Brk im murinen Darmepithel zu untersuchen, wurde das brk Gen in der Maus inaktiviert. Brk knockout Mäuse zeigten keine offensichtlichen Defekte in ihrer Entwicklung jedoch eine erweiterte Proliferationszone in den Krypten des Darmepithels und verlängerte Villi. Die Inaktivierung von Brk führte zu einer erhöhten Akkummulation von nukleärem (-catenin sowie einer Hochregulierung des (-catenin Zielgens c-myc in den Krypten der knockout Mäuse. Zusätzlich zeigten Brk knockout Mäuse eine Aktivierung des Akt-Signaltransduktionswegs in ihrem Darmepithel. Im Gegensatz zu Wildtyp Mäusen waren Brk knockout Mäuse resistent gegenüber (-Strahlung, was die Anhäufung onkogener Mutationen und damit die Entwicklung von Krebs fördert. Eine Induktion der Expression des Brk-Proteins im Darmepithel behandelter Wildtyp Mäuse wurde festgestellt. Weiterhin traten bei Brk knockout Mäusen chronische Entzündungen des Darmepithels sowie eine erhöhte Sensibilität gegenüber dem Reizmittel DSS auf. Im Gegensatz dazu, zeigten Wildtyp Mäuse eine mit der Literatur Übereinstimmende Reaktion zu DSS verbunden mit einer Induktion der Brk Expression im Darmepithel. Zusammenfassend kann gesagt werden, dass die Brk Tyrosin Kinase eine entscheidende Rolle in der Aufrechterhaltung der Homöstase und Integrität des Darmepithels spielt. Insbesondere scheint Brk als wichtiger Faktor zur Bestimmung der Sensitivität epithelialer Zellen zu genotoxischem Stress zu fungieren. Entgegen der bisher vermuteten onkogenen Funktion in epithelialen Tumoren scheint Brk im normalen Darmepithel "Tumor Suppressor" Ähnliche Funtionen innezuhaben.
The Breast tumor kinase Brk is a prototypical non-myristoylated, non-receptor tyrosine kinase. Brk expression is epithelial-specific and ,in normal tissues, restricted to cells exiting the cell cycle and undergoing terminal differentiation. To determine the biological role of Brk in the gastrointestinal tract, we disrupted mouse brk by homologous recombination. Loss of Brk in the mouse resulted in increased intestinal epithelial cell turnover and the appearance of longer small intestinal villi. Brk deficient mice displayed enhanced accumulation of nuclear (-catenin and upregulation of the (-catenin target gene c-myc in the crypt compartment of small and large intestine. In addition, Brk deficient mice exhibited increased Akt kinase activity. Even though, there was no corresponding difference in base-line apoptosis in untreated wild-type and knockout animals. However, subjected to (-irradiation, Brk deficient animals were significantly impaired in the apoptotic response. Wild-type mice, however, exhibited normal levels of apoptosis following (-irradiation accompanied by a rapid induction of Brk expression in crypt cells. Furthermore, chronic inflammation was observed in Brk deficient mice, and they showed increased susceptibility to a colon injury model utilizing DSS. Interestingly, wild-type mice exhibited a significant upregulation of nuclear Brk protein throughout the intestinal epithelium in response to DSS. These recent findings suggest that Brk plays a crucial role in the maintenance of intestinal tissue homeostasis and integrity. In addition, Brk may function to protect the intestinal epithelium against DNA-replication-induced errors and hence the development of cancer. Contrary to reported oncogenic properties of Brk in other epithelial tissues, Brk appears to have tumor suppressor-like functions in the mouse gastrointestinal epithelium.

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李震威 and Chun-wai Davy Lee. "RET receptor tyrosine kinase in developing, adult and polycystic kidneys." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31241931.

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Lee, Sungsoo. "Functional and structural study of the protein tyrosine kinase CSK, as a model system /." View online ; access limited to URI, 2005. http://0-wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3188063.

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Ayrapetov, Marina K. "Structural and functional studies of the Csk and Src family protein tyrosine kinases /." View online ; access limited to URI, 2006. http://0-wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3225312.

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Summy, Justin Matthew. "Functional domain contributions to signaling specificity between the non-receptor tyrosine kinases c-src and c-yes." Morgantown, W. Va. : [West Virginia University Libraries], 2001. http://etd.wvu.edu/templates/showETD.cfm?recnum=2239.

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Thesis (Ph. D.)--West Virginia University, 2001.
Title from document title page. Document formatted into pages; contains vi, 195 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 182-190).

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35

Gruninger, Robert J., and University of Lethbridge Faculty of Arts and Science. "Structure and mechanism of protein tyrosine phosphatase-like phytases." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Chemistry and Biochemistry, c2009, 2009. http://hdl.handle.net/10133/2473.

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The structure and mechanism of the Protein Tyrosine Phosphatase-like Phytases (PTPLPs) from Selenomonas ruminantium (PhyAsr) and Mitsuokella multacida (PhyAmm) were investigated using a combination of enzyme kinetics, site-directed mutagenesis, and X-ray crystallography. I show that PTPLPs use a classical protein tyrosine phosphatase catalytic mechanism and adopt a core PTP fold. Several unique structural features of PTPLPs confer specificity for inositol phosphates. The effect of ionic strength and oxidation on the kinetics and structure of PTPLPs was investigated. The structural consequences of reversible and irreversible oxidation on PTPLPs and PTPs are compared and discussed. We determine the structural basis of substrate specificity in PTPLPs and propose a novel reaction mechanism for the hydrolysis of inositol polyphosphates by PTPLPs. Finally, the structure and function of a unique tandemly repeated phytase has been determined. We show that the active sites of the tandem repeat possess significantly different specificities for inositol polyphosphate.
xix, 148 leaves : ill. (some col.) ; 29 cm

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Gnangnon, Bénédicte. "Caractérisation moléculaire et fonctionnelle de la pseudo-tyrosine kinase-like (pTKL) de plasmodium." Thesis, Lille 2, 2019. http://www.theses.fr/2019LIL2S003/document.

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Le paludisme, première endémie parasitaire mondiale ayant engendré près d’un demi-million de morts en 2017 (d’après l’OMS), est due à une infection par un parasite du genre Plasmodium. Cet apicomplexe infecte, au cours de son cycle de vie, un hôte définitif, un moustique femelle du genre Anopheles, et un hôte intermédiaire homéotherme (l’Homme pour au moins 6 espèces). Chez ce dernier, après une phase de développement hépatique, le parasite envahit puis lyse les érythrocytes. L’accroissement exponentiel de la parasitémie engendre les symptômes du paludisme et permet la production de formes sexuées (gamétocytes) qui seront transmises au vecteur arthropode, permettant ainsi la complétion du cycle de vie du parasite.Plasmodium a co-évolué avec ses hôtes et mis en place divers modes de régulation de l’expression de ses gènes. La phosphorylation est l’une des modifications post-traductionnelles majeures et rapides qu’il utilise pour répondre aux changements environnementaux auxquels il est confronté au cours de son cycle de vie. Nombre de ses kinases et phosphatases jouent un rôle essentiel dans l’invasion de cellules hôtes, la croissance et la division cellulaires, ainsi que la motilité de certains stades. En revanche, le rôle des cinq pseudokinases de Plasmodium dans son développement n’a jusqu’ici pas été exploré.Durant ma thèse, j’ai caractérisé l’unique pseudo-Tyrosine Kinase-like (pTKL) de Plasmodium et étudié son rôle au cours du cycle intra-érythrocytaire du parasite.L’annotation de la pTKL de P. falciparum (PfpTKL) m’a permis d’identifier différents domaines et motifs, et notamment un domaine SAM (Sterile Alpha Motif), deux motifs RVxF (connus pour leur capacité d’interaction avec la Protéine Phosphatase de type 1, PP1) et un pseudo-domaine kinase appartenant à la famille des Tyrosine Kinases-like (TKL). Nous avons montré que ce pseudo-domaine kinase est capable de lier l’ATP de manière cation-indépendante, mais est dépourvu d’activité enzymatique. Des études d’interaction in vitro couplées à l’utilisation de modèles hétérologues (Levure, ovocytes de Xénope) m’ont permis d’identifier deux protéines parasitaires partenaires de PfpTKL : le domaine SAM de PfpTKL interagit directement avec la pseudo-protéase PfSERA5 (SErine Repeat Antigen 5), alors que les deux régions de la protéine contenant les motifs RVxF de PfpTKL interagissent avec PfPP1c (phosphatase majeure de Plasmodium). De façon intéressante, le deuxième motif RVxF est directement impliqué dans l’interaction avec PP1c et serait capable de moduler l’activité de cette dernière de manière allostérique.La localisation de la pTKL de P. berghei (PbpTKL) a ensuite été étudiée par immunofluorescence et confirmée par des expériences de fractionnement cellulaire. Nous avons ainsi observé que PbpTKL est exportée dans l’érythrocyte infecté au stade trophozoïte, puis retenue dans le parasite et la vacuole parasitophore au stade schizonte. L’étude de l’interactome de PbpTKL par IP/MS au stade trophozoïte a montré que PbpTKL s’associe à diverses protéines impliquées dans l’organisation du cytosquelette de l’érythrocyte, ainsi que dans l’érythropoïèse et l’homéostasie cellulaire. Ces observations suggèrent que pTKL joue un rôle, direct ou via ses partenaires, à l’interface entre le parasite et sa cellule hôte.Enfin, afin d’approcher la fonction de pTKL chez le parasite, nous avons généré différentes lignées génétiquement modifiées. L’étude phénotypique des souches de P. berghei KO et iKD pour pTKL a montré qu’elle était dispensable pour la complétion du cycle intra-érythrocytaire, l’expression des gamétocytes ainsi que l’activation des gamétocytes mâles. Ces données suggèrent que pTKL est dispensable pour ces stades de développement ou que l’expression de gènes redondants compense son absence. Quoi qu’il en soit, il est important de poursuivre les recherches sur le rôle de cette protéine aux autres stades de développement du parasite, notamment du zygote aux stades hépatiques
Malaria is the first endemic parasitic disease in the world with nearly half million deaths in 2017 according to the WHO. This disease is the result of an infection by an agent belonging to the Plasmodium genus. This apicomplexan parasite infects two hosts over its complex life cycle: a definitive one – a mosquito belonging to the Anopheles genus – and a homoeothermic intermediate host. At least six Plasmodium species can infect humans. In its intermediate host, Plasmodium first replicates in hepatocytes before releasing erythrocyte-infectious stages in the bloodstream. Once there, parasites invade and replicate within erythrocytes, before lysing them to release other infectious stages. This triggers an exponential rise in the parasitemia, as well as malaria symptoms. Sexual stages, called gametocytes, are produced over this intra-erythrocytic cycle to be transmitted to the arthropod vector, thus allowing the completion of the parasite life cycle.Plasmodium co-evolved with its hosts and set up diverse gene expression regulation pathways accordingly. Phosphorylation is one of the major and fastest post-translational modifications used by the parasite to respond to environmental changes. Many of its kinases and phosphatases play key roles in host cell invasion, cellular growth and division, as well as motility of specific developmental stages. However, the role of the five pseudo-kinases expressed by Plasmodium has not been explored yet.During my PhD project, I have performed the characterization of the unique Plasmodium pseudo-Tyrosine Kinase-like (pTKL) and explored its role over the parasite intra-erythrocytic cycle.P. falciparum pTKL (PfpTKL) in silico annotation allowed the delineation of the protein domains. Notably, a SAM (Sterile Alpha Motif) domain, two RVxF motifs (known for their binding potential with the major protein phosphatase type 1, PP1) and a pseudo-kinase domain belonging to Tyrosine Kinase-like (TKL) family were found. This pseudo-kinase domain was found to be able to bind ATP in a cation-independent way although devoid of kinase activity. Two parasite protein partners of PfpTKL have been identified using in vitro protein-protein interaction studies together with heterologous models (yeast, Xenopus ovocytes). First, PfSERA5 (SErine Repeat Antigen 5) specifically and strongly interacts with PfpTKL SAM domain and second, PfPP1c binds the two RVxF-containing regions of PfpTKL. Interestingly, the second RVxF motif, which is located within the pseudo-kinase domain, directly binds PfPP1c and seems to be involved in the allosteric regulation of the phosphatase activity. The subcellular localization of P. berghei pTKL (PbpTKL) was studied by IFA as well as sequential lysis of erythrocytes followed by immunoprecipitation assays. PbpTKL was shown to be exported to the host cell cytosol at the trophozoite stage, but retained in the parasitophorous vacuole and the parasite cytosol at the schizont stage. Furthermore, our interactome analysis conducted at the trophozoite stage by IP/MS showed that PbpTKL binds many host cell proteins involved in erythrocyte cytoskeleton organization, as well as erythropoiesis and cell homeostasis. These data suggest that pTKL plays a role at the parasite/host interface, either directly or via its protein partners.Finally, in an attempt to understand the role of pTKL for the parasite development, we generated genetically modified P. berghei strains. The phenotypic study of PbpTKL KO and iKD strains did not show any difference between the defective parasites and the parental wild type ones during the intra-erythrocytic cycle, gametocyte expression and male gametocyte activation. These data suggest the dispensability of pTKL or the expression of redundant gene(s) with similar functions in these parasite stages. Whatever the explanation, it is still important to follow up this investigation in other parasite stages, from zygotes to hepatic stages

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37

Chiang, Gary Gene. "Regulation of activation loop phosphorylation in the Lck tyrosine protein kinase /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9993989.

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38

Dillon, Anne M. R. "An investigation of protein tyrosine phosphorylation in equine blood platelets." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390250.

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Young, Stephen W. "The insulin receptor tyrosine kinase and the activation of the map kinase cascade : interactions with the protein kinase C and protein kinase A signalling pathways." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238958.

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Gervais, François G. "Regulation of lymphocyte-specific tyrosine protein kinase p56[superscript]l[superscript]c[superscript]k by tyrosine phosphorylation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0023/NQ29945.pdf.

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41

Hatahet, Laith. "Regulation of lymphocyte specific protein tyrosine kinase, Lck, by tyrosine phosphorylation : evaluation of the tail-bite model." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78375.

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Several studies show that the catalytic function of the Src-family protein kinase Lck is repressed by phosphorylation of a conserved carboxyl-terminal residue (Y505). This phosphorylation allows the molecule to bind to its SH2 domain rendering the protein in an inactive state, a proposed model called the tail-bite mechanism. However, previous findings demonstrated that the activity of Lck from several T cell lines lacking CD45, which is the phosphatase known to dephosphorylate Y505, was significantly elevated. Herein, we are evaluating the tail bite mechanism model by examining the major regulatory sites of Lck, Y394 and Y505, in several T cell lines and assessing the catalytic function of Lck tail mutants on its substrates in JCaM1 cells in vivo . Utilizing phospho-specific antibodies, we provide evidence that Lck from activated T cells is phosphorylated both at Y394 and Y505.

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Bennett, Haley Lorraine Garvan Institute of Medical Research Faculty of Medicine UNSW. "Co-operation between the docking protein GAB2 and the protein tyrosine kinase src in human mammary epithelial cells." Awarded by:University of New South Wales, 2008. http://handle.unsw.edu.au/1959.4/39486.

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The Gab2 docking protein is a target of several oncogenic protein tyrosine kinases and potentiates activation of the Ras/extracellular signal regulated kinase and phosphatidylinositol 3-kinase (PI3-kinase) pathways. The prototypical member of the Src family of protein tyrosine kinases, c-Src, phosphorylates Gab2 and both proteins are overexpressed in breast cancers. However, whether overexpression of these two proteins contributes to mammary tumourigenesis had not been previously investigated. Pharmacological inhibition of c-Src in breast cancer cell lines reduced Gab2 tyrosine phosphorylation while overexpression of these two proteins increased this effect, demonstrating a contribution of c-Src to Gab2 tyrosine phosphorylation in breast cancer cells. The biological effects of Gab2 and c-Src overexpression were determined in a three-dimensional cell culture model using the human mammary epithelial cell line MCF-10A. When cultured on a basement membrane, MCF10A cells form acini that model mammary lobules in vivo. Overexpression of Gab2 in MCF10As conferred increased acinar size and independence of the morphogenetic program from exogenous EGF. While overexpression of c-Src alone did not affect acinar morphogenesis, it potentiated the EGF-independent acinar growth induced by Gab2 overexpression. As enhanced c-Src kinase activity is often observed in breast cancer, the effect of Gab2 co-expression with active Src constructs was next determined. Expression of v-Src or c-SrcY527F altered acinar morphology and the resulting structures were categorised as spheroidal, discohesive or dispersed, according to the degree of phenotypic disruption. Gab2 co-expression shifted the proportion of structures towards the dispersed phenotype. This shift reflects a negative role for Gab2 at adherens junctions in the context of active Src expression, as in monolayer cells Gab2 significantly decreased E-cadherin-based adhesive strength without altering the surface expression of this adhesion molecule. Furthermore, Gab2 associated with the E-cadherin complex. The ability of Gab2 to weaken the strength of cell-cell contacts in active Src-expressing cells may be due to enhanced activation of PI3-kinase signalling at adherens junctions, as the potentiating effects of Gab2 in both monolayer and three-dimensional cultures were dependent upon Gab2 recruitment of the p85 subunit of PI3-kinase. Finally, Gab2 increased migration and invasion of v-Src-expressing cells in transwell assays, however these effects were p85-independent. This is the first study to demonstrate Gab2 co-operation with various forms of Src to augment proliferative, invasive and migratory signals, as well as revealing a novel mechanism whereby Gab2 may promote metastatic spread. This study thus demonstrates multiple roles for Gab2 in contributing to breast cancer progression.

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Crosby, David. "Cross-talk between tyrosine kinases and members of the protein kinase C family in human platelets." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288410.

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Krishnan, Kadalmani. "Characterisation of the G protein controlled tyrosine kinase, ACK1 and its interaction with nucleolar partner proteins." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610698.

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Rivera, Reyes Brenda Mariola. "Regulation of the TCR signaling pathway." Connect to text online, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1132588714.

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BOUGERET, CECILE. "Mecanismes de regulation de la proteine tyrosine kinase p50csk responsable de l'inhibition des proteines tyrosine kinases de la famille src." Paris 7, 1994. http://www.theses.fr/1994PA077207.

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L'activite kinase des proteines tyrosine kinases (ptks) de la famille src est regulee par phosphorylation de deux residus tyrosine tres conserves, l'un localise dans le domaine catalytique et implique dans une regulation positive par autophosphorylation, l'autre localise dans le domaine regulateur carboxy-terminal et implique dans une regulation negative. La kinase responsable de la phosphorylation du site de regulation negative est la ptk ubiquitaire p50csk qui contient les domaines src homology 3 et 2 (sh3 et sh2) impliques dans les interactions proteine-proteine permettant la transduction des signaux. La proteine csk est unique parmi les membres des ptks car elle a ete decrite comme ne possedant pas les sites tyrosine conserves de regulation de l'activite kinase, de ce fait les mecanismes de regulation de la fonction de csk ne sont pas connus. Le role majeur de la proteine csk dans l'inhibition des ptks de la famille src nous a conduit a etudier les mecanismes impliques dans la regulation de son activite kinase. D'une part, nous avons observe que dans un systeme surexpression procaryote, la proteine csk est capable de s'autophosphoryler sur residu tyrosine. Cette autophosphorylation a lieu suivant un mecanisme intermoleculaire et semble impliquee dans une regulation negative de l'activite kinase. D'autre part, nous avons detecte une interaction fonctionnelle entre csk et l'un de ses substrats, la ptk de la famille src p561ck. Cette interaction implique le domaine sh2 de csk et requiert l'autophosphorylation de lck sur son site de regulation positive, ce qui suggere que cette interaction est regulee par l'etat d'activation de lck. Nous proposons donc deux mecanismes de regulation de la fonction de csk, (1) une regulation directe par autophosphorylation de csk, et (2) une regulation indirecte via le domaine sh2 de csk par interaction de ce domaine avec les substrats de csk, ces deux mecanismes n'etant pas exclusifs l'un de l'autre

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Annerén, Cecilia. "The Tyrosine Kinase GTK : Signal Transduction and Biological Function." Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1384.

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Protein tyrosine kinases play an important role in the regulation of various cellular processes such as

growth, differentiation and survival. GTK, a novel SRC-like cytoplasmic tyrosine kinase, was recently cloned from a mouse insulinoma cell line and the present work was conducted in order to find a biological function of GTK in insulin producing and neuronal cells. It was observed that kinase active GTK-mutants, expressed in RINm5F cells, transferred to the cell nucleus and increased the levels of the cell cycle regulatory protein p27^KIP1, reduced cell growth and stimulated glucagon mRNA expression. Furthermore, wild type GTK induces neurite outgrowth in the rat adrenal pheochromocytoma PC12 cell line, through activation of the RAP1-pathway, suggesting a role of GTK for cell differentiation. Studies using transgenic mice, expressing GTK under the control of the rat insulin 1 promoter, demonstrated a dual role of GTK for β-cell growth: Whereas GTK increases the β-cell mass and causes enhanced β-cell proliferation in response to partial pancreatectomy it also induced β-cell death in response to proinflammatory cytokines and impaired the glucose tolerance in mice treated with the β-cell toxin streptozotocin suggesting a possible role of GTK for β-cell destruction in Type 1 diabetes. We have also observed that GTK-transgenic islets and GTK-expressing RINm5F cells exhibit a reduced insulininduced activation of the insulin receptor substrate (IRS-1 and IRS-2)-pathways, partly due to an increased basal activity of these. GTK was found to associate with and phosphorylate the SH2 domain adapter protein SHB, which could explain many of the GTK-dependent effects both in vitro and in vivo. In summary, the present work suggests that the novel tyrosine kinase GTK is involved in various signal transduction pathways, regulating different cellular responses, such as proliferation, differentiation and survival.

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Edling, Charlotte. "Receptor tyrosine kinase c-Kit signalling in hematopoietic progenitor cells." Doctoral thesis, Umeå : Umeå University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-888.

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Naudin, Cécile. "Régulation de la signalisation oncogénique de Src par l'adaptateur SLAP dans les cellules de cancer colorectal." Thesis, Montpellier 2, 2012. http://www.theses.fr/2012MON20082.

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La tyrosine kinase cytoplasmique Src est un régulateur clé de la signalisation induite par les facteurs de croissance et les intégrines. Src présente des propriétés oncogéniques lorsqu'elle est dérégulée, une situation fréquemment retrouvée dans les cancers colorectaux (CCR). Sous sa forme activée, Src participe à la croissance tumorale et à la formation de métastases. Cependant, les mécanismes de dérégulation impliqués sont mal connus. En effet, SRC est rarement muté dans ces cancers. Mon travail de thèse a mis en évidence un nouveau mécanisme de dérégulation de Src via l'inactivation de SLAP. SLAP est une protéine de signalisation de type adaptateur qui régule négativement la signalisation lymphocytaire. De part son association avec l'E3-ligase Cbl, il induit la dégradation de substrats importants de la tyrosine kinase Lck nécessaires à l'activation lymphocytaire. Je montre que SLAP est également exprimé dans le tissu épithélial colique et que son expression est fréquemment perdue au cours de la progression tumorale colorectale. SLAP inhibe la tumorigénicité et le potentiel métastasant des cellules de CCR. Sur le plan moléculaire, SLAP définit une boucle de rétrocontrôle d'une voie oncogénique Src/EphA2/Akt initiée par Src via la dégradation protéasome-dépendante du récepteur EphA2 impliquant l'ubiquitine E4-ligase UBE4A. Ces résultats révèlent un nouveau mécanisme d'induction oncogénique de Src, une fonction insoupçonnée de suppresseur de tumeurs de SLAP et montrent l'importance d'une E4-ligase et des protéines adaptatrices dans la régulation négative de la signalisation initiée par les tyrosine kinases dans la progression tumorale
The cytoplasmic tyrosine kinase Src mediates intracellular signaling induced by growth factors and integrins. When deregulated, Src acquires oncogenic properties. Src deregulation largely occurs in the absence of mutation of the corresponding gene but the underlying molecular mechanisms involved in this process are still unclear. Here I uncovered a novel mechanism of Src oncogenic induction in colorectal cancer (CRC) via SLAP silencing. SLAP is an adaptor protein and signaling molecule that controls lymphocytes activation. By association with E3-ligase Cbl, SLAP induces proteasomal degradation of important components of T cell receptor signaling, which impedes lymphocytes activation. I show that SLAP is also expressed in the epithelial tissue of the colon, but its expression is frequently lost during tumorigenesis. I also show that SLAP controls tumorigenicity and invasiveness of CRC cells. At the molecular level, SLAP specifies a feedback loop of a Src/EphA2/Akt oncogenic signaling that is initiated by Src itself. Precisely, phosphorylation of EphA2 on Tyr594 by Src creates a binding site for SLAP-SH2 to elicit receptor degradation. This novel SLAP function is independent of Cbl but requires its interaction with the E4-ligase UBE4A. SLAP down-regulation observed in cancer cells dramatically increases EphA2 levels and amplifies a Src/EphA2/Akt signaling required for cell tumorigenicity. Thus, SLAP inactivation defines a novel mechanism of Src oncogenic induction in human cancer

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50

Zhang, Deyong, and 張德勇. "The regulation of cardiac potassium channels by protein tyrosine kinases." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41508294.

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Dissertations / Theses on the topic 'Tyrosine‐protein kinase (tyrosine kinase)'

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