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Dissertations / Theses on the topic 'Protein-tyrosine kinase'

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Published: 4 June 2021

Last updated: 3 March 2023

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1

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).

2

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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3

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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4

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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5

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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6

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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7

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.

8

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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9

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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10

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.

11

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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12

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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13

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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14

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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15

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.

16

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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17

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.

18

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.

19

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.

20

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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21

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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22

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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23

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.

24

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.

25

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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26

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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27

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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28

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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29

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

30

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).

31

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.

32

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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33

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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34

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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35

Kim, Jae-Hwan. "Involvement of G protein and protein tyrosine kinase signal transduction in pig oocyte activation /." free to MU campus, to others for purchase, 1999. http://wwwlib.umi.com/cr/mo/fullcit?p9946271.

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36

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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37

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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38

Zhang, Deyong. "The regulation of cardiac potassium channels by protein tyrosine kinases." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41508294.

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39

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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40

Read, Stuart Hamilton. "Production and function of a soluble c-Kit molecule." Title page, abstract and contents only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phr2845.pdf.

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Abstract:

"Research conducted at the Department of Haematology, Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science."--T.p. Includes bibliographical references (leaves 170-214). Elevated levels of receptor tyrosine kinases have been implicated in carcinogenesis. It is possible that high expression of c-Kit by the leukaemic cell provides them with a growth advantage over their normal counterparts in the bone marrow microenvironment. Thus, a means of inhibiting the interaction of c-Kit on these cells with ligand Steel Factor may remove proliferation and survival signals. Main aim of the study was to produce a biological inhibitor of this interaction and evaluate its ability to prevent ligand Steel Factor from binding to c-Kit on live cells.

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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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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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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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Hung, Kwok Wang. "Identification of the EphA4-interacting proteins by yeast two-hybrid screening /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BICH%202006%20HUNG.

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Tse, Tak-fong. "Role of RON activation on chemoresistance in gastric cancer." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38592253.

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Chan, Chi-wai Michael. "Characterization and regulation of expression of tyrosine kinase receptors rse, axl, mer and their ligand gas6 in the testis /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20357758.

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Allsebrook, Andrew M. "QPRTase : quinolinic acid analogue synthesis and non-enzymic decarboxylation of N-alkylquinolinic acids." Thesis, University of St Andrews, 1998. http://hdl.handle.net/10023/14376.

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Abstract:

Quinolinate phosphoribosyltransferase (QPRTase, E.C. 2.4.2.19) is considered to be a unique enzyme in that it is thought to catalyse two distinct chemical reactions. Both the transfer of a phosphoribosyl group from 5-phosphoribosyl-1- pyrophosphate onto the nitrogen of quinolinic acid and the subsequent decarboxylation of the intermediate to form nicotinic acid mononucleotide are thought to be catalysed by the QPRTase system. Analogues of quinolinic acid were designed as potential inhibitors of QPRTase. These contain acidic groups at the 2- and 3- positions but are unable to decarboxylate. However, such compounds may be able to undergo the phosphoribosyl transfer reaction, potentially increasing their inhibitory potency. These compounds may be useful as "biological tools" allowing the neurological effects of an increase in quinolinic acid levels to be investigated. The compounds may show anti-fungal activity blocking the kynurenine pathway for NAD production. 2-Sulfonicotinic acid was synthesised by the oxidation of 2-mercaptonicotinic acid by either basic potassium permanganate, or iodine, with the structure was confirmed by X-ray crystallography. In biological testing the acid was shown to be neither an agonist nor antagonist of the NMDA receptor, or to be neurotoxic. A number of synthetic routes towards 2-phosphononicotinic acid, an alternative quinolinic acid analogue, were attempted though none were successful. These included orthometallation strategies and palladium coupling reactions to incorporate the phosphonic acid group at the 2- position. Nucleophilic addition routes, methods of building up the pyridine ring and including non-selective phosphonic acid addition were also examined. However, a related derivative, 2-(phosphonomethyl)nicotinic acid, was successfully synthesised. The non-enzymic decarboxylation of N-alkyl quinolinic acids was investigated, for comparison with the decarboxylation reaction catalysed by QPRTase. Both N- methyl and N-ethylquinolinic acid were synthesised, and the pH versus rate profiles measured. The rate maximum for both compounds was at pH 1.5, with the rate decreasing both above and below the maximum. N-Methylquinolinic acid was 10 times faster than quinolinic acid itself, demonstrating the effect of the nitrogen substituent. The N-ethyl derivative decarboxylated a further 1.5 times faster, showing the effect of increasing the size of the substituent. An Arrhenius plot was also carried out, giving an activation energy for the reaction of 153 kJ mol-1. Attempts to prepare the N-propyl derivative were unsuccessful, as decarboxylation occurred very readily to give N- propylnicotinic acid.

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Corwin, Thomas [Verfasser]. "Deciphering Human Cytoplasmic Protein Tyrosine Kinase Phosphorylation Specificity In Yeast / Thomas Corwin." Berlin : Freie Universität Berlin, 2016. http://d-nb.info/1081935510/34.

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Caron, Lorraine. "Structure-function analyses of the tyrosine protein kinase p56lck in T lymphocytes." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56963.

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p56$ sp{ rm lck}$ is a member of the Src-family of tyrosine protein kinases which is abundantly expressed in T lymphocytes. Increasing evidence indicates that p56$ sp{ rm lck}$ participates in T-cell receptor-mediated signalling. Firstly, this enzyme is physically associated with the CD4 and CD8 T-cell surface glycoproteins. CD4 and CD8 are respectively involved in the recognition of major histocompatibility complex class II and class I, that are expressed on antigen presenting cells. Secondly, expression of activated p56$ sp{ rm lck}$ polypeptides in CD4- and CD8-negative T cells has been documented to enhance antigen-induced T-cell responsiveness. To understand the mechanism(s) by which p56$ sp{ rm lck}$ participates in this process, the effects of mutations in known regulatory domains of p56$ sp{ rm lck}$ on the ability of activated p56$ sp{ rm lck}$ to enhance antigen-induced T-cell responses have been examined. Our results indicate that p56$ sp{ rm lck}$ regulates T-cell antigen receptor signalling through a complex process requiring multiple distinct structural domains of the enzyme.

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Corwin, Thomas Georg [Verfasser]. "Deciphering Human Cytoplasmic Protein Tyrosine Kinase Phosphorylation Specificity In Yeast / Thomas Corwin." Berlin : Freie Universität Berlin, 2016. http://d-nb.info/1081935510/34.

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