Дисертації з теми "Receptor tyrosine kinase family"
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Lorén, Christina. "Investigating the function of the Receptor Tyrosine Kinase ALK during Drosophila melanogaster development /." Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-411.
Повний текст джерелаGuiton, Michelle. "Molecular basis of signal transduction by the Trk family of receptor tyrosine kinases." Thesis, University of Bristol, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296366.
Повний текст джерелаKIM, SOYEON. "INVESTIGATING THE MOLECULAR INTERACTION OF ERBB RECEPTOR TYROSINE KINASES USING FLUORESCENCE CROSS CORRELATION SPECTROSCOPY." University of Akron / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=akron1632756640189756.
Повний текст джерелаReschke, Markus Oliver. "Mitogen-inducible gene-6 is a negative regulator of the HER-family of receptor tyrosine kinases." kostenfrei, 2008. http://mediatum2.ub.tum.de/doc/654949/654949.pdf.
Повний текст джерелаQi, Wenqing, Larry Cooke, Amy Stejskal, Christopher Riley, Kimiko Croce, Jose Saldanha, David Bearss, and Daruka Mahadevan. "MP470, a novel receptor tyrosine kinase inhibitor, in combination with Erlotinib inhibits the HER family/PI3K/Akt pathway and tumor growth in prostate cancer." BioMed Central, 2009. http://hdl.handle.net/10150/610342.
Повний текст джерелаBeji, Abdelhamid [Verfasser], Kay Akademischer Betreuer] Schneitz, and Axel [Akademischer Betreuer] [Ullrich. "Significance of the Negative Regulator of HER Receptor Tyrosine Kinase Family, mig-6 Protein, in Colon Cancer and Glioblastoma / Abdelhamid Beji. Gutachter: Axel Ullrich. Betreuer: Kay Schneitz." München : Universitätsbibliothek der TU München, 2012. http://d-nb.info/1019590297/34.
Повний текст джерелаGoebel, Susan Michelle. "Phospho-regulation of hippocampal NMDA receptor localization and function /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.
Знайти повний текст джерелаTypescript. Includes bibliographical references (leaves 200-233). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
Zhao, Haotian. "Exploring the role of fibroblast growth factor (FGF) signaling in mouse lens fiber differentiation through tissue-specific disruption of FGF receptor gene family." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1072722841.
Повний текст джерелаTitle from first page of PDF file. Document formatted into pages; contains xii, 203 p.; also includes graphics (some col.) Includes bibliographical references (p. 179-203). Available online via OhioLINK's ETD Center
Lennmyr, Fredrik. "Signal Transduction in Focal Cerebral Ischemia : Experimental Studies on VEGF, MAPK and Src family kinases." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5267-1/.
Повний текст джерелаLjuslinder, Ingrid. "Studies of LRIG1 and the ERBB receptor family in breast and colorectal cancer." Doctoral thesis, Umeå : Umeå university, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-25678.
Повний текст джерелаFischer, Oliver Martin. "Receptor Tyrosine Kinase Activation in Human Carcinoma Cells." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-17997.
Повний текст джерелаCheung, Man-ting, and 張敏婷. "Expression of met receptor tyrosine kinase in hepatocellularcarcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B4669965X.
Повний текст джерелаMeyer, Sara. "The Ron Receptor Tyrosine Kinase in Tissue Morphogenesis." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1258666269.
Повний текст джерелаThobe, Megan. "The Ron Receptor Tyrosine Kinase in Prostate Cancer." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1273006729.
Повний текст джерелаRobertson, Sears Heather C. 1975. "The receptor tyrosine phosphatase Ptp69D and the receptor tyrosine kinase Pvr in Drosophila nervous system development." Thesis, Massachusetts Institute of Technology, 2004. http://hdl.handle.net/1721.1/32254.
Повний текст джерелаIncludes bibliographical references.
Cell migration and axon guidance are highly similar processes important for the development of the nervous system. Both processes involve the transduction of signals across the membrane, resulting in changes in the cytoskeleton. I have examined the roles of two receptors that are involved in axon guidance and cell migration in Drosophila. Ptp69D is a receptor tyrosine phosphatase required for axon guidance in the developing embryo and for layer-specific axon targeting in the developing visual system. Using a dominant-negative form of Ptp69D, I have identified several genes with which Ptp69D genetically interacts in photoreceptor axon targeting. Removing a single dose of the cytoplasmic tyrosine kinases Src64 or Abl or the repulsive axon guidance receptor robo enhanced the Ptp69D dominant-negative phenotype. In mammalian systems, Src plays a key role in the regulation of cell adhesion, and Abl is a known regulator of actin cytoskeletal dynamics. Removing a single dose of the EGF receptor or Ras85D suppressed the Ptp69D dominant negative phenotype. Interestingly, the cytoplasmic tyrosine kinase PR2 binds Ptp69D, and the C. elegans homolog of PR2 has been found to suppress the Egfr/Ras pathway. Other evidence suggests that the Egfr/Ras pathway may be required for axon outgrowth. In addition to PR2, I also identified the receptor tyrosine kinase Pvr in a biochemical screen for proteins that bind Ptp69D. I generated mutants in Pvr by gene disruption and EMS mutagenesis. These mutants have disruptions in the embryonic central nervous system, including mispositioning of axon tracts and the glia that wrap them. However, these defects are not inherent to the CNS.
(cont.) Rather, they result from a failure of hemocytes to migrate out of the head and engulf dead cells in the CNS. To identify proteins that signal downstream of Pvr in cell migration, I used a yeast two-hybrid screen to identify 15 proteins that bind the intracellular domain of kinase-active Pvr. One of these proteins, drk, is required for Pvr-dependent Erk MAP kinase activation. None has defects in hemocyte migration when disrupted by RNA interference. Whether these proteins have redundant functions or function downstream of Pvr in other systems remains to be determined.
by Heather C. Robertson Sears.
Ph.D.
Burgar, Helen Rachel. "Fibroblast growth factor receptor signalling." Thesis, University of Birmingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275129.
Повний текст джерелаFox, Gavin Connor. "Structural studies on MAP kinase phosphatases and the receptor tyrosine kinase TrkA." Thesis, Birkbeck (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268768.
Повний текст джерелаDoepfner, Kathrin T. "Targeting receptor tyrosine kinase signaling in acute myeloid leukemia /." Zürich, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253043.
Повний текст джерелаPaliouras, Grigorios. "Regulation of met receptor tyrosine kinase signalling and biology." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86661.
Повний текст джерелаThe Met RTK and its ligand, hepatocyte growth factor (HGF), are positive regulators of epithelial morphogenesis, scatter, and survival. However little was known regarding the proteins responsible for attenuating Met receptor activation. In Chapter II, I demonstrated that the Met receptor was hyperphopshorylated in PTP1B-null mice in response to Fas-induced liver damage. Inhibition of Met signaling with PHA665752, removed protection from liver failure in PTP1B-null hepatocytes, demonstrating that PTP1B was a negative regulator of the Met RTK and its removal promoted cell survival against Fas-induced hepatic failure.
In response to Met receptor stimulation, the Gab1 scaffold protein is the prominent protein recruited and phosphorylated downstream from Met and is critical in mediating Met-dependent biological responses. In chapters III and IV, I identified the serine/threonine kinase Pak4 and the microtubule-bound guanine nucleotide exchange factor GEF-H1 as novel proteins recruited to Gab1 following Met receptor activation. I demonstrate that Gab1 and Pak4 synergize to enhance migration and invasion following HGF stimulation. Furthermore, the recruitment of Pak4 to Gab1 is important for its subcellular localization to lamellipodia and critical for epithelial cell dispersal and morphogenesis downstream from Met. In addition, GEF-H1 is important in focal adhesion formation and turnover and this correlates with the ability of GEF-H1 to promote epithelial migration and invasion downstream from Met.
Overall, these studies investigate molecular mechanisms regulating Met-dependent signals and demonstrate for the first time that the Met receptor is a substrate for PTP1B and identify Pak4 and GEF-H1 as key integrators of Met dependent cellular migration and invasion.
Les récepteurs tyrosine kinase aux facteurs de croissance sont des initiateurs critiques des voies de signalisation nécessaires à la croissance, la différentiation, la migration et la survie cellulaire. Beaucoup de ces signaux sont coordonnés par des protéines d'échafaudage qui sont phosphorylées au cours de leur recrutement au complexe de récepteurs activés. Ceci fournit des sites de liaison à de multiples protéines permettant l'activation et la génération de différentes réponses biologiques. L'amplitude et la durée d'un signal est régulée via la déphosphorylation et la dégradation des protéines cibles. De cette façon, la régulation du signal agit pour promouvoir la formation et le désassemblage de complexes protéiques et pour diversifier et localiser les signaux en aval des récepteurs tyrosine kinase.
Le récepteur Met et son ligand HGF (Hepatocyte Growth Factor) sont des régulateurs de la morphogenèse, la dispersion et la survie des cellules épithéliales. Toutefois, peu d'informations sont disponibles sur les protéines responsables de l'extinction des signaux issus du récepteur Met. Dans le chapitre II, je démontre que le récepteur Met est hyperphosphorylé dans les souris knock-out pour PTP1B en réponse aux dommages induits par Fas. L'inhibition par le composé PHA665752 de la signalisation par Met, relève la protection contre les crises hépatiques dans les souris KO pour PTP1B. Ceci démontre que PTP1B est un régulateur négatif de Met et son retrait permet la survie cellulaire contre les crises hépatiques induites par Fas.
En réponse à la stimulation du récepteur Met, la protéine d'échafaudage Gab1 est la plus importante des protéines recrutées et phosphorylées en aval de Met et cette protéine est critique dans la médiation des réponses biologiques dépendantes de Met. Dans les chapitres III et IV, j'ai identifié la kinase Ser/Thr Pak4 et le facteur d'échange de guanine lié aux microtubules (GEF-H1) en tant que nouvelles protéines recrutées à Gab1 suite à l'activation de Met. Je démontre que Gab1 et Pak4 agissent de façon synergique pour promouvoir la migration et l'invasion suite à la stimulation par HGF. De plus, le recrutement de Pak4 à Gab1 est important pour sa localisation cellulaire dans les lamellipodes et est critique pour la dispersion et la morphogenèse des cellules épithéliales en aval de Met. En outre, GEF-H1 est important pour la formation et le roulement des points d'adhésion focaux ce qui est en corrélation avec la capacité de GEF-H1 de promouvoir la migration et l'invasion épithéliale en aval de Met.
Ces études ont pour but d'investiguer les mécanismes moléculaires régulant les signaux dépendants de Met et démontrent pour la première fois que le récepteur Met est un substrat pour PTP1B. Finalement, Pak4 et GEF-H1 sont identifiés comme des intégrateurs clés de la migration et l'invasion cellulaire dépendante de Met.
Park, Eun-Hee 1971. "Mechanisms of translation initiation of receptor tyrosine kinase Tie2." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=102690.
Повний текст джерелаTie2, an endothelial-specific receptor tyrosine kinase, plays an essential role in normal blood vessel maturation, remodeling, and stability. Tie2 expression is also upregulated in various cancers indicating a role in tumor angiogenesis. The human Tie2 mRNA transcript contains an unusually long (372 nucleotides) 5' untranslated region (UTR) with five upstream open reading frames (uORFs). In this thesis, we demonstrate that the Tie2 5' UTR promotes cap-independent translation, indicating the presence of functional internal ribosome entry site (IRES). In addition, we illustrate that Tie2 IRES activity is maintained, and even slightly stimulated, under hypoxic conditions when cap-dependent protein synthesis is attenuated. We further show that the Tie2 IRES is functional during quiescence, another condition known to compromise cap-dependent translation. These results present how Tie2 mRNA is translated despite a cumbersome structured 5' UTR and how its production is secured under unfavorable environmental conditions.
We define experimental conditions where the Tie2 IRES is not active, allowing us to assess the contribution of cap-dependent translation to Tie2 protein synthesis. We demonstrate evidence that Tie2 mRNA can be translated via both cap-dependent scanning mechanism and internal initiation. Moreover, we show that the presence of the uORFs within the 5' UTR is inhibitory to downstream translation initiation. Our results suggest that the uORFs serve to decrease the proportion of ribosomes competent for reinitiation as they traverse the mRNA 5' UTR and thus minimizing interference with the IRES and/or mediating inefficient translation of the potent protein under normal conditions. Like many other cellular IRESes, the entire Tie2 5' UTR appears to be required for maximum IRES activity.
Taken together, our results underscore the complex mechanisms to control gene expression at the level of translation initiation of the Tie2 mRNA.
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.
Повний текст джерелаWagner, Joel Patrick. "Multivariate studies of receptor tyrosine kinase function in cancer." Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/81672.
Повний текст джерелаCataloged from PDF version of thesis.
Includes bibliographical references (p. 215-232).
Receptor tyrosine kinases (RTKs) are critical regulators of cellular homeostasis in multicellular organisms. They influence cell proliferation, migration, differentiation, and transcriptional activation, among other processes, and are therefore also relevant to cancer biology. Upon interaction with cognate ligand, RTKs initiate signaling cascades dependent in part on the phosphorylation of proteins. From a computational perspective, this thesis has studied methods for quantifying relationships between measured signals (using Bayesian network inference, correlation, and mutual information-based methods), and between signals and cellular phenotypes (using linear regression, partial least squares regression, and feature selection methods). From a biological perspective, this thesis has studied signaling between RTKs, signaling and cell migration downstream of RTKs in epithelial versus mesenchymal cell states, and comparative signaling across six RTKs. In the latter case, the results show that the six RTKs cluster into three classes based on their inferred signaling networks. Using publicly available transcriptional and pharmacological profiling data from hundreds of cancer cell lines, it was determined that expression of same-class RTK genes or their cognate ligands can correlate with insensitivity to drugs targeting other RTKs in that class. This suggests that resistance to RTK-targeted therapies in cancer may emerge in part because same-class RTKs can compensate for the reduced signaling of the inhibited receptor. The thesis concludes by quantitatively exploring the features of experimental data that improve model accuracy.
by Joel Patrick Wagner.
Ph.D.
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.
Повний текст джерелаHocker, Samuel. "Receptor tyrosine kinase expression and phosphorylation in canine nasal carcinoma." Thesis, Kansas State University, 2018. http://hdl.handle.net/2097/38648.
Повний текст джерелаDepartment of Clinical Sciences
Mary Lynn Higginbotham
This study evaluated sixteen canine nasal carcinoma and five normal nasal epithelium samples for expression and phosphorylation of known targets of toceranib [vascular endothelial growth factor receptor-2 (VEGR2), platelet derived growth factor alpha (PDGFR-[alpha]), platelet derived growth factor receptor beta (PDGFR-[beta]), and stem cell factor receptor (c-KIT)] and epidermal growth factor receptor 1 (EGFR1) using immunohistochemistry, RT-PCR and a receptor tyrosine kinase (RTK) phosphorylation panel. Protein for VEGFR2 was expressed in neoplastic cells of all carcinomas, PDGFR-[alpha] was noted in 15/16, whereas PDGFR-[beta] was detected in 3/16 samples, but showed primarily stromal staining. Protein expression for c-KIT was present in 4/16 and EGFR1 was noted in 14/16 samples. Normal tissue showed variable protein expression of the RTKs. Messenger RNA for VEGFR2, PDGFR-[beta], and c-KIT were noted in all samples. Messenger RNA for PDGFR-[alpha] and EGFR1 were detected in 15/16 samples. All normal nasal tissue detected messenger RNA for all RTKs of interest. Constitutive phosphorylation of VEGFR2, PDGFR-[alpha], PDGFR-[beta] and c-KIT was not observed in any carcinoma or normal nasal sample, but phosphorylation of EGFR1 was noted in 10/16 carcinoma and 3/5 normal samples. The absence of major phosphorylated RTK targets of toceranib suggests the clinical effect of toceranib may occur through inhibition of alternative and currently unidentified RTK pathways in canine nasal carcinomas. The observed protein and message expression and phosphorylation of EGFR1 in the nasal carcinoma samples merits further inquiry into EGFR1 as a therapeutic target for this cancer.
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.
Повний текст джерелаEdling, 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.
Повний текст джерелаCoonan, Jason R. "Regulation of neural connectivity by the EphA4 receptor tyrosine kinase /." Connect to thesis, 2001. http://eprints.unimelb.edu.au/archive/00000727.
Повний текст джерелаSchuller, 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/.
Повний текст джерела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.
Повний текст джерелаReynolds, Andrew Robert. "Functional fluorescence imaging of receptor tyrosine kinase activity in cells." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398898.
Повний текст джерелаGoodman, 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/.
Повний текст джерелаAubertin, Johannes. "Characterization of receptor tyrosine kinase signaling pathways in bladder cancer." Paris 11, 2009. http://www.theses.fr/2009PA11T047.
Повний текст джерелаLee, 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.
Повний текст джерелаWong, Wai-lap. "Signal transduction pathways of ret receptor tuyrosine kinase." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22786478.
Повний текст джерела王偉立 and Wai-lap Wong. "Signal transduction pathways of ret receptor tuyrosine kinase." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31225354.
Повний текст джерелаChan, Richard Muller William J. "In vivo structure-function studies of the ErbB2 receptor tyrosine kinase /." *McMaster only, 2004.
Знайти повний текст джерелаShulman, Johanna. "Biochemical analysis of activating mutations of the kit receptor tyrosine kinase." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0003/MQ40794.pdf.
Повний текст джерелаSo, Wai Kin. "Role of receptor tyrosine kinase regulator Sprouty in ovarian cancer cells." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42242.
Повний текст джерелаPetkiewicz, Stephanie L. "The Met receptor tyrosine kinase in mammary gland tumorigenesis and development /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103278.
Повний текст джерелаThrough assays of overexpression in vivo and inhibition in vitro, Met receptor signaling has been correlated with the development of the mammary gland. To examine the effects of loss of Met receptor signaling on mammary gland development I have utilized the Cre/LoxP1 recombination system to knock-out the Met receptor from the mammary epithelium. Mammary-specific Cre recombinase efficiently excised floxed DNA as visualized by activation of a beta-galactosidase reporter In Met+/+ glands, however, few beta-galactosidase positive cells are retained In the Mefl/fl glands and an intermediate number are retained in the Met fl/+ glands. This indicates that Met-null cells are selected against and supports a role for Met in the development of the mammary gland.
Luzac, Michal Leonie. "Small Molecules as Potential Inhibitors of the Met Tyrosine Kinase Receptor." Thesis, University College London (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498510.
Повний текст джерелаIrving, Carol. "Characterisation of the receptor tyrosine kinase, Sek-1, during vertebrate embryogenesis." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263644.
Повний текст джерелаGirlalt-Pujol, Marta. "Investigating the regulation of the endocytosis of tyrosine kinase receptor Tie2." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/18527/.
Повний текст джерелаMcCarthy, Mark John. "Studies on the endothelial cell specific receptor tyrosine kinase, tie-1." Thesis, University of Leicester, 1999. http://hdl.handle.net/2381/34159.
Повний текст джерелаMyers, Samuel Harry. "Development of novel receptor tyrosine kinase inhibitors by a chemocentric approach." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28769.
Повний текст джерелаTuzi, Nadia Lucia. "The Eph growth factor receptor." Thesis, Open University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294878.
Повний текст джерелаLam, 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.
Повний текст джерелаLam, 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.
Повний текст джерелаPaluch, Andrew M. "The Ron Receptor Tyrosine Kinase as a Mediator of Inflammation and Tumorigenesis." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1455208865.
Повний текст джерелаZhao, Tong Tong. "Mechanism and Therapeutic Potential of Statin-Mediated Inhibition of Tyrosine Kinase Receptors." Thesis, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20334.
Повний текст джерелаHantschel, Oliver. "Structural and functional analysis of the non receptor tyrosine kinase c-Abl." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=970379552.
Повний текст джерела