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dc.contributor.advisorHitchcock, Ian Sen_US
dc.contributor.authorCorbo, Lana Marieen_US
dc.contributor.otherDepartment of Biochemistry and Cell Biologyen_US
dc.date.accessioned2013-05-22T17:34:21Z
dc.date.available2013-05-22T17:34:21Z
dc.date.issued1-Dec-11en_US
dc.date.submitted11-Decen_US
dc.identifierCorbo_grad.sunysb_0771M_10769en_US
dc.identifier.urihttp://hdl.handle.net/1951/59620
dc.description30 pg.en_US
dc.description.abstractJanus kinase (JAK) 2 is a critical secondary signaling protein and is ubiquitously expressed in hematopoietic cells. One of the major roles of JAK2 is to trigger signal transduction following binding of the hematopoietic growth factor thrombopoietin (TPO), to its receptor c-Mpl, which initiates megakaryopoiesis. Previous findings focused on other hematopoietic growth factor receptors suggest that JAK2 is critical for translocation of the receptor to the membrane. Using hematopoietic cell lines, in which we transiently overexpressed human JAK2, we found that increased JAK2 expression had no effect on cell surface membrane localization. We also studied the effects of c-Mpl cell surface localization following over-expression of mutant forms of JAK2 (JAK2V617F and JAK2R564Q) which have been shown to cause myeloproliferative diseases in humans. Interestingly, contrary to previous reports, we found no difference in cell surface localization, following overexpression of mutant JAK2. Finally, we determined the effects of the JAK2R564Q mutation on cellular proliferation, survival, and signaling, comparing its effect to those of the more common JAK2V617F mutation. Although the JAK2R564Q mutation occurs within the same pseudokinase domain as JAK2V617F, the functionality of the mutations differs. Our results suggest that the JAK2R564Q mutation has the ability to prevent apoptosis while the JAKV617F contributes to hyperproliferation.en_US
dc.description.sponsorshipStony Brook University Libraries. SBU Graduate School in Department of Biochemistry and Cell Biology. Charles Taber (Dean of Graduate School).en_US
dc.formatElectronic Resourceen_US
dc.language.isoen_USen_US
dc.publisherThe Graduate School, Stony Brook University: Stony Brook, NY.en_US
dc.subject.lcshMolecular biology--Cellular biology--Biologyen_US
dc.titleJanus kinase (JAK) 2 regulation and the novel activating mutation, JAK2R546Qen_US
dc.typeThesisen_US
dc.description.advisorAdvisor(s): Hitchcock, Ian S. Committee Member(s): Dean, Neta ; Erster, Susan.en_US
dc.mimetypeApplication/PDFen_US


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