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dc.contributor.supervisor Mishra, Suresh (Physiology) en_US
dc.contributor.author Salter, Neil William
dc.date.accessioned 2011-09-01T19:21:19Z
dc.date.available 2011-09-01T19:21:19Z
dc.date.issued 2011-09-01
dc.identifier.uri http://hdl.handle.net/1993/4825
dc.description.abstract Transglutaminase 2 (TG2) is a functionally and structurally complex ubiquitous protein. TG2 has Ca2+-dependent transamidating activity, can bind and hydrolyze ATP/GTP, function as a G-protein in intracellular signaling, and has reported kinase activity. TG2 knockout mice are observed to have impaired glucose-stimulated insulin secretion (GSIS). Three naturally occurring mutations, including Met330Arg, Ile331Asn, and Asn333Ser, have been reported in the TG2 protein and observed to be related with maturity onset diabetes of the young (MODY). Overexpression of the naturally occurring Myc-tag mutants in INS-1E cells generated a loss in GSIS compared to wild type-TG2 overexpression. Each mutant was shown to have diminished transamidation and kinase activities, along with altered GTP-binding which was responsive to glucose stimulation. Naturally occurring mutations in TG2 impact the transamidation, kinase, and GTP-binding functions of TG2. The GTP-binding function of TG2 has a significant impact on GSIS from pancreatic beta cells in addition to its transamidating activity. en_US
dc.rights info:eu-repo/semantics/openAccess
dc.subject TG2 en_US
dc.subject Diabetes en_US
dc.title Functional characterization of naturally occurring mutant transglutaminase 2 en_US
dc.type info:eu-repo/semantics/masterThesis
dc.degree.discipline Physiology en_US
dc.contributor.examiningcommittee Dodd, Janice (Physiology) Nyomba, Gregoire (Physiology) Murphy, Leigh (Biochemistry and Medical Genetics) en_US
dc.degree.level Master of Science (M.Sc.) en_US
dc.description.note October 2011 en_US


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