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E-GEOD-59928 - Expression data from 24 hours of Sox17 overexpression in pancreatic islets of a 16-week old mice
Released on 31 July 2014, last updated on 28 July 2015
Secretion of insulin by pancreatic β cells in response to glucose is central for glucose homeostasis, and dysregulation of this process is a hallmark of the early stages of diabetes. We utilized a tetracycline-inducible approach to investigate the immediate impact of a pulse of Sox17 expression on the insulin secretory pathway. Sox17 gain-of-function animals (Sox17-GOF) were generated using an Ins2-rtTA mouse line and a line in which Sox17 expression is regulated by the tetracycline transactivator (tetO-Sox17). Administering doxycycline to 16-week old mice resulted in Sox17 overexpression in mature β cells in the islets. In order to identify the molecular basis by which Sox17 regulates the secretory pathway in β cells, we performed microarray analysis on isolated islets following a 24-hour pulse of Sox17 overexpression. We chose to analyze a 24 hour pulse of Sox17 for islet pancreas RNA extraction and hybridization on Affymetrix microarrays since it was sufficient to stimulate the insulin secretory pathway without causing changes in islet architecture.
transcription profiling by array
James Wells <James.Wells@cchmc.org>, Jim Wells
Sox17 regulates insulin secretion in the normal and pathologic mouse β cell. Jonatan D, Spence JR, Method AM, Kofron M, Sinagoga K, Haataja L, Arvan P, Deutsch GH, Wells JM.