Gene expression profiling of HUH7-ins: lack of a granulogenic function for chromogranin A.

Lutherborrow, MA; Appavoo, M; Simpson, AM; Tuch, BE

Gene expression profiling of HUH7-ins: lack of a granulogenic function for chromogranin A.

Lutherborrow, MA Appavoo, M Simpson, AM

Tuch, BE

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Publication Type:: Journal Article
Citation:: Islets, 2009, 1 (1), pp. 62 - 74
Issue Date:: 2009-07

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Field	Value	Language
dc.contributor.author	Lutherborrow, MA	en_US
dc.contributor.author	Appavoo, M	en_US
dc.contributor.author	Simpson, AM https://orcid.org/0000-0002-2249-5097	en_US
dc.contributor.author	Tuch, BE	en_US
dc.date.issued	2009-07	en_US
dc.identifier.citation	Islets, 2009, 1 (1), pp. 62 - 74	en_US
dc.identifier.uri	http://hdl.handle.net/10453/13048
dc.description.abstract	Previously, the insulin producing liver cell line HUH7-ins has been shown to synthesize, store and secrete insulin in response to glucose via secretory granules. The current study characterized the gene expression profile of HUH7-ins with the aim to identify changes possibly involved in the formation of granules. Additionally, experiments were conducted to determine the influence of chromogranin A (CgA) on secretory granule biogenesis (SGB) in HUH7-ins. Expression of 165 genes were significantly changed in HUH7-ins,though interestingly the majority of secretory granule associated genes, such as the chromogranins were unchanged. CgA was over-expressed in glucose unresponsive HUH7-ins cells to test whether CgA played a role in SGB and would restore the regulated secretory phenotype. Over-expression affected neither the storage nor regulated secretion of insulin. These data suggest that SGB may by regulated at a post-transcriptional level with no evidence to indicate that CgA regulates SGB in the cell line HUH7-ins.	en_US
dc.language	eng	en_US
dc.relation.ispartof	Islets	en_US
dc.relation.isbasedon	10.4161/isl.1.1.8994	en_US
dc.subject.mesh	Cell Line, Tumor	en_US
dc.subject.mesh	Secretory Vesicles	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Insulin	en_US
dc.subject.mesh	Glucose	en_US
dc.subject.mesh	Microarray Analysis	en_US
dc.subject.mesh	Gene Expression Profiling	en_US
dc.subject.mesh	Gene Expression Regulation	en_US
dc.subject.mesh	Middle Aged	en_US
dc.subject.mesh	Male	en_US
dc.subject.mesh	Insulin-Secreting Cells	en_US
dc.subject.mesh	Chromogranin A	en_US
dc.subject.mesh	Validation Studies as Topic	en_US
dc.title	Gene expression profiling of HUH7-ins: lack of a granulogenic function for chromogranin A.	en_US
dc.type	Journal Article
utslib.citation.volume	1	en_US
utslib.location.activity	United States	en_US
utslib.for	1108 Medical Microbiology	en_US
utslib.for	1116 Medical Physiology	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
utslib.copyright.status	closed_access
pubs.issue	1	en_US
pubs.publication-status	Published	en_US
pubs.volume	1	en_US

Abstract:

Previously, the insulin producing liver cell line HUH7-ins has been shown to synthesize, store and secrete insulin in response to glucose via secretory granules. The current study characterized the gene expression profile of HUH7-ins with the aim to identify changes possibly involved in the formation of granules. Additionally, experiments were conducted to determine the influence of chromogranin A (CgA) on secretory granule biogenesis (SGB) in HUH7-ins. Expression of 165 genes were significantly changed in HUH7-ins,though interestingly the majority of secretory granule associated genes, such as the chromogranins were unchanged. CgA was over-expressed in glucose unresponsive HUH7-ins cells to test whether CgA played a role in SGB and would restore the regulated secretory phenotype. Over-expression affected neither the storage nor regulated secretion of insulin. These data suggest that SGB may by regulated at a post-transcriptional level with no evidence to indicate that CgA regulates SGB in the cell line HUH7-ins.

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http://hdl.handle.net/10453/13048