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Article: BIG3 inhibits insulin granule biogenesis and insulin secretion.

TitleBIG3 inhibits insulin granule biogenesis and insulin secretion.
Authors
Issue Date2014
PublisherNature Publishing Group. The Journal's web site is located at http://www.emboreports.org
Citation
EMBO Reports, 2014, v. 15 n. 6, p. 714-722 How to Cite?
AbstractWhile molecular regulation of insulin granule exocytosis is relatively well understood, insulin granule biogenesis and maturation and its influence on glucose homeostasis are relatively unclear. Here, we identify a novel protein highly expressed in insulin-secreting cells and name it BIG3 due to its similarity to BIG/GBF of the Arf-GTP exchange factor (GEF) family. BIG3 is predominantly localized to insulin- and clathrin-positive trans-Golgi network (TGN) compartments. BIG3-deficient insulin-secreting cells display increased insulin content and granule number and elevated insulin secretion upon stimulation. Moreover, BIG3 deficiency results in faster processing of proinsulin to insulin and chromogranin A to β-granin in β-cells. BIG3-knockout mice exhibit postprandial hyperinsulinemia, hyperglycemia, impaired glucose tolerance, and insulin resistance. Collectively, these results demonstrate that BIG3 negatively modulates insulin granule biogenesis and insulin secretion and participates in the regulation of systemic glucose homeostasis. © 2014 Singapore Bioimaging Consortium, A*STAR.
Persistent Identifierhttp://hdl.handle.net/10722/196793
ISSN
2015 Impact Factor: 7.739
2015 SCImago Journal Rankings: 4.291
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorLi, H-
dc.contributor.authorWei, S-
dc.contributor.authorCheng, KY-
dc.contributor.authorGounko, NV-
dc.contributor.authorEricksen, RE-
dc.contributor.authorXu, A-
dc.contributor.authorHong, W-
dc.contributor.authorHan, W-
dc.date.accessioned2014-04-29T03:41:33Z-
dc.date.available2014-04-29T03:41:33Z-
dc.date.issued2014-
dc.identifier.citationEMBO Reports, 2014, v. 15 n. 6, p. 714-722-
dc.identifier.issn1469-221X-
dc.identifier.urihttp://hdl.handle.net/10722/196793-
dc.description.abstractWhile molecular regulation of insulin granule exocytosis is relatively well understood, insulin granule biogenesis and maturation and its influence on glucose homeostasis are relatively unclear. Here, we identify a novel protein highly expressed in insulin-secreting cells and name it BIG3 due to its similarity to BIG/GBF of the Arf-GTP exchange factor (GEF) family. BIG3 is predominantly localized to insulin- and clathrin-positive trans-Golgi network (TGN) compartments. BIG3-deficient insulin-secreting cells display increased insulin content and granule number and elevated insulin secretion upon stimulation. Moreover, BIG3 deficiency results in faster processing of proinsulin to insulin and chromogranin A to β-granin in β-cells. BIG3-knockout mice exhibit postprandial hyperinsulinemia, hyperglycemia, impaired glucose tolerance, and insulin resistance. Collectively, these results demonstrate that BIG3 negatively modulates insulin granule biogenesis and insulin secretion and participates in the regulation of systemic glucose homeostasis. © 2014 Singapore Bioimaging Consortium, A*STAR.-
dc.languageeng-
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.emboreports.org-
dc.relation.ispartofEMBO Reports-
dc.titleBIG3 inhibits insulin granule biogenesis and insulin secretion.-
dc.typeArticle-
dc.identifier.emailCheng, KY: dorncky@hkucc.hku.hk-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.authorityCheng, KY=rp01672-
dc.identifier.authorityXu, A=rp00485-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/embr.201338181-
dc.identifier.pmid24711543-
dc.identifier.pmcidPMC4197882-
dc.identifier.hkuros228676-
dc.identifier.volume15-
dc.identifier.issue6-
dc.identifier.spage714-
dc.identifier.epage722-
dc.publisher.placeUnited Kingdom-

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