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10.1002/embr.201338181 http://scihub22266oqcxt.onion/10.1002/embr.201338181 C4197882!4197882!24711543     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Rep 2014 ; 15 (6): 714-22 Nephropedia Template TP {{tp|p=24711543|t=2014. BIG3 inhibits insulin granule biogenesis and insulin secretion |pdf=|usr=}}{{24711543}} gab.com Text BIG3 inhibits insulin granule biogenesis and insulin secretion JO: EMBO Rep http://www.kidney.de/pget.php?&tw=1&pmid=24711543 #FOAvip While 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 ?-granin in ?-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. Twit Text FOAVip BIG3 inhibits insulin granule biogenesis and insulin secretion ????EMBO Rep http://www.kidney.de/pget.php?&tw=1&pmid=24711543 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24711543 #FOAvip English Wikipedia <ref>{{Cite pmid|24711543}}</ref> BIG3 inhibits insulin granule biogenesis and insulin secretion #MMPMID24711543 Li H; Wei S; Cheng K; Gounko NV; Ericksen RE; Xu A; Hong W; Han W EMBO Rep 2014[Jun]; 15 (6): 714-22 PMID24711543show ga While 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 ?-granin in ?-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. äBIG3 inhibits insulin granule biogenesis and insulin secretion (epmc).pdf DeepDyve Pubget Overpricing