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58篇 您的检索式：作者名="Winnay"

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	题名	作者	年代	出处	被引量
1	Tissuespecific knockout of the insulin receptor in pancreatic β cells creates an insulin secretary defect similar to that in type 2 diabetes显示文摘	Kulkarni RN Brtining JC Winnay JN	1999	Cell1999，96，3：	1
2	Tissue-specific knockout of the insulin receptor in pancreatic beta cell creates an insulin secretory defect similar to that in type 2 diabetes显示文摘	Kulkarni RN Braining JC Winnay JN	1999	Cell1999，96，3：	1
3	Glucose effects on betacell growth and survival require activation of insulin receptors and insulin receptor substrate 2 显示文摘	Assmann A Ueki K Winnay JN	2009	Mol Cell Biol2009，29，11：	1
4	Gab-1-mediated IGF-I signaling in IRS-1-deficient 3T3 fibroblasts显示文摘	Winnay JN Bruning JC Burks DJ	2000	Biol Chem2000，275，10：	1
5	The phosphoinositide 3- kinase regulatory subunit p85alpha can exert tumor suppressor properties through negative regulation of growth factor signaling显示文摘	Taniguchi CM Winnay J Kondo T	2010	Cancer Res2010，70，13：	1
6	Differential signaling by insulinreceptor substrate 1 (IRS-1) and IRS-2 in IRS-1-deficient cells显示文摘	Bruning JC Winnay J Cheatham B et al	1997	Mol Cell Biol1997，17，3：	1
7	Tissue-specific knockout of the insulin receptor in pancreatic beta ceils creates an insulin secretory defect similar to that in type 2 diabetes 显示文摘	Kulkarni RN Bruning JC Winnay JN	1999	Cell1999，96，：	1
8	A muscle specific insulin receptor nockout exhibils features of the metabolic syndrome of NIDDM without altering glucose to leranee显示文摘	BRUNING JG MICHAEL MD WINNAY JN	1998	Mol Cell1998，2，5：	1
9	A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance显示文摘	BruningJC Michael MD Winnay JN	1998	Mol Cell1998，2，：	1
10	Tissue-specific knockout of the insulin receptor in pancreatic beta cells creates an insulin secretory defect similar to that in type 2 diabetes显示文摘	Kulkarni RN Bruning JC Winnay JN	1999	Cell1999，96，：	1
11	Differential signaling by insulin receptor substrate 1 (IRS-1) and IRS-2 in IRS-l-defierent cells显示文摘	BRUNING J C WINNAY J CHEATHAM B	1997	ol Cell Biol1997，17，：	1
12	The phosphoinositide 3- kinase regulatory subunit p85alpha can exert tumor suppressor pro- perties through negative regulation of growth factor signaling 显示文摘	Taniguchi CM Winnay J Kondo T	2010	Cancer Res2010，70，13：	1
13	Glucoseeffects on beta-cell growth and survival require activation of insulin receptors and insulin receptor substrate 2 显示文摘	Assmann A Ueki K Winnay J N	2009	Mol Cell Biol2009，29，11：	1
14	Tissue-specific knockout of the insulin receptor in pancreatic beta cells creates an insulin secretory defect similar to that in type 2 diabetes显示文摘	Kulkarni R N Bruning J C Winnay J N	1999	Cell1999，96，：	1
15	PDX-1 haploinsufficiency limits the compensatory islet hyperplasia that occurs in response to Insulin resistance 显示文摘	Kulkarni RN Jhala US Winnay JN	2004	J Chin Invesl2004，114，6：	1
16	Tissue-specific knockout of the insulin receptor in pancreatic beta cells creates an insulin secretory defect similar to that in type 2 diabetes显示文摘	Kulkarni RN Bruning JC Winnay JN	1999	Cell1999，96，3：	1
17	Glucose effects on beta- cell growth and survival require activation of insulin receptors and insulin receptor substrate 2显示文摘	Asmann A Ueki K Winnay JN	2009	Mol Cell Biol2009，29，11：	1
18	Altered function of insulin reeptor substrate-1-deficientmouse islets and cultured betacell fines显示文摘	Kulkarni RN Winnay JN Daniels M	1999	J Clin Invest1999，104，12：	1
19	Tissue-specific knockout of the insulin receptor in pancreatic beta cells creates an insulin secretory defect similar to that in type 2 diabetes显示文摘	Kulkarni RN Bruning JC Winnay JN	1999	Cell1999，96，：	1
20	A regulatory subunit of phosphoinositide 3-kinase increases the nuclear accumulation of X-box-binding protein-1 to modulate the unfolded protein response显示文摘	Winnay JN Boucher J Mori MA	2010	Nat Med2010，16，4：	1

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