Ignet

Gene Information

Gene symbol: SH2B2

Gene name: SH2B adaptor protein 2

HGNC ID: 17381

Synonyms: APS

Related Genes

#	Gene Symbol	Number of hits
1	ADIPOQ	1 hits
2	AKT1	1 hits
3	INS	1 hits
4	INSR	1 hits
5	IRS1	1 hits
6	LEP	1 hits
7	PDLIM5	1 hits
8	PIK3CA	1 hits
9	SH2B1	1 hits
10	SH2B3	1 hits

Related Sentences

#	PMID	Sentence
1	14578283	Increased insulin sensitivity and hypoinsulinemia in APS knockout mice.
2	14578283	A tyrosine kinase adaptor protein containing pleckstrin homology and SH2 domains (APS) is rapidly and strongly tyrosine phosphorylated by insulin receptor kinase upon insulin stimulation.
3	14578283	The function of APS in insulin signaling has heretofore remained unknown.
4	14578283	The blood glucose-lowering effect of insulin, as assessed by the intraperitoneal insulin tolerance test, was increased in APS(-/-) mice.
5	14578283	Plasma insulin levels during fasting and in the intraperitoneal glucose tolerance test were lower in APS(-/-) mice.
6	14578283	However, overexpression of wild-type or dominant-negative APS in 3T3L1 adipocytes did not affect insulin receptor numbers, phosphorylations of insulin receptor, insulin receptor substrate-1, or Akt and mitogen-activated protein kinase.
7	14578283	The glucose uptake and GLUT4 translocation were not affected by insulin stimulation in these cells.
8	14578283	Nevertheless, the insulin-stimulated glucose transport in isolated adipocytes of APS(-/-) mice was increased over that of APS(+/+) mice.
9	14578283	APS(-/-) mice also showed increased serum levels of leptin and adiponectin, which might explain the increased insulin sensitivity of adipocytes.
10	14578283	Increased insulin sensitivity and hypoinsulinemia in APS knockout mice.
11	14578283	A tyrosine kinase adaptor protein containing pleckstrin homology and SH2 domains (APS) is rapidly and strongly tyrosine phosphorylated by insulin receptor kinase upon insulin stimulation.
12	14578283	The function of APS in insulin signaling has heretofore remained unknown.
13	14578283	The blood glucose-lowering effect of insulin, as assessed by the intraperitoneal insulin tolerance test, was increased in APS(-/-) mice.
14	14578283	Plasma insulin levels during fasting and in the intraperitoneal glucose tolerance test were lower in APS(-/-) mice.
15	14578283	However, overexpression of wild-type or dominant-negative APS in 3T3L1 adipocytes did not affect insulin receptor numbers, phosphorylations of insulin receptor, insulin receptor substrate-1, or Akt and mitogen-activated protein kinase.
16	14578283	The glucose uptake and GLUT4 translocation were not affected by insulin stimulation in these cells.
17	14578283	Nevertheless, the insulin-stimulated glucose transport in isolated adipocytes of APS(-/-) mice was increased over that of APS(+/+) mice.
18	14578283	APS(-/-) mice also showed increased serum levels of leptin and adiponectin, which might explain the increased insulin sensitivity of adipocytes.
19	14578283	Increased insulin sensitivity and hypoinsulinemia in APS knockout mice.
20	14578283	A tyrosine kinase adaptor protein containing pleckstrin homology and SH2 domains (APS) is rapidly and strongly tyrosine phosphorylated by insulin receptor kinase upon insulin stimulation.
21	14578283	The function of APS in insulin signaling has heretofore remained unknown.
22	14578283	The blood glucose-lowering effect of insulin, as assessed by the intraperitoneal insulin tolerance test, was increased in APS(-/-) mice.
23	14578283	Plasma insulin levels during fasting and in the intraperitoneal glucose tolerance test were lower in APS(-/-) mice.
24	14578283	However, overexpression of wild-type or dominant-negative APS in 3T3L1 adipocytes did not affect insulin receptor numbers, phosphorylations of insulin receptor, insulin receptor substrate-1, or Akt and mitogen-activated protein kinase.
25	14578283	The glucose uptake and GLUT4 translocation were not affected by insulin stimulation in these cells.
26	14578283	Nevertheless, the insulin-stimulated glucose transport in isolated adipocytes of APS(-/-) mice was increased over that of APS(+/+) mice.
27	14578283	APS(-/-) mice also showed increased serum levels of leptin and adiponectin, which might explain the increased insulin sensitivity of adipocytes.
28	14578283	Increased insulin sensitivity and hypoinsulinemia in APS knockout mice.
29	14578283	A tyrosine kinase adaptor protein containing pleckstrin homology and SH2 domains (APS) is rapidly and strongly tyrosine phosphorylated by insulin receptor kinase upon insulin stimulation.
30	14578283	The function of APS in insulin signaling has heretofore remained unknown.
31	14578283	The blood glucose-lowering effect of insulin, as assessed by the intraperitoneal insulin tolerance test, was increased in APS(-/-) mice.
32	14578283	Plasma insulin levels during fasting and in the intraperitoneal glucose tolerance test were lower in APS(-/-) mice.
33	14578283	However, overexpression of wild-type or dominant-negative APS in 3T3L1 adipocytes did not affect insulin receptor numbers, phosphorylations of insulin receptor, insulin receptor substrate-1, or Akt and mitogen-activated protein kinase.
34	14578283	The glucose uptake and GLUT4 translocation were not affected by insulin stimulation in these cells.
35	14578283	Nevertheless, the insulin-stimulated glucose transport in isolated adipocytes of APS(-/-) mice was increased over that of APS(+/+) mice.
36	14578283	APS(-/-) mice also showed increased serum levels of leptin and adiponectin, which might explain the increased insulin sensitivity of adipocytes.
37	14578283	Increased insulin sensitivity and hypoinsulinemia in APS knockout mice.
38	14578283	A tyrosine kinase adaptor protein containing pleckstrin homology and SH2 domains (APS) is rapidly and strongly tyrosine phosphorylated by insulin receptor kinase upon insulin stimulation.
39	14578283	The function of APS in insulin signaling has heretofore remained unknown.
40	14578283	The blood glucose-lowering effect of insulin, as assessed by the intraperitoneal insulin tolerance test, was increased in APS(-/-) mice.
41	14578283	Plasma insulin levels during fasting and in the intraperitoneal glucose tolerance test were lower in APS(-/-) mice.
42	14578283	However, overexpression of wild-type or dominant-negative APS in 3T3L1 adipocytes did not affect insulin receptor numbers, phosphorylations of insulin receptor, insulin receptor substrate-1, or Akt and mitogen-activated protein kinase.
43	14578283	The glucose uptake and GLUT4 translocation were not affected by insulin stimulation in these cells.
44	14578283	Nevertheless, the insulin-stimulated glucose transport in isolated adipocytes of APS(-/-) mice was increased over that of APS(+/+) mice.
45	14578283	APS(-/-) mice also showed increased serum levels of leptin and adiponectin, which might explain the increased insulin sensitivity of adipocytes.
46	14578283	Increased insulin sensitivity and hypoinsulinemia in APS knockout mice.
47	14578283	A tyrosine kinase adaptor protein containing pleckstrin homology and SH2 domains (APS) is rapidly and strongly tyrosine phosphorylated by insulin receptor kinase upon insulin stimulation.
48	14578283	The function of APS in insulin signaling has heretofore remained unknown.
49	14578283	The blood glucose-lowering effect of insulin, as assessed by the intraperitoneal insulin tolerance test, was increased in APS(-/-) mice.
50	14578283	Plasma insulin levels during fasting and in the intraperitoneal glucose tolerance test were lower in APS(-/-) mice.
51	14578283	However, overexpression of wild-type or dominant-negative APS in 3T3L1 adipocytes did not affect insulin receptor numbers, phosphorylations of insulin receptor, insulin receptor substrate-1, or Akt and mitogen-activated protein kinase.
52	14578283	The glucose uptake and GLUT4 translocation were not affected by insulin stimulation in these cells.
53	14578283	Nevertheless, the insulin-stimulated glucose transport in isolated adipocytes of APS(-/-) mice was increased over that of APS(+/+) mice.
54	14578283	APS(-/-) mice also showed increased serum levels of leptin and adiponectin, which might explain the increased insulin sensitivity of adipocytes.
55	14578283	Increased insulin sensitivity and hypoinsulinemia in APS knockout mice.
56	14578283	A tyrosine kinase adaptor protein containing pleckstrin homology and SH2 domains (APS) is rapidly and strongly tyrosine phosphorylated by insulin receptor kinase upon insulin stimulation.
57	14578283	The function of APS in insulin signaling has heretofore remained unknown.
58	14578283	The blood glucose-lowering effect of insulin, as assessed by the intraperitoneal insulin tolerance test, was increased in APS(-/-) mice.
59	14578283	Plasma insulin levels during fasting and in the intraperitoneal glucose tolerance test were lower in APS(-/-) mice.
60	14578283	However, overexpression of wild-type or dominant-negative APS in 3T3L1 adipocytes did not affect insulin receptor numbers, phosphorylations of insulin receptor, insulin receptor substrate-1, or Akt and mitogen-activated protein kinase.
61	14578283	The glucose uptake and GLUT4 translocation were not affected by insulin stimulation in these cells.
62	14578283	Nevertheless, the insulin-stimulated glucose transport in isolated adipocytes of APS(-/-) mice was increased over that of APS(+/+) mice.
63	14578283	APS(-/-) mice also showed increased serum levels of leptin and adiponectin, which might explain the increased insulin sensitivity of adipocytes.
64	14578283	Increased insulin sensitivity and hypoinsulinemia in APS knockout mice.
65	14578283	A tyrosine kinase adaptor protein containing pleckstrin homology and SH2 domains (APS) is rapidly and strongly tyrosine phosphorylated by insulin receptor kinase upon insulin stimulation.
66	14578283	The function of APS in insulin signaling has heretofore remained unknown.
67	14578283	The blood glucose-lowering effect of insulin, as assessed by the intraperitoneal insulin tolerance test, was increased in APS(-/-) mice.
68	14578283	Plasma insulin levels during fasting and in the intraperitoneal glucose tolerance test were lower in APS(-/-) mice.
69	14578283	However, overexpression of wild-type or dominant-negative APS in 3T3L1 adipocytes did not affect insulin receptor numbers, phosphorylations of insulin receptor, insulin receptor substrate-1, or Akt and mitogen-activated protein kinase.
70	14578283	The glucose uptake and GLUT4 translocation were not affected by insulin stimulation in these cells.
71	14578283	Nevertheless, the insulin-stimulated glucose transport in isolated adipocytes of APS(-/-) mice was increased over that of APS(+/+) mice.
72	14578283	APS(-/-) mice also showed increased serum levels of leptin and adiponectin, which might explain the increased insulin sensitivity of adipocytes.
73	16803868	Enigma interacts with adaptor protein with PH and SH2 domains to control insulin-induced actin cytoskeleton remodeling and glucose transporter 4 translocation.
74	16803868	APS (adaptor protein with PH and SH2 domains) initiates a phosphatidylinositol 3-kinase-independent pathway involved in insulin-stimulated glucose transport.
75	16803868	We recently identified Enigma, a PDZ and LIM domain-containing protein, as a partner of APS and showed that APS-Enigma complex plays a critical role in actin cytoskeleton organization in fibroblastic cells.
76	16803868	Because actin rearrangement is important for insulin-induced glucose transporter 4 (Glut 4) translocation, we studied the potential involvement of Enigma in insulin-induced glucose transport in 3T3-L1 adipocytes.
77	16803868	Expression of an APS mutant unable to bind Enigma increased the insulin-induced Glut 4 translocation to the plasma membrane.
78	16803868	Using time-lapse fluorescent microscopy of green fluorescent protein-actin, we demonstrated that the overexpression of Enigma altered insulin-induced actin rearrangements, whereas the expression of Enigma without its LIM domains was without effect.
79	16803868	Taken together, these data strongly suggest that the interaction between APS and Enigma is involved in insulin-induced Glut 4 translocation by regulating cortical actin remodeling and raise the possibility that modification of APS/Enigma ratio could participate in the alteration of insulin-induced glucose uptake in adipose tissue.
80	16803868	Enigma interacts with adaptor protein with PH and SH2 domains to control insulin-induced actin cytoskeleton remodeling and glucose transporter 4 translocation.
81	16803868	APS (adaptor protein with PH and SH2 domains) initiates a phosphatidylinositol 3-kinase-independent pathway involved in insulin-stimulated glucose transport.
82	16803868	We recently identified Enigma, a PDZ and LIM domain-containing protein, as a partner of APS and showed that APS-Enigma complex plays a critical role in actin cytoskeleton organization in fibroblastic cells.
83	16803868	Because actin rearrangement is important for insulin-induced glucose transporter 4 (Glut 4) translocation, we studied the potential involvement of Enigma in insulin-induced glucose transport in 3T3-L1 adipocytes.
84	16803868	Expression of an APS mutant unable to bind Enigma increased the insulin-induced Glut 4 translocation to the plasma membrane.
85	16803868	Using time-lapse fluorescent microscopy of green fluorescent protein-actin, we demonstrated that the overexpression of Enigma altered insulin-induced actin rearrangements, whereas the expression of Enigma without its LIM domains was without effect.
86	16803868	Taken together, these data strongly suggest that the interaction between APS and Enigma is involved in insulin-induced Glut 4 translocation by regulating cortical actin remodeling and raise the possibility that modification of APS/Enigma ratio could participate in the alteration of insulin-induced glucose uptake in adipose tissue.
87	16803868	Enigma interacts with adaptor protein with PH and SH2 domains to control insulin-induced actin cytoskeleton remodeling and glucose transporter 4 translocation.
88	16803868	APS (adaptor protein with PH and SH2 domains) initiates a phosphatidylinositol 3-kinase-independent pathway involved in insulin-stimulated glucose transport.
89	16803868	We recently identified Enigma, a PDZ and LIM domain-containing protein, as a partner of APS and showed that APS-Enigma complex plays a critical role in actin cytoskeleton organization in fibroblastic cells.
90	16803868	Because actin rearrangement is important for insulin-induced glucose transporter 4 (Glut 4) translocation, we studied the potential involvement of Enigma in insulin-induced glucose transport in 3T3-L1 adipocytes.
91	16803868	Expression of an APS mutant unable to bind Enigma increased the insulin-induced Glut 4 translocation to the plasma membrane.
92	16803868	Using time-lapse fluorescent microscopy of green fluorescent protein-actin, we demonstrated that the overexpression of Enigma altered insulin-induced actin rearrangements, whereas the expression of Enigma without its LIM domains was without effect.
93	16803868	Taken together, these data strongly suggest that the interaction between APS and Enigma is involved in insulin-induced Glut 4 translocation by regulating cortical actin remodeling and raise the possibility that modification of APS/Enigma ratio could participate in the alteration of insulin-induced glucose uptake in adipose tissue.
94	16803868	Enigma interacts with adaptor protein with PH and SH2 domains to control insulin-induced actin cytoskeleton remodeling and glucose transporter 4 translocation.
95	16803868	APS (adaptor protein with PH and SH2 domains) initiates a phosphatidylinositol 3-kinase-independent pathway involved in insulin-stimulated glucose transport.
96	16803868	We recently identified Enigma, a PDZ and LIM domain-containing protein, as a partner of APS and showed that APS-Enigma complex plays a critical role in actin cytoskeleton organization in fibroblastic cells.
97	16803868	Because actin rearrangement is important for insulin-induced glucose transporter 4 (Glut 4) translocation, we studied the potential involvement of Enigma in insulin-induced glucose transport in 3T3-L1 adipocytes.
98	16803868	Expression of an APS mutant unable to bind Enigma increased the insulin-induced Glut 4 translocation to the plasma membrane.
99	16803868	Using time-lapse fluorescent microscopy of green fluorescent protein-actin, we demonstrated that the overexpression of Enigma altered insulin-induced actin rearrangements, whereas the expression of Enigma without its LIM domains was without effect.
100	16803868	Taken together, these data strongly suggest that the interaction between APS and Enigma is involved in insulin-induced Glut 4 translocation by regulating cortical actin remodeling and raise the possibility that modification of APS/Enigma ratio could participate in the alteration of insulin-induced glucose uptake in adipose tissue.
101	19122374	Sh2b3/Lnk consisting of an N-terminal proline-rich region, PH-, SH2-domains and a tyrosine phosphorylation site, forms an intracellular adaptor protein family conserved from drosophila to mammals, together with Sh2b1/SH2-B and Sh2b2/APS (adaptor protein with PH and SH2 domains).