Ignet

Gene Information

Gene symbol: SNW1

Gene name: SNW domain containing 1

HGNC ID: 16696

Synonyms: NCoA-62, SKIP, Prp45, PRPF45, Bx42

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	INPP5D	1 hits
3	INPP5E	1 hits
4	INPPL1	1 hits
5	INS	1 hits
6	IRF6	1 hits
7	PIB5PA	1 hits
8	PIK3CA	1 hits
9	PTEN	1 hits
10	SRC	1 hits
11	SYNJ1	1 hits

Related Sentences

#	PMID	Sentence
1	16842857	Lipid phosphatases, src homology 2 domain containing inositol 5'-phosphatase 2 (SHIP2) and skeletal muscle and kidney-enriched inositol phosphatase (SKIP) hydrolyze PI(3,4,5)P(3) to PI(3,4)P(2) and phosphatase and tensin homolog deleted on chromosome ten (PTEN) hydrolyzes PI(3,4,5)P(3) to PI(4,5)P(2).
2	16842857	SHIP2 negatively regulates insulin signaling relatively specifically via its 5'-phosphatase activity.
3	16842857	Targeted disruption of the SHIP2 gene in mice resulted in increased insulin sensitivity and conferred protection from obesity induced by a high-fat diet.
4	16842857	Polymorphisms in the human SHIP2 gene are associated, at least in part, with the insulin resistance of type 2 diabetes.
5	16842857	Importantly, inhibition of endogenous SHIP2 through the liver-specific expression of a dominant-negative SHIP2 improves glucose metabolism and insulin resistance in diabetic db/db mice.
6	16842857	Overexpression of PTEN and SKIP also inhibited insulin-induced phosphorylation of Akt and the uptake of glucose in cultured cells.
7	16842857	Taken together, inhibition of endogenous SHIP2 in the whole body appears to be effective at improving the insulin resistance associated with type 2 diabetes and/or obesity.
8	16842857	Inhibition of PTEN in the tissues specifically targeted, including skeletal muscle and fat, may result in an amelioration of insulin resistance in type 2 diabetes, although caution against the formation of tumors is needed.
9	16842857	Lipid phosphatases, src homology 2 domain containing inositol 5'-phosphatase 2 (SHIP2) and skeletal muscle and kidney-enriched inositol phosphatase (SKIP) hydrolyze PI(3,4,5)P(3) to PI(3,4)P(2) and phosphatase and tensin homolog deleted on chromosome ten (PTEN) hydrolyzes PI(3,4,5)P(3) to PI(4,5)P(2).
10	16842857	SHIP2 negatively regulates insulin signaling relatively specifically via its 5'-phosphatase activity.
11	16842857	Targeted disruption of the SHIP2 gene in mice resulted in increased insulin sensitivity and conferred protection from obesity induced by a high-fat diet.
12	16842857	Polymorphisms in the human SHIP2 gene are associated, at least in part, with the insulin resistance of type 2 diabetes.
13	16842857	Importantly, inhibition of endogenous SHIP2 through the liver-specific expression of a dominant-negative SHIP2 improves glucose metabolism and insulin resistance in diabetic db/db mice.
14	16842857	Overexpression of PTEN and SKIP also inhibited insulin-induced phosphorylation of Akt and the uptake of glucose in cultured cells.
15	16842857	Taken together, inhibition of endogenous SHIP2 in the whole body appears to be effective at improving the insulin resistance associated with type 2 diabetes and/or obesity.
16	16842857	Inhibition of PTEN in the tissues specifically targeted, including skeletal muscle and fat, may result in an amelioration of insulin resistance in type 2 diabetes, although caution against the formation of tumors is needed.
17	18573875	Increased insulin action in SKIP heterozygous knockout mice.
18	18573875	Previous studies showed that SKIP negatively regulates insulin-induced phosphatidylinositol 3-kinase signaling (Ijuin and Takenawa, Mol.
19	18573875	We now have generated mice with a targeted mutation of the mouse ortholog of the human SKIP gene, Pps.
20	18573875	Adult heterozygous Pps mutant mice show increased insulin sensitivity and reduced diet-induced obesity with increased Akt/protein kinase B (PKB) phosphorylation in skeletal muscle but not in adipose tissue.
21	18573875	The insulin-induced uptake of 2-deoxyglucose into the isolated soleus muscle was significantly enhanced in Pps mutant mice.
22	18573875	Furthermore, in vitro knockdown studies in L6 myoblast cells revealed that reduction of SKIP expression level increased insulin-stimulated Akt/PKB phosphorylation and 2-deoxyglucose uptake.
23	18573875	These results imply that SKIP regulates insulin signaling in skeletal muscle.
24	18573875	Thus, SKIP may be a promising pharmacologic target for the treatment of insulin resistance and diabetes.
25	18573875	Increased insulin action in SKIP heterozygous knockout mice.
26	18573875	Previous studies showed that SKIP negatively regulates insulin-induced phosphatidylinositol 3-kinase signaling (Ijuin and Takenawa, Mol.
27	18573875	We now have generated mice with a targeted mutation of the mouse ortholog of the human SKIP gene, Pps.
28	18573875	Adult heterozygous Pps mutant mice show increased insulin sensitivity and reduced diet-induced obesity with increased Akt/protein kinase B (PKB) phosphorylation in skeletal muscle but not in adipose tissue.
29	18573875	The insulin-induced uptake of 2-deoxyglucose into the isolated soleus muscle was significantly enhanced in Pps mutant mice.
30	18573875	Furthermore, in vitro knockdown studies in L6 myoblast cells revealed that reduction of SKIP expression level increased insulin-stimulated Akt/PKB phosphorylation and 2-deoxyglucose uptake.
31	18573875	These results imply that SKIP regulates insulin signaling in skeletal muscle.
32	18573875	Thus, SKIP may be a promising pharmacologic target for the treatment of insulin resistance and diabetes.
33	18573875	Increased insulin action in SKIP heterozygous knockout mice.
34	18573875	Previous studies showed that SKIP negatively regulates insulin-induced phosphatidylinositol 3-kinase signaling (Ijuin and Takenawa, Mol.
35	18573875	We now have generated mice with a targeted mutation of the mouse ortholog of the human SKIP gene, Pps.
36	18573875	Adult heterozygous Pps mutant mice show increased insulin sensitivity and reduced diet-induced obesity with increased Akt/protein kinase B (PKB) phosphorylation in skeletal muscle but not in adipose tissue.
37	18573875	The insulin-induced uptake of 2-deoxyglucose into the isolated soleus muscle was significantly enhanced in Pps mutant mice.
38	18573875	Furthermore, in vitro knockdown studies in L6 myoblast cells revealed that reduction of SKIP expression level increased insulin-stimulated Akt/PKB phosphorylation and 2-deoxyglucose uptake.
39	18573875	These results imply that SKIP regulates insulin signaling in skeletal muscle.
40	18573875	Thus, SKIP may be a promising pharmacologic target for the treatment of insulin resistance and diabetes.
41	18573875	Increased insulin action in SKIP heterozygous knockout mice.
42	18573875	Previous studies showed that SKIP negatively regulates insulin-induced phosphatidylinositol 3-kinase signaling (Ijuin and Takenawa, Mol.
43	18573875	We now have generated mice with a targeted mutation of the mouse ortholog of the human SKIP gene, Pps.
44	18573875	Adult heterozygous Pps mutant mice show increased insulin sensitivity and reduced diet-induced obesity with increased Akt/protein kinase B (PKB) phosphorylation in skeletal muscle but not in adipose tissue.
45	18573875	The insulin-induced uptake of 2-deoxyglucose into the isolated soleus muscle was significantly enhanced in Pps mutant mice.
46	18573875	Furthermore, in vitro knockdown studies in L6 myoblast cells revealed that reduction of SKIP expression level increased insulin-stimulated Akt/PKB phosphorylation and 2-deoxyglucose uptake.
47	18573875	These results imply that SKIP regulates insulin signaling in skeletal muscle.
48	18573875	Thus, SKIP may be a promising pharmacologic target for the treatment of insulin resistance and diabetes.
49	18573875	Increased insulin action in SKIP heterozygous knockout mice.
50	18573875	Previous studies showed that SKIP negatively regulates insulin-induced phosphatidylinositol 3-kinase signaling (Ijuin and Takenawa, Mol.
51	18573875	We now have generated mice with a targeted mutation of the mouse ortholog of the human SKIP gene, Pps.
52	18573875	Adult heterozygous Pps mutant mice show increased insulin sensitivity and reduced diet-induced obesity with increased Akt/protein kinase B (PKB) phosphorylation in skeletal muscle but not in adipose tissue.
53	18573875	The insulin-induced uptake of 2-deoxyglucose into the isolated soleus muscle was significantly enhanced in Pps mutant mice.
54	18573875	Furthermore, in vitro knockdown studies in L6 myoblast cells revealed that reduction of SKIP expression level increased insulin-stimulated Akt/PKB phosphorylation and 2-deoxyglucose uptake.
55	18573875	These results imply that SKIP regulates insulin signaling in skeletal muscle.
56	18573875	Thus, SKIP may be a promising pharmacologic target for the treatment of insulin resistance and diabetes.
57	18573875	Increased insulin action in SKIP heterozygous knockout mice.
58	18573875	Previous studies showed that SKIP negatively regulates insulin-induced phosphatidylinositol 3-kinase signaling (Ijuin and Takenawa, Mol.
59	18573875	We now have generated mice with a targeted mutation of the mouse ortholog of the human SKIP gene, Pps.
60	18573875	Adult heterozygous Pps mutant mice show increased insulin sensitivity and reduced diet-induced obesity with increased Akt/protein kinase B (PKB) phosphorylation in skeletal muscle but not in adipose tissue.
61	18573875	The insulin-induced uptake of 2-deoxyglucose into the isolated soleus muscle was significantly enhanced in Pps mutant mice.
62	18573875	Furthermore, in vitro knockdown studies in L6 myoblast cells revealed that reduction of SKIP expression level increased insulin-stimulated Akt/PKB phosphorylation and 2-deoxyglucose uptake.
63	18573875	These results imply that SKIP regulates insulin signaling in skeletal muscle.
64	18573875	Thus, SKIP may be a promising pharmacologic target for the treatment of insulin resistance and diabetes.
65	19272022	Growth factor or insulin stimulation induces a canonical cascade resulting in the transient phosphorylation of PtdIns(4,5)P(2) by PI3K (phosphoinositide 3-kinase) to form PtdIns(3,4,5)P(3), which is rapidly dephosphorylated either by PTEN (phosphatase and tensin homologue deleted on chromosome 10) back to PtdIns(4,5)P(2), or by the 5-ptases (inositol polyphosphate 5-phosphatases), generating PtdIns(3,4)P(2).
66	19272022	Futhermore, the 5-ptases SHIP [SH2 (Src homology 2)-domain-containing inositol phosphatase] 2, SKIP (skeletal muscle- and kidney-enriched inositol phosphatase) and 72-5ptase (72 kDa 5-ptase)/Type IV/Inpp5e (inositol polyphosphate 5-phosphatase E) are implicated in negatively regulating insulin signalling and glucose homoeostasis in specific tissues.
67	19272022	SHIP2 polymorphisms are associated with a predisposition to insulin resistance.
68	19272022	In addition, 5-ptases such as SHIP1, SHIP2 and 72-5ptase/Type IV/Inpp5e regulate macrophage phagocytosis, and SHIP1 also controls haemopoietic cell proliferation.