Ignet

Gene Information

Gene symbol: PTEN

Gene name: phosphatase and tensin homolog

HGNC ID: 9588

Synonyms: MMAC1, TEP1, PTEN1

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	CTNNB1	1 hits
3	FASN	1 hits
4	FFAR3	1 hits
5	FOXO1	1 hits
6	IGF1	1 hits
7	IGF2	1 hits
8	INS	1 hits
9	IRS2	1 hits
10	JUN	1 hits
11	MAPK14	1 hits
12	MAPK8	1 hits
13	MIRN192	1 hits
14	MIRN21	1 hits
15	MIRN214	1 hits
16	NOS3	1 hits
17	PARK7	1 hits
18	PDPK1	1 hits
19	PIK3CA	1 hits
20	PPARG	1 hits
21	PPP2R4	1 hits
22	PRKAA1	1 hits
23	PRKCA	1 hits
24	SLC37A4	1 hits
25	SOD1	1 hits
26	SPARC	1 hits
27	SREBF1	1 hits
28	STK11	1 hits
29	TGFB1	1 hits
30	TNS1	1 hits
31	TRIB3	1 hits

Related Sentences

#	PMID	Sentence
1	11916922	PTEN (MMAC1) is a lipid/protein phosphatase that can negatively regulate the PI3K pathway by dephosphorylating phosphatidylinositol (3,4,5)-triphosphate, but it is unclear whether PTEN is physiologically relevant to insulin signaling in vivo.
2	11916922	Transfection of cells in culture with ASO targeting PTEN reduced PTEN mRNA and protein levels and increased insulin-stimulated Akt phosphorylation in alpha-mouse liver-12 (AML12) cells.
3	11916922	Inhibition of PTEN expression also dramatically reduced insulin concentrations in ob/ob mice, improved the performance of db/db mice during insulin tolerance tests, and increased Akt phosphorylation in liver in response to insulin.
4	11916922	These results suggest that PTEN plays a significant role in regulating glucose metabolism in vivo by negatively regulating insulin signaling.
5	15855265	In mice, a heterozygous deletion of the Pten gene is associated with increased activation of AKT and with development of pheochromocytomas.
6	16061670	Here we show for the first time in vivo that overexpression of PTEN in the Wnt-1 transgenic mice resulted in a marked decrease in the insulin-like growth factor (IGF)-I receptor levels leading to a reduced IGF-I-mediated mitogenesis.
7	16061670	Moreover, the percentage of BrdUrd-positive epithelial nuclei was decreased by 48%. beta-Catenin immunoreactivity was significantly decreased and the percentage of signal transducer and activator of transcription 5a (stat5a)-positive mammary epithelial cells was increased by 2-fold in Wnt-1 mice overexpressing PTEN.
8	16061670	The present study shows that PTEN can partially inhibit the Wnt-1-induced mammary tumorigenesis in early neoplastic stages by blocking the AKT pathway and by reducing the IGF-I receptor levels in mammary gland.
9	16170201	Pten insufficiency increased peripheral insulin sensitivity in wild type and Irs2(-/-) mice and increased Akt and Foxo1 phosphorylation in the islets.
10	16170201	Compared with Irs2(-/-) mice, the Irs2(-/-)::Pten(+/-) mice displayed nearly normal glucose tolerance and survived without diabetes, because normal but small islets produced sufficient insulin until the mice died of lymphoproliferative disease at 12 months age.
11	16873694	We further found that activated stress signaling p38, but not Jun NH(2)-terminal kinase, was involved in PTEN upregulation.
12	16873694	The p38 target transcriptional factor activating transcription factor (ATF)-2 bound to the PTEN promoter, which was increased by palmitic acid treatment.
13	16873694	Palmitic acid inhibits insulin signaling by promoting PTEN activity and its transcription through p38 and its downstream transcription factor ATF-2.
14	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.
15	17218436	In addition, the expression of the protein tribbles-3 and the phosphatase enzyme activity of phosphatase and tensin homolog deleted on chromosome 10 (PTEN), which prevent Akt activation, were increased in muscle from EtOH-exposed rats.
16	17337625	Here we show by using two synthetic PPARgamma agonists (rosiglitazone and KR-62776, a novel PPARgamma agonist) that phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a key downstream mediator of PPARgamma signaling.
17	17337625	The effects of PPARgamma agonists on PTEN expression and glucose uptake disappeared by pretreatment with a PPARgamma antagonist or by knockdown of PPARgamma expression.
18	17623817	In cultured C2C12 myotubes, acute suppression of PI3K activity led to decreased PTEN expression, while palmitic acid increased PTEN in myotubes in a p38-dependent fashion.
19	17875968	Exposure of cultured human umbilical vein endothelial cells to either peroxynitrite (ONOO-) or high glucose significantly inhibited both basal and insulin-stimulated Akt phosphorylation at Ser473 and Akt activity in parallel with increased apoptosis, phosphorylation, and activity of phosphatase and tensin homologue deleted on chromosome 10 (PTEN).
20	17875968	Furthermore, protein kinase B/Akt inhibition induced by ONOO- or high glucose and apoptosis triggered by high glucose could be abolished by transfection of PTEN-specific small interfering RNA, suggesting that PTEN mediated the Akt inhibition by ONOO-.
21	17875968	Consistently, LKB1 phosphorylated PTEN at Ser380/Thr382/383 in vitro, suggesting that LKB1 might act as an upstream kinase for PTEN.
22	17875968	Furthermore, administration of PTEN-specific small interfering RNA suppressed diabetes-enhanced apoptosis and Akt inhibition.
23	17875968	Finally, treatment with Tempol, a superoxide dismutase mimetic, and insulin, both of which reduced the ONOO- formation, markedly reduced diabetes-enhanced LKB1-Ser428 phosphorylation, PTEN, and apoptosis in the endothelium of mouse aortas.
24	17875968	We conclude that hyperglycemia triggers apoptosis by inhibiting Akt signaling via ONOO(-)-mediated LKB1-dependent PTEN activation.
25	18387000	In the present study, we investigated the importance of the LKB1-AMPK pathway in regulating tumorigenesis in mice resulting from deficiency of the PTEN (phosphatase and tensin homologue deleted on chromosome 10) tumour suppressor, which drives cell growth through overactivation of the Akt and mTOR (mammalian target of rapamycin) kinases.
26	18387000	We demonstrate that inhibition of AMPK resulting from a hypomorphic mutation that decreases LKB1 expression does not lead to tumorigenesis on its own, but markedly accelerates tumour development in PTEN(+/-) mice.
27	18387000	We demonstrate that LKB1 is required for activators of AMPK to inhibit mTORC1 signalling as well as cell growth in PTEN-deficient cells.
28	19543271	Here we show that TGF-beta activates Akt in glomerular mesangial cells by inducing the microRNAs (miRNAs) miR-216a and miR-217, both of which target PTEN (phosphatase and tensin homologue), an inhibitor of Akt activation.
29	19543271	These studies reveal a mechanism of Akt activation through PTEN downregulation by two miRs, which are regulated by upstream miR-192 and TGF-beta.
30	19879746	Moreover, folic acid caused a reduction in PTEN (phosphatase and tensin homolog deleted on chromosome 10) expression, an increase in the phosphorylation of endothelial nitric oxide synthase (eNOS(Ser1177)) and Akt(Ser473), and an enhanced interaction of heat shock protein 90 (HSP90) with eNOS in both strains, with greater magnitude observed in +db/+db mice.
31	19879746	The mechanism may be, at least partly, attributed to enhancement of PI3K/HSP90/eNOS/Akt cascade, reduction in plasma resistin level, down-regulation of PTEN and slight modification of oxidative state.
32	20872961	The phosphoinositide 3-kinase (PI3K)/phosphatase and tensin homolog (PTEN)/Akt axis is a key signal transduction node that regulates crucial cellular functions, including insulin and other growth factors signaling, lipid and glucose metabolism, as well as cell survival and apoptosis.
33	20872961	In this pathway, PTEN acts as a phosphoinositide phosphatase, which terminates PI3K-propagated signaling by dephosphorylating PtdIns(3,4)P(2) and PtdIns(3,4,5)P(3).
34	20929508	The results suggest the following molecular etiopathophysiology of DN: (i) hyperglycemia upregulates IGF2, which initiates PTEN, a regulator of IGF2 signaling; (ii) loss of this IGF2-PTEN feedback loop causes changes that are characteristic of DN; and (iii) lowered expression of the repair modulator SPARC results in the development and/or progression of DN.
35	20852026	Under basal conditions, enhanced insulin-PI3K signaling via deletion of phosphatase with tensin homology (PTEN), a negative regulator of this pathway, leads to increased ?-cell mass and function.
36	21136963	Of interest, the increase in protein kinase C signaling responses with phorbol esters was associated with activation of the lipid phosphatase PTEN and a 27?kDa HSP.
37	21073655	Furthermore, high glucose concentrations led to apoptosis of ?-cells by activation of p38MAPK and p53, and dysfunction of ?-cells through phosphatase and tensih homolog (PTEN)-dependent Jun N-terminal kinase (JNK) activation and protein kinase B (AKT/PKB) inhibition, which induced the translocation of forkhead box O1 and pancreatic duodenal homeobox-1, followed by reduced insulin expression and secretion.
38	21073655	In conclusion, NOX2-derived ROS could play a critical role in high glucose-induced ?-cell dysfunction through PTEN-dependent JNK activation and AKT inhibition.
39	17130482	We report here a stable isotope flux phenotyping study of this "silent" phenotype, in which tissue-specific insulin effects in whole-body Pten(+/-)-deficient mice were dissected in vivo.
40	17130482	Glucose-6-phosphatase expression was the same for Pten(+/-) and Pten(+/+) mice in the fasted state, and its expression for Pten(+/-) was 25% of Pten(+/+) in the fed state.
41	21205932	Additionally, PKC activation did not impair phosphatidylinositol 3-kinase activity, phosphoinositide-dependent kinase phosphorylation, lipid phosphatase (PTEN), or protein phosphatase 2A activities.
42	21228352	Luciferase reporter assay showed that miR-214 specifically binds to the phosphatase and tensin homolog (PTEN) mRNA 3'-untranslated region, implicating PTEN as a target gene of miR-214.
43	21228352	Overexpression of pre-miR-214 led to impaired PTEN expression and delayed apoptosis of THP-1 cells, whereas knockdown of miR-214 level largely abolished AGE-induced cell survival.
44	21426932	Interestingly, DJ-1 was associated with PTEN and this interaction was significantly increased in response to high glucose.
45	21320485	Decreased PTEN and increased phospho-Akt were found in kidney of diabetic rats, and in vitro research revealed that high glucose attenuated PTEN expression in a time-dependent manner, concomitant with activation of Akt.
46	21320485	Again, expression of PTEN significantly inhibited high glucose-caused increased phospho-Akt and lipogenic genes including SREBP-1, fatty acid synthase (FASN) and acetyl-CoA carboxylase (ACC).
47	21613227	Renal cortices from OVE26 type 1 diabetic mice showed significantly elevated levels of miR-21 associated with reduced PTEN and increased fibronectin content.
48	21613227	Overexpression of miR-21 mimicked the action of high glucose, which included a reduction in PTEN expression and a concomitant increase in Akt phosphorylation.
49	21568903	PDK1 has an essential role in regulating cell migration especially in the context of PTEN deficiency.
50	21960994	Expression of insulin-signaling molecules Akt, PTEN, GSK3?, and eNOS receptors for short-chain fatty acids GPR41, and GPR43 as well as protein phosphatase PP2AA, PP2AB, PP2C were evaluated using Western blot analysis.
51	19365404	PTEN, a negative regulator of the phosphatidylinositol-3-kinase/AKT pathway, is an important modulator of insulin signaling.
52	19365404	We found that Pten loss in the pancreas causes the elevation of AKT signaling in the liver.
53	19365404	The phosphorylation of AKT and its downstream substrate GSK3beta was increased in the liver of PPKO mice, while PTEN level was decreased without detectable excision of Pten allele in the liver of PPKO mice.