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phosphorylated-Pten promotes the proliferation and differentiation of hematopoietic stem cells.
Results indicate miR (zeige MLXIP Antikörper)-130a as an oncogenic miRNA that targets PTEN to drive malignant cell survival and tumor growth.
PTEN loss and activation of K-RAS (zeige HRAS Antikörper) and beta-catenin (zeige CTNNB1 Antikörper) cooperate to accelerate prostate tumourigenesis.
Data show that PTEN plays a key role in Th17 cell differentiation by blocking IL-2 (zeige IL2 Antikörper) expression.
Collectively, these findings provide a mechanistic account of how Rac1-dependent membrane raft localization regulates differential activation of distinct phosphoinositide 3-kinase isoforms and offer insight into why PTEN-deficient cancers depend on p110beta.
SHP2 (zeige PTPN11 Antikörper) and PTEN deficiencies were detected in liver cancer patients with poor prognosis. These data depict a mechanism of hepato-oncogenesis and suggest a potential therapeutic strategy.
Mechanistically, ligation of alpha8beta1 by the milk protein Mfge8 (zeige MFGE8 Antikörper) reduces antral smooth muscle contractile force by preventing RhoA (zeige RHOA Antikörper) activation through a PTEN-dependent mechanism.
We have found a prospective targeted therapy for PTEN-deficient tumors, with efficacy in vitro and in vivo in tumors derived from different tissues. This is based upon the changes in glutamine (zeige GFPT1 Antikörper) metabolism, DNA replication, and DNA damage response which are consequences of inactivation of PTEN.
Suggest a role for PI(3,4)P2 in the phenotype caused by loss-of-function mutations or deletions in PTEN in breast/prostate tumor cells.
embryonic myogenic progenitors lacking the phosphatase and tensin homolog (Pten) exhibit enhanced proliferation and differentiation, resulting in muscle hypertrophy.
PTEN loss has a negative prognostic impact in both adult and paediatric patients. The negative clinical outcome of PTEN loss is, however, limited to cases harbouring large genomic deletions, indicating that a detailed analysis of the type of abnormality is indispensable to refine risk stratification and treatment.
Low PTEN expression is associated with esophageal carcinoma.
Bmi-1 (zeige BMI1 Antikörper) binds to PTEN promoter and directly inhibits PTEN and thereafter activates AKT (zeige AKT1 Antikörper)
showed that PTEN induced miR (zeige MLXIP Antikörper)-26b expression by regulating the differential expression of Ikaros (zeige IKZF1 Antikörper) isoforms that are transcriptional regulators of miR (zeige MLXIP Antikörper)-26b
This study reveals the presence of a PTEN Alu insertion hotspot involved in Cowden syndrome, and suggests that undetected PTEN pathogenic variants could contribute to CS.
might induce cell invasion and migration via regulating AKT (zeige AKT1 Antikörper)/GSK-3beta (zeige GSK3b Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) signaling pathway, playing a vital role in the progression of gastric cancer
We show that elevated levels of PPARG (zeige PPARG Antikörper) strongly correlate with elevation of FASN (zeige FASN Antikörper) in human prostate cancer (CaP) and that high levels of PPARG (zeige PPARG Antikörper)/FASN (zeige FASN Antikörper) and PI3K (zeige PIK3CA Antikörper)/pAKT (zeige AKT1 Antikörper) pathway activation confer a poor prognosis.These data suggest that CaP patients could be stratified in terms of PPARG (zeige PPARG Antikörper)/FASN (zeige FASN Antikörper) and PTEN levels to identify patients with aggressive CaP who may respond favorably to PPARG (zeige PPARG Antikörper)/FASN (zeige FASN Antikörper) inhibition.
Deregulated expression of miR (zeige MLXIP Antikörper)-107 inhibits metastasis of pancreatic ductal adenocarcinoma through inhibition PI3K (zeige PIK3CA Antikörper)/Akt (zeige AKT1 Antikörper) signaling via caveolin-1 (zeige CAV1 Antikörper) and PTEN.
PTEN/Akt (zeige AKT1 Antikörper) signaling pathway contributes to cardiomyocyte apoptosis after coronary microembolization.
PTEN, FOXO3A (zeige FOXO3 Antikörper) and PKB (zeige AKT1 Antikörper) were expressed in a stage- and cell-specific manner during ovarian follicle formation and development in the fetal and neonatal pig.
the miR-17-92 cluster is involved in granulosa cell proliferation and differentiation by coordinately targeting the PTEN and BMPR2 (zeige BMPR2 Antikörper) genes.
miR (zeige MYLIP Antikörper)-26b participates in the inflammatory response of LPS (zeige IRF6 Antikörper)-stimulated bAMs by modulating the NF-kappaB (zeige NFKB1 Antikörper) pathway through targeting PTEN.
Pten expression levels in the mammary glands of dairy cows, was investigated.
These studies identify a key role for PTEN in the modulation of lipid mediators involved in adenosine diphosphate receptor-regulated endothelial signaling pathways involving eNOS (zeige NOS3 Antikörper) activation in vascular endothelial cells.
Overexpressing PTEN enhanced fatty acid oxidation and assembly and secretion of VLDL in cultured hepatocytes.
Inhibition of PTEN activity had no effect on cyclic strain-mediated cell proliferation but inhibited cyclic strain-mediated suppression of apoptosis
PTEN plays an important role in multicilia formation and cilia disassembly by controlling the phosphorylation of Dishevelled (zeige DVL2 Antikörper).
PTEN negatively regulates growth cone phosphatidylinositol 3,4,5-trisphosphate levels and mediates chemorepulsion, whereas chemoattraction is PTEN-independent.
PTEN-dependent slowing of axonal growth enables the establishment of stable nerve-muscle contacts that develop into neuromuscular junctions.
This gene was identified as a tumor suppressor that is mutated in a large number of cancers at high frequency. The protein encoded this gene is a phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase. It contains a tensin like domain as well as a catalytic domain similar to that of the dual specificity protein tyrosine phosphatases. Unlike most of the protein tyrosine phosphatases, this protein preferentially dephosphorylates phosphoinositide substrates. It negatively regulates intracellular levels of phosphatidylinositol-3,4,5-trisphosphate in cells and functions as a tumor suppressor by negatively regulating AKT\\/PKB signaling pathway.
mutated in multiple advanced cancers 1
, phosphatidylinositol 3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN
, phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN
, protein tyrosine phosphatase and tensin-like protein
, phosphatase and tensin homolog deleted on chromosome ten
, phosphatase and tensin homolog (mutated in multiple advanced cancers 1)
, MMAC1 phosphatase and tensin homolog deleted on chromosome 10
, phosphatase and tensin-like protein
, homolog of human mutated in multiple advanced cancers
, protein/lipid phosphatase Pten