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PTEN loss in E-cadherin (显示 CDH1 抗体)-deficient mouse mammary epithelial cells rescues apoptosis and results in development of classical invasive lobular carcinoma.
Pten modulates the hematopoietic stem cells response to inflammatory cytokines.
PTEN counteracts FBXL2 (显示 FBXL2 抗体) to promote IP3R3 (显示 ITPR3 抗体)- and Ca(2 (显示 CA2 抗体)+)-mediated apoptosis limiting tumour growth
Theca cell-selective Pten mutation (tPtenMT) in mice resulted in increases in PDK1 (显示 PDPK1 抗体) and Akt (显示 AKT1 抗体) phosphorylation, indicating an over-activation of PI3K signaling in the ovaries.
We further demonstrate that loss of one allele of PTEN is sufficient to shift isoform dependency from p110alpha (显示 PIK3CA 抗体) to p110beta in vivo. These results provide insight into the molecular mechanism by which ErbB2 (显示 ERBB2 抗体)-positive breast cancer escapes p110alpha (显示 PIK3CA 抗体) inhibition.
Low PTEN expression is associated with Prostate Cancer Progression.
Findings indicate that the ovary is highly resistant to tumorigenic changes due to selective global or granulosa cells-specific Pten disruption and rising FSH (显示 BRD2 抗体) levels.
The results identify a novel miR (显示 MLXIP 抗体)-682/PTEN/NF-kappaB (显示 NFKB1 抗体) p65 (显示 NFkBP65 抗体) signaling pathway in intestinal epithelial cells injury induced by ischemia-reperfusion that could be targeted for therapy.
This is the first report of a viral-Cre mediated Trp53 (显示 TP53 抗体)/Pten mouse model of undifferentiated pleomorphic sarcoma. The bioluminescence imaging feature, along with high penetrance of the model and its immunological characteristics, makes it suited for pre-clinical studies of soft tissue sarcoma
miR (显示 MLXIP 抗体)-214 regulates renal cell hypertrophy and matrix protein expression by directly acting on PTEN and modulating the PRAS40 (显示 AKT1S1 抗体)/tuberin (显示 TSC2 抗体) and mTORC1 axis in response to high glucose.
The silencing of PTEN by siRNA increased the proliferation and promoted cell invasion of Tca8113 cells (squamous carcinoma). PTEN gene silencing may accelerate the EMT (显示 ITK 抗体) in Tca8113 cells.
35 SNPs of the human phosphatase and tensin homolog (PTEN) gene were analyzed by mutational analysis for functional significance, and five were found to be deleterious based on different computational tools, including molecular dynamics simulations.
These data suggest the involvement of IGF-2, IGF-1R (显示 IGF1R 抗体), IGF-2R and PTEN in temporo-spatial patterning of basic cellular processes (proliferation, differentiation) during normal tooth development.
miR (显示 MLXIP 抗体)-221/222 play a critical role in the propagation of breast cancer stem cells and tumor growth possibly through targeting PTEN, which in turn activating the Akt (显示 AKT1 抗体)/NF-kappaB (显示 NFKB1 抗体)/COX-2 (显示 COX2 抗体) pathway.
Targeting of PTEN by miR (显示 MLXIP 抗体)-486-5p observed in endothelial cells
miR (显示 MLXIP 抗体)-221-3p targets PTEN mRNA and downregulates PTEN, which is the possible mechanism of miR (显示 MLXIP 抗体)-221-3p-induced oncogenic properties. Collectively, we reveal a critical role for miR (显示 MLXIP 抗体)-221-3p in gastric carcinoma development and progression.
The c.80-96A.G (rs1903858) polymorphism was identified in one individual. In a single SPS (显示 SMS 抗体) individual, we also identified a novel variant in intron 2 (c.164+223T.C) of PTEN, which was predicted by in silico analysis to have no functional consequences.
Well-differentiated laryngeal squamous cell carcinomas express moderate to high protein levels of PTEN, an evidence of normal gene function, whereas loss of its expression correlates with a progressive tumor dedifferentiation.
These results suggest that the activation of NF-kappabeta (显示 NFKB1 抗体) by MMA(III) may participate in UROtsa cells malignant transformation through the negative regulation of PTEN expression involving p50 (显示 CD40 抗体) homodimers-mediated chromatin remodeling around the PTEN promoter.
PTEN/Akt (显示 AKT1 抗体) signaling pathway contributes to cardiomyocyte apoptosis after coronary microembolization.
PTEN, FOXO3A (显示 FOXO3 抗体) and PKB (显示 AKT1 抗体) 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 (显示 BMPR2 抗体) genes.
miR (显示 MYLIP 抗体)-26b participates in the inflammatory response of LPS (显示 IRF6 抗体)-stimulated bAMs by modulating the NF-kappaB (显示 NFKB1 抗体) 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 (显示 NOS3 抗体) 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 (显示 DVL2 抗体).
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