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PTEN loss in E-cadherin (Montrer CDH1 Anticorps)-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 (Montrer FBXL2 Anticorps) to promote IP3R3 (Montrer ITPR3 Anticorps)- and Ca(2 (Montrer CA2 Anticorps)+)-mediated apoptosis limiting tumour growth
Theca cell-selective Pten mutation (tPtenMT) in mice resulted in increases in PDK1 (Montrer PDPK1 Anticorps) and Akt (Montrer AKT1 Anticorps) 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 (Montrer PIK3CA Anticorps) to p110beta in vivo. These results provide insight into the molecular mechanism by which ErbB2 (Montrer ERBB2 Anticorps)-positive breast cancer escapes p110alpha (Montrer PIK3CA Anticorps) 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 (Montrer BRD2 Anticorps) levels.
The results identify a novel miR (Montrer MLXIP Anticorps)-682/PTEN/NF-kappaB (Montrer NFKB1 Anticorps) p65 (Montrer NFkBP65 Anticorps) 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 (Montrer TP53 Anticorps)/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 (Montrer MLXIP Anticorps)-214 regulates renal cell hypertrophy and matrix protein expression by directly acting on PTEN and modulating the PRAS40 (Montrer AKT1S1 Anticorps)/tuberin (Montrer TSC2 Anticorps) 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 (Montrer ITK Anticorps) 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 (Montrer IGF1R Anticorps), IGF-2R and PTEN in temporo-spatial patterning of basic cellular processes (proliferation, differentiation) during normal tooth development.
miR (Montrer MLXIP Anticorps)-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 (Montrer AKT1 Anticorps)/NF-kappaB (Montrer NFKB1 Anticorps)/COX-2 (Montrer COX2 Anticorps) pathway.
Targeting of PTEN by miR (Montrer MLXIP Anticorps)-486-5p observed in endothelial cells
miR (Montrer MLXIP Anticorps)-221-3p targets PTEN mRNA and downregulates PTEN, which is the possible mechanism of miR (Montrer MLXIP Anticorps)-221-3p-induced oncogenic properties. Collectively, we reveal a critical role for miR (Montrer MLXIP Anticorps)-221-3p in gastric carcinoma development and progression.
The c.80-96A.G (rs1903858) polymorphism was identified in one individual. In a single SPS (Montrer SMS Anticorps) 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 (Montrer NFKB1 Anticorps) by MMA(III) may participate in UROtsa cells malignant transformation through the negative regulation of PTEN expression involving p50 (Montrer CD40 Anticorps) homodimers-mediated chromatin remodeling around the PTEN promoter.
PTEN/Akt (Montrer AKT1 Anticorps) signaling pathway contributes to cardiomyocyte apoptosis after coronary microembolization.
PTEN, FOXO3A (Montrer FOXO3 Anticorps) and PKB (Montrer AKT1 Anticorps) 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 (Montrer BMPR2 Anticorps) genes.
miR (Montrer MYLIP Anticorps)-26b participates in the inflammatory response of LPS (Montrer IRF6 Anticorps)-stimulated bAMs by modulating the NF-kappaB (Montrer NFKB1 Anticorps) 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 (Montrer NOS3 Anticorps) 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 (Montrer DVL2 Anticorps).
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