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Glandular epithelial androgen receptor (AR (show AR Antibodies)) inactivation (with persistent stromal AR action) enhanced PTEN deletion-induced uterine pathology possibly by downregulating progesterone receptor (show PGR Antibodies) expression in the uterus.
ompounding a previously described Bmi1 (show BMI1 Antibodies)-transgene and Pten-deficiency prostate cancer mouse model with the Ezh2 (show EZH2 Antibodies) transgene did not enhance tumour progression or drive metastasis formation. In conclusion, we here report the generation of a wildtype Ezh2 (show EZH2 Antibodies) overexpression mouse model that allows for intravital surveillance of tissues with activated transgene
In conclusion, our data indicated that miR (show MLXIP Antibodies)-26a potentially contributes to the beta-cell dysfunction in T2DM, and miR (show MLXIP Antibodies)-26a may be a new therapeutic strategy against T2DM.
CFTR (show CFTR Antibodies) attaches tumor suppressor PTEN to the membrane and promotes anti Pseudomonas aeruginosa immunity.
These findings indicate that PTEN not only targets tumor cells themselves by impacting cell behaviors, but also blocks osteoclast-mediated bone destruction, leading to interruption of the vicious cycle during osteosarcomagenesis
further molecular mechanisms of HOTAIR action in cardiac hypertrophy (CH) demonstrated that HOTAIR may act as a competing endogenous RNA (ceRNA) for miR (show MLXIP Antibodies)-19, thereby modulating the dis-inhibition of its endogenous target PTEN and playing an important role in inhibiting CH progress.
Setdb1 (show SETDB1 Antibodies) regulates PTEN/AKT (show AKT1 Antibodies)/FOXO1 (show FOXO1 Antibodies) pathway to inhibit Spermatogonial stem cells apoptosis.
Data indicate a functional circuit linking PTEN and LXRs, and highlights LXRs as metabolic gatekeepers that are able to constrain prostate cancer (PCa (show ENPP1 Antibodies)) progression.
phosphorylated-Pten promotes the proliferation and differentiation of hematopoietic stem cells.
Results indicate miR (show MLXIP Antibodies)-130a as an oncogenic miRNA that targets PTEN to drive malignant cell survival and tumor growth.
Data show that ten-eleven translocation 1 (TET1 (show TET1 Antibodies)) suppresses tumor cell growth, migration and invasion through demethylation of CpG island in PTEN promoter by increasing 5-hmC content.
Out of 171 EGFR (show EGFR Antibodies) mutated tumor-patient cases, 20 were sequenced using at least a limited comprehensive genomic profiling platform. 50% harbored concurrent TP53 (show TP53 Antibodies) mutation, 10% PIK3CA (show PIK3CA Antibodies) mutation, 5% PTEN mutation, among others.
inhibition of miR (show MLXIP Antibodies)-19b suppresses the progression of WT by modulating the PTEN/PI3K (show PIK3CA Antibodies)/AKT (show AKT1 Antibodies) signaling pathway.
findings shed new light on the STAT1 (show STAT1 Antibodies)/miR (show MLXIP Antibodies)-181a/PTEN pathway in colorectal cancer and add new insight regarding the carcinogenesis of colorectal cancer.
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 (show BMI1 Antibodies) binds to PTEN promoter and directly inhibits PTEN and thereafter activates AKT (show AKT1 Antibodies)
PTEN/Akt (show AKT1 Antibodies) signaling pathway contributes to cardiomyocyte apoptosis after coronary microembolization.
PTEN, FOXO3A (show FOXO3 Antibodies) and PKB (show AKT1 Antibodies) 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 (show BMPR2 Antibodies) genes.
miR (show MYLIP Antibodies)-26b participates in the inflammatory response of LPS (show IRF6 Antibodies)-stimulated bAMs by modulating the NF-kappaB (show NFKB1 Antibodies) 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 (show NOS3 Antibodies) 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 (show DVL2 Antibodies).
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