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these results identify the PI3K-GSK3-SMAD1 (show SMAD1 Proteins) axis as a central node integrating multiple signaling networks that govern bone formation and homeostasis.
Data suggest a critical role for KDM3A (show KDM3A Proteins) in the PI3K/AP-1 (show JUN Proteins) oncogenic axis and propose a novel strategy for inhibition of KDM3A (show KDM3A Proteins) against liver tumor development under PI3K pathway activation.
Data show that tumors lacking PSMA had less than half the abundance of type 1 insulin-like growth factor receptor (IGF-1R), less activity in the survival pathway mediated by PI3K-AKT signaling, and more activity in the proliferative pathway mediated by MAPK-ERK1/2 signaling.
Both PIK3CA mutants H1047R and E545K are able to activate the AKT/mTOR pathway. An intact AKT2/mTOR complex 1 cascade is required for tumourigenesis induced by H1047R/c-Met or E545K/c-Met in the liver in mice.
Loss of HDAC (show HDAC3 Proteins)-mediated repression and gain of NF-kappaB (show NFKB1 Proteins) activation underlie cytokine induction in ARID1A- and PIK3CA-mutation-driven ovarian cancer.
We further demonstrate that loss of one allele of PTEN is sufficient to shift isoform dependency from p110alpha to p110beta in vivo. These results provide insight into the molecular mechanism by which ErbB2 (show ERBB2 Proteins)-positive breast cancer escapes p110alpha inhibition.
Studies indicate that the Pten+/- genotype displayed neoplasia in multiple organs, including the endometrium and that the Pten is a key regulatory player in the PI3K/PTEN/AKT (show AKT1 Proteins) pathway.
our results offer significant insight into how PIK3CA overexpression drives squamous cell carcinoma (HNSCC) invasion and metastasis, providing a rationale for targeting PI3K/PDK1 (show PDPK1 Proteins) and TGFb (show TGFB1 Proteins) signaling in advanced HNSCC patients with PIK3CA amplification
Data show that docetaxel, rapamycin and tanespimycin multi-drug loaded micelles targeted against HSP90 (show HSP90 Proteins) and the PI3K/AKT (show AKT1 Proteins)/mTOR (show FRAP1 Proteins) pathway in prostate cancer.
Data indicate that chlorogenic acid (CGA (show CGA Proteins)) protected osteoblast MC3T3-E1 cells against oxidative damage via PI3K/Akt (show AKT1 Proteins)-mediated activation of Nrf2 (show NFE2L2 Proteins)/HO-1 (show HMOX1 Proteins) pathway, which may be an effective drug in treatment of osteoporosis.
Concomitant inhibition of PIM (show PIM1 Proteins) kinase and p110alpha activities inhibits glioma stem cell function and survival.
Study shows that PIK3CA is required for the proliferation, migration, invasion and clone formation of gallbladder carcinoma (GBC) cells in vitro and that the E545K mutation of PIK3CA promotes GBC progression through its enhanced binding to EGFR (show EGFR Proteins).
Our findings suggest that PIK3CA mutation has the neutral prognostic effects on colorectal cancers (CRC (show CALR Proteins)) OS and progression-free survival. Evidence was accumulating for the establishment of CRC (show CALR Proteins) survival between PIK3CA mutations and patient-specific clinical or molecular profiles.
Sixteen of 20 patients treated at the MTD had reduced (18)FDG-PET uptake; 7 (33%) had a reduction >25%. One patient achieved a complete response (CR; endometrial carcinoma exhibiting both PIK3CA and PTEN mutations and complete PTEN loss) and two had a partial response (PR; both metastatic breast cancer).
Ehrlichia chaffeensis infection activated the phosphatidylinositol 3-kinase (PI3K)-Akt (show AKT1 Proteins)-mTOR (mechanistic target of rapamycin (show FRAP1 Proteins)) pathway, and activation was induced by three ehrlichial tandem repeat protein (TRP (show TBPL1 Proteins)) effectors, with TRP120 inducing the strongest activation.
Overexpression of KAT6A or TRIM24 (show TRIM24 Proteins) promoted PIK3CA expression, AKT (show AKT1 Proteins) phosphorylation, and cell proliferation.
Combined PI3Kalpha and CDK4/6 (show CDK4 Proteins) inhibition significantly improved disease control in human xenograft models compared with either monotherapy.
Data show that cancer-associated fibroblasts (CAFs (show TBX1 Proteins))-derived hepatocyte growth factor (HGF (show HGF Proteins)) or recombinant HGF (show HGF Proteins) activated c-Met/phosphoinositide 3-kinase (PI3K)/Akt (show AKT1 Proteins) and glucose-regulated protein 78 (GRP78 (show HSPA5 Proteins)) signalling pathways in ovarian cancer cells.
Compared to single-gene-targeted cells and parental controls, cells with both a PIK3CA mutation and TP53 (show TP53 Proteins) alteration had increased cancerous phenotypes including cell proliferation, soft agar colony formation, aberrant morphology in acinar formation assays, and genomic heterogeneity.
Data indicate that PIK3CA copy number gain was an independent poor prognostic factor for disease-free survival (DFS (show FST Proteins)).
There are multiple conformations in equilibrium during the course of PI3K SH3 domain unfolding.
PI3K has a role in activation of 5'-AMP (show TMPRSS5 Proteins)-activated kinase during hypoxia-reoxygenation of bovine aortic endothelial cells
Production of PtdIns3P by PI3K-C2alpha (show PIK3C2A Proteins) is required for acquisition of fusion competence in neurosecretion.
crystallographic and biochemical approaches used to gain insight into activating mutations in two noncatalytic p110alpha domains-the adaptor-binding and the helical domains
Phosphatidylinositol 3-kinase is composed of an 85 kDa regulatory subunit and a 110 kDa catalytic subunit. The protein encoded by this gene represents the catalytic subunit, which uses ATP to phosphorylate PtdIns, PtdIns4P and PtdIns(4,5)P2. This gene has been found to be oncogenic and has been implicated in cervical cancers.
phosphoinositide-3-kinase, catalytic, alpha polypeptide
, Phosphoinositide-3-kinase, catalytic, alpha polypeptide
, PI3-kinase subunit alpha
, phosphatidylinositol 4,5-bisphosphate 3-kinase 110 kDa catalytic subunit alpha
, phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform
, phosphatidylinositol-4,5-bisphosphate 3-kinase 110 kDa catalytic subunit alpha
, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha isoform
, phosphoinositide-3-kinase catalytic alpha polypeptide
, ptdIns-3-kinase subunit alpha
, ptdIns-3-kinase subunit p110-alpha
, serine/threonine protein kinase PIK3CA
, PI3-kinase p110 subunit alpha
, phosphatidylinositol 3-kinase, catalytic, 110-KD, alpha
, phosphatidylinositol 3-kinase, catalytic, alpha polypeptide
, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit, alpha isoform
, ptdIns-3-kinase p110
, phosphoinositide 3-kinase catalytic subunit