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these results identify the PI3K-GSK3 (show GSK3b ELISA Kits)-SMAD1 (show SMAD1 ELISA Kits) axis as a central node integrating multiple signaling networks that govern bone formation and homeostasis.
Data suggest a critical role for KDM3A (show KDM3A ELISA Kits) in the PI3K/AP-1 (show JUN ELISA Kits) oncogenic axis and propose a novel strategy for inhibition of KDM3A (show KDM3A ELISA Kits) against liver tumor development under PI3K pathway activation.
Data show that tumors lacking PSMA (show FOLH1 ELISA Kits) had less than half the abundance of type 1 insulin (show INS ELISA Kits)-like growth factor receptor (show RYK ELISA Kits) (IGF-1R (show IGF1R ELISA Kits)), less activity in the survival pathway mediated by PI3K-AKT (show AKT1 ELISA Kits) signaling, and more activity in the proliferative pathway mediated by MAPK (show MAPK1 ELISA Kits)-ERK1/2 (show MAPK1/3 ELISA Kits) 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 ELISA Kits)-mediated repression and gain of NF-kappaB (show NFKB1 ELISA Kits) activation underlie cytokine induction in ARID1A (show ARID1A ELISA Kits)- 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 ELISA Kits)-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 ELISA Kits) 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 ELISA Kits) and TGFb (show TGFB1 ELISA Kits) signaling in advanced HNSCC patients with PIK3CA amplification
Data show that docetaxel, rapamycin and tanespimycin multi-drug loaded micelles targeted against HSP90 (show HSP90 ELISA Kits) and the PI3K/AKT (show AKT1 ELISA Kits)/mTOR (show FRAP1 ELISA Kits) pathway in prostate cancer.
Data indicate that chlorogenic acid (CGA (show CGA ELISA Kits)) protected osteoblast MC3T3-E1 cells against oxidative damage via PI3K/Akt (show AKT1 ELISA Kits)-mediated activation of Nrf2 (show NFE2L2 ELISA Kits)/HO-1 (show HMOX1 ELISA Kits) pathway, which may be an effective drug in treatment of osteoporosis.
FBS (show FBXO8 ELISA Kits). Following stimulation of RTKs (receptor tyrosine kinases), microinjected PI3Kalpha was recruited to the PM, but oncogenic forms of PI3Kalpha were not recruited to the PM to a greater extent and did not reside at the PM longer than the wild-type PI3Kalpha. Instead, the E545K mutant specifically bound activated Cdc42 (show CDC42 ELISA Kits)
AQP9 (show AQP7 ELISA Kits) overexpression decreased the protein levels of phosphatidylinositol-3-kinase (PI3K), leading to reduced phosphorylation of Akt (show AKT1 ELISA Kits), and subsequently the protein levels of forkhead box protein O1 (FOXO1 (show FOXO1 ELISA Kits)) were increased.
PI3K catalytic-alpha (show POLG ELISA Kits)(PIK3CA) mutations assessed from circulating tumor DNA represent the first potentially viable serum biomarker for the selection of ET combinations, and new data demonstrate the feasibility of this minimally invasive technique as an alternative to traditional tissue analysis
We identified a de novo phosphatidylinositol-4,5- bisphosphate 3-kinase catalytic subunit alpha gene (PIK3CA) mutation as a potential drug resistance mechanism.
Overall PIK3CA mutant/HER2 (show ERBB2 ELISA Kits)+ tumours had significantly lower pCR rates compared with wild-type tumours, however mainly confined to the HR+/PIK3CA mutant population. No definite conclusions can be drawn regarding survival
The primary end point was progression-free survival (PFS) in the intention-to-treat (ITT) population and patients with PIK3CA-mutated tumours.In patients with PIK3CA-mutated tumours, the median PFS was 7.3 months for pictilisib (n = 32) versus 5.8 months with placebo (n = 30) (HR, 1.06; 95% CI 0.52-2.12; P = 0.88)
PIK3CA mutations have a role in breast tumor response to targeting mTOR (show FRAP1 ELISA Kits)-mediated MCL-1 (show MCL1 ELISA Kits) translation
Data show that long noncoding RNA RMEL3 is required for MAPK (show MAPK1 ELISA Kits) and PI3K signaling, and its knockdown decrease BRAFV600E melanoma cell survival and proliferation.
Results indicate that des (show DES ELISA Kits)-gamma-carboxy prothrombin (show F2 ELISA Kits) (DCP (show ACE ELISA Kits)) antagonizes the inhibitory effects of Sorafenib on hepatocellular carcinoma (HCC (show FAM126A ELISA Kits)) through activation of the Raf (show RAF1 ELISA Kits)/MEK (show MAP2K1 ELISA Kits)/ERK (show EPHB2 ELISA Kits) and PI3K/Akt (show AKT1 ELISA Kits)/mTOR (show FRAP1 ELISA Kits) signaling pathways.
Together, dual inhibition of BRD4 (show BRD4 ELISA Kits) and PI3K by SF2523 suppresses human prostate cancer cell growth in vitro and in vivo.
There are multiple conformations in equilibrium during the course of PI3K SH3 domain (show ITSN1 ELISA Kits) unfolding.
PI3K has a role in activation of 5'-AMP (show TMPRSS5 ELISA Kits)-activated kinase during hypoxia-reoxygenation of bovine aortic endothelial cells
Production of PtdIns3P by PI3K-C2alpha (show PIK3C2A ELISA Kits) 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