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High PI3K expression is sensitive to initial injury intensity induced by freeze damage.
excessive proliferation of endometrial epithelial cells was observed in Pik3cad/d mice. Our studies suggest that Pik3ca has a critical role in uterine gland development and female fertility
Long latency DMBA induced mouse mammary tumors reproduce the molecular profile of human luminal breast carcinomas, displaying a high incidence of activating Pik3caH1047 and loss of function Pten mutations.
Data show that the phosphoinositide 3-kinase (PI3K) inhibitor BKM120 led to a precipitous drop in DNA synthesis within 8 h of drug treatment, whereas DNA synthesis in normal tissues was less affected.
Using genetic inactivation of the growth and metabolism regulator, Pik3ca (encoding PIK3CA also known as p110alpha, alpha/+), the interplay between the maternal genome and the fetal genome on placental phenotype, was examined.
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.
p110alpha subunit of PI3K and PKD (show PRKD1 Proteins) mediate YAP (show YAP1 Proteins) activation in response to insulin (show INS Proteins) and neurotensin (show NTS Proteins) in pancreatic cancer cells. Inhibitors of PI3K or PKD (show PRKD1 Proteins) disrupt crosstalk between insulin receptor (show INSR Proteins) and GPCR (show NMUR1 Proteins) signaling systems by blocking YAP (show YAP1 Proteins)/TEAD-regulated gene expression in pancreatic cancer cells
PI3K overexpression is associated with colorectal cancer metastasis.
PIK3CA gene mutations were not found; however, a synonymous single nucleotide polymorphism (SNP) [rs17849079] was observed frequently [35/96 (36.4%)] in oral cancer samples.
Preliminary data consistent with preclinical data indicate increased antitumor activity of taselisib in patients with PIK3CA-mutant tumors (in comparison with patients with tumors without known activating PIK3CA hotspot mutations) starting at the lowest dose tested of 3 mg, thereby supporting higher potency for taselisib against PIK3CA-mutant tumors.
In vivo single-agent mTORC inhibition inhibited growth of one PIK3CA-mutant cancer, but had little effect on any PIK3CA(WT) or a second PIK3CA-mutant model. In all models, the combination therapy showed greater growth delay than monotherapy. The uniform ability of PI3K and mTORC inhibition to suppress the growth of Head and neck squamous cell carcinomas (HNSCC) cells highlights the pathway's role in driving proliferation
A mosaic gain-of-function mutation in PIK3CA was identified in a patient with gait disturbance, leg pain, isolated macrodactyly of the foot, and mild intellectual disability.
The lack of KRAS, NRAS (show NRAS Proteins), BRAF (show BRAF Proteins), and PIK3CA mutation in our study may suggest that a subset of eyelid sebaceous carcinomas is unlike that of eyelid sebaceous carcinomas of western countries.
Phosphatidylinositol-3-kinase signaling is regulated by INPP4B and PTEN in the triple-negative breast cancer cells.
PIK3CA mutations can lead to resistance to MET inhibition, supporting future clinical evaluation of combinations of PI3K and MET inhibitors in common scenarios of malignant neoplasms featuring aberrant MET expression and PIK3CA mutations.
We find that both primary and recurrent Squamous cell carcinoma of the anal canal (ASCC) tumors harbor mutations in genes, such as PIK3CA and FBXW7 (show FBXW7 Proteins), that are also mutated in other HPV-associated cancers. Overall mutational burden was not significantly different in pre- versus post-CRT (show SLC6A8 Proteins) tumors, and several examples of shared clonal driver mutations were identified
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