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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 (显示 HDAC3 ELISA试剂盒)-mediated repression and gain of NF-kappaB (显示 NFKB1 ELISA试剂盒) activation underlie cytokine induction in ARID1A (显示 ARID1A ELISA试剂盒)- 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 (显示 ERBB2 ELISA试剂盒)-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 (显示 AKT1 ELISA试剂盒) 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 (显示 PDPK1 ELISA试剂盒) and TGFb (显示 TGFB1 ELISA试剂盒) signaling in advanced HNSCC patients with PIK3CA amplification
Data show that docetaxel, rapamycin and tanespimycin multi-drug loaded micelles targeted against HSP90 (显示 HSP90 ELISA试剂盒) and the PI3K/AKT (显示 AKT1 ELISA试剂盒)/mTOR (显示 FRAP1 ELISA试剂盒) pathway in prostate cancer.
Data indicate that chlorogenic acid (CGA (显示 CGA ELISA试剂盒)) protected osteoblast MC3T3-E1 cells against oxidative damage via PI3K/Akt (显示 AKT1 ELISA试剂盒)-mediated activation of Nrf2 (显示 NFE2L2 ELISA试剂盒)/HO-1 (显示 HMOX1 ELISA试剂盒) pathway, which may be an effective drug in treatment of osteoporosis.
Data show that macrophage M2 polarization was mediated through PTEN/PI3k/AKT (显示 AKT1 ELISA试剂盒) pathway activation.
Constitutive Activation of PI3K is associated with Ovarian Granulosa Cell Tumors.
Together with recent identification of somatic mutations in p110a (encoded by PIK3CA), our data establish a potential mechanistic link between AGGF1 (显示 AGGF1 ELISA试剂盒) and PIK3CA, the two genes identified for Klippel-Trenaunay syndrome (KTS)
Study found that PIK3CA mutation occurred in approximately 2.8% of patients with lung adenocarci- noma in a cohort of Chinese patients.
PIK3CA mutations are associated with esophageal squamous cell carcinoma.
This is the first report on phosphorylation of p53 (显示 TP53 ELISA试剂盒) serine 46 as a modulator of p53 (显示 TP53 ELISA试剂盒)-PIK3CA promoter interaction.
KRAS mutations and AKT (显示 AKT1 ELISA试剂盒) activation are present in Wilms tumors (WT) and may represent novel therapeutic targets for this tumor.
relevant genomic aberrations such as mutations in the hotspot regions of exon 9 and 20 of the PIK3CA gene can be detected in single circulating tumor cells and might provide insights into mechanisms of resistance to HER2 (显示 ERBB2 ELISA试剂盒)-targeted therapies.
the expression of 3 miRs and 9 mRNAs associate with the PIK3CA status. Expression of LRG1 (显示 LRG1 ELISA试剂盒) is independent of luminal (A or B) subtype, decreased after neo-adjuvant aromatase (显示 CYP19A1 ELISA试剂盒) inhibitor treatment.
Somatic mutations affecting PI3K pathway genes were found to be highly prevalent in infiltrating epitheliosis, suggesting that these lesions may be neoplastic rather than hyperplastic.
Somatic PIK3CA mutations in seven patients with PIK3CA-related overgrowth spectrum have been reported.
These results indicated that dual targeting of PI3K and PERK pathways might improve clinical prognosis and enhance the treatment of ESCC patients.
These data indicate that increased irisin (显示 FNDC5 ELISA试剂盒) levels may have protective roles in liver cancer cells through partial activation of the PI3K/AKT (显示 AKT1 ELISA试剂盒) pathway, which may facilitate liver cancer progression and decrease the sensitivity to chemotherapy.
There are multiple conformations in equilibrium during the course of PI3K SH3 domain (显示 ITSN1 ELISA试剂盒) unfolding.
PI3K has a role in activation of 5'-AMP (显示 TMPRSS5 ELISA试剂盒)-activated kinase during hypoxia-reoxygenation of bovine aortic endothelial cells
Production of PtdIns3P by PI3K-C2alpha (显示 PIK3C2A ELISA试剂盒) 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