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anti-Mouse (Murine) PIK3CA Antibodies:
anti-Human PIK3CA Antibodies:
anti-Rat (Rattus) PIK3CA Antibodies:
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Human Polyclonal PIK3CA Primary Antibody for WB - ABIN6672113
Dinesh, Rasool et al.: Berberine inhibits IL-21/IL-21R mediated inflammatory proliferation of fibroblast-like synoviocytes through the attenuation of PI3K/Akt signaling pathway and ameliorates IL-21 mediated ... in Cytokine 2018
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Mouse (Murine) Polyclonal PIK3CA Primary Antibody for WB - ABIN3020829
Zhang, Chen, Tao, Kang, Xiong, Zeng, Liu, Jiang, Chen: miR-25-3p, Positively Regulated by Transcription Factor AP-2α, Regulates the Metabolism of C2C12 Cells by Targeting Akt1. in International journal of molecular sciences 2018
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Human Monoclonal PIK3CA Primary Antibody for ICC, FACS - ABIN969555
Edwards, Witherspoon, Wang, Afrasiabi, Pham, Birnbaumer, Lipkin: Epigenetic repression of DNA mismatch repair by inflammation and hypoxia in inflammatory bowel disease-associated colorectal cancer. in Cancer research 2009
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Human Polyclonal PIK3CA Primary Antibody for ELISA, IHC - ABIN188684
López-Knowles, Hernández, Malats, Kogevinas, Lloreta, Carrato, Tardón, Serra, Real: PIK3CA mutations are an early genetic alteration associated with FGFR3 mutations in superficial papillary bladder tumors. in Cancer research 2006
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Human Polyclonal PIK3CA Primary Antibody for ELISA, IHC - ABIN334459
Abubaker, Bavi, Al-Haqawi, Jehan, Munkarah, Uddin, Al-Kuraya: PIK3CA alterations in Middle Eastern ovarian cancers. in Molecular cancer 2009
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Human Polyclonal PIK3CA Primary Antibody for IF (p), IHC (p) - ABIN677198
Paul-Samojedny, Suchanek, Borkowska, Pude?ko, Owczarek, Kowalczyk, Machnik, Fila-Dani?ow, Kowalski: Knockdown of AKT3 (PKB?) and PI3KCA suppresses cell viability and proliferation and induces the apoptosis of glioblastoma multiforme T98G cells. in BioMed research international 2014
High PI3KCA expression is associated with brain cancer.
Despite the induction of oxidative and metabolic stresses, Shp2 deletion in hepatocytes suppressed hepatocarcinogenesis driven by overexpression of oncoproteins MET/CAT or MET/PIK. Shp2 loss inhibited proliferative signaling from c-Met, Wnt/beta-catenin, Ras/Erk and PI3K/Akt pathways, but triggered cell senescence following exogenous expression of the oncogenes.
present study highlighted that overexpression of miR-203 may function as a cardioprotective regulator in DCM by targeting PIK3CA via inactivation of PI3K/Akt signaling pathway.
The major role in stimulation of the synthesis of granulocytic CSF during stressful stimulation is played by PI3K/Akt signaling cascade.
RAS signaling through PI3K is necessary for normal lymphatic vasculature development and for RAS-induced transformation in vitro and in vivo, especially in lung cancer, where it is essential for tumor initiation and necessary for tumor maintenance. [review]
High Pik3ca expression is associated with abdominal aortic aneurysm.
Data show that oncogenic phosphatidylinositol 3-kinase, catalytic, alpha polypeptide (PI3K)-proto-oncogene protein Akt (AKT)-activated epidermis exhibits a growth disadvantage even though its cells are more proliferative.
PI3K p110alpha plays a significant role in antigen activation and differentiation of CD4(+) and CD8(+) T lymphocytes modulating antitumor immunity.
Phospholipase C-related catalytically inactive protein (PRIP)-deficient mouse embryonic fibroblasts exhibited increased cell migration, and was significantly attenuated upon transfection with a siRNA targeting p110alpha, a catalytic subunit of class I phosphoinositide 3-kinases (PIK3CA).
Here, we demonstrated that inducible MuSC-specific deletion of p110alpha, a catalytic subunit of phosphatidylinositol 3-kinase (PI3K), rendered MuSCs unable to exit quiescence, resulting in severely impaired MuSC proliferation and muscle regeneration.
miR152 may have an important role in pancreatic beta cell function, and established an association between miR152 and the PI3Kalpha axis.
H1047R mutation of Pik3ca induces centrosome amplification in cultured mouse cells.
The crucial role of p110beta and the more subtle role of p110alpha in the production of PIP3 molecular species following platelet stimulation has been demonstrated.
Here, we describe a role for PI3K/AKT in the regulation of TRF1, an essential component of the shelterin complex. PI3K and AKT chemical inhibitors reduce TRF1 telomeric foci and lead to increased telomeric DNA damage and fragility. We identify the PI3Kalpha isoform as responsible for this TRF1 inhibition.
The data establish oncogenic PIK3CA mutations as a cause of glutamine dependency in colorectal cancer.
High PI3k expression is associated with gastrointestinal stromal tumor.
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.
IL1B promotes the nuclear translocaiton of S100A4 protein in gastric cancer cells and the cell's stem-like properties through PI3K pathway.
This study determined the mutation frequencies and prognostic values of KRAS exon 2, 3 and 4, NRAS exon 2 and 3, PIK3CA exon 9 and 20, and BRAF exon 15 by PCR and direct sequencing in 353 colorectal cancer patients from two Chinese clinical centers.
Study shows that ARQ092 counteracts overactivation of PI3K signal pathway in primary fibroblast cells derived from patients with PIK3CA-related overgrowth spectrum.
We detected the same PIK3CA mutation in her affected tissue, urine, and tumor, indicating Wilms tumors probably arise from PIK3CA mutant cells in patients with CLOVES. No urine sample from a participant with Klippel-Trenaunay (KTS) had detectable PIK3CA mutations.
Expression of Phosphoinositide 3-Kinase p110alpha and p110beta Subunits and PIK3CA Mutation in Patients With Advanced Gastric Carcinoma.
To investigate the reasons for which miR-375 holds a special place among circulating miRNAs in Acute myocardial infarction (MI), enrichment and network analyses of miR-375 target genes and their interactions were carried out. PIK3CA and TP53 genes, regulated by miR-375, were identified as the key players of MI disease module.
We report the first characterization of clinical acquired resistance to MEKi + CDK4i, identifying a rare preexisting PIK3CA(E545K) subpopulation that expands upon therapy and exhibits drug resistance.
Data suggest that receptor-tyrosine kinase HEK2 (EphB3) and phosphatidylinositol 3-kinase catalytic alpha polypeptide (PIK3CA) are cooperating oncogenes that contribute toward its pathogenesis.
THE DIAGNOSIS AND RELAPSE PREDICTION OF PATIENTS WITH NON-MUSCLE INVASIVE BLADDER CANCER WITH FGFR3,TP53 AND PIK3CA GENE MUTATION POSSESSED HIGH ACCURACY
Results show PIK3CA mutation correlates with poor prostate cancer prognosis and causes prostate cancer in mice. Moreover, PIK3CA mutation and PTEN loss coexist in prostate cancer and can cooperate in vivo to accelerate tumorigenesis and facilitate castration-resistant prostate cancer.
H2O2 induces oxidative stress to breast cancer tumor cell line MCF-7 in a dose dependent manner. Over-expression of p110alpha protein restores pro-survival effects against H2O2 induced apoptosis and increase phosphorylated proto-oncogene proteins c-akt levels.
Study identified a novel F977Y kinase domain PIK3CA mutation exclusively present in a recurrent cell line of head and neck squamous cell carcinoma (HNSCC), potentially conferring resistance to PI3K inhibitors.
KRAS wild-type metastatic colorectal cancer patients with mutant type phosphatidylinositol 3-kinases receiving an epidermal growth factor receptor monoclonal antibody (anti-EGFR) inhibitor as first-line therapy have significantly lower overall response rate, shorter progression-free survival and overall survival.
The study shows a high concordance of KRAS, NRAS, BRAF and PIK3CA gene mutations in plasma against mutation status in tumor tissue.
Study data from human hepatocellular carcinoma (HCC) liver samples, human HCC cells, and Sgk3 knockout mice model suggest that SGK3 plays a role in transducing helical domain mutant PIK3CA signaling during liver tumor development.
AR + /FOXA1 + expression defines a luminal-like TNBC subgroup affected with a worse outcome compared to other TNBC and a higher risk of late recurrences. This subgroup appears enriched in PIK3CA mutations, suggesting a role for PI3K inhibitors in this subgroup.
PIK3CA expression in triple negative breast cancer is not associated with specific clinical or diagnostic features. Further molecular studies and meta-analysis are warranted to clarify the prognostic and predictive role of PIK3CA protein expression.
In this large pooled analysis, PIK3CA mutations were significantly associated with a better IDFS, DDFS, and OS, but had a lesser prognostic effect after adjustment for other prognostic factors.
PIK3CA gene fusion and expression is associated with poor outcome in the hormone receptor-positive breast cancer.
The expression levels of ARID1A and PIK3CA in gastric cancer were significantly associated with the depth of invasion of gastric cancer.
Data show that both class I and III phosphoinositide 3-kinases (PI3Ks) re present in trafficking vesicles.
There are multiple conformations in equilibrium during the course of PI3K SH3 domain unfolding.
PI3K has a role in activation of 5'-AMP-activated kinase during hypoxia-reoxygenation of bovine aortic endothelial cells
Production of PtdIns3P by PI3K-C2alpha 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