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anti-Mouse (Murine) PIK3CA Antibodies:
anti-Human PIK3CA Antibodies:
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Mouse (Murine) Polyclonal PIK3CA Primary Antibody for WB - ABIN3020829
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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Human Polyclonal PIK3CA Primary Antibody for WB - ABIN6672113
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 FACS, IHC (p) - ABIN1882113
Singh, Reddy, Goberdhan, Walsh, Dao, Ngai, Chou, O-Charoenrat, Levine, Rao, Stoffel: p53 regulates cell survival by inhibiting PIK3CA in squamous cell carcinomas. in Genes & development 2002
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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 IHC (p), ELISA - ABIN547797
Abubaker, Bavi, Al-Haqawi, Jehan, Munkarah, Uddin, Al-Kuraya: PIK3CA alterations in Middle Eastern ovarian cancers. in Molecular cancer 2009
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
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.
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 axis as a central node integrating multiple signaling networks that govern bone formation and homeostasis.
Data suggest a critical role for KDM3A in the PI3K/AP-1 oncogenic axis and propose a novel strategy for inhibition of KDM3A 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-mediated repression and gain of NF-kappaB activation underlie cytokine induction in ARID1A- and PIK3CA-mutation-driven ovarian cancer.
PIK3CA mutations are found in benign overgrowth syndromes, collectively known as PIK3CA-related overgrowth spectrum. (Review)
Gene alterations, such as TP53 mutation, PIK3CA mutation, ERBB2 amplification and CCND1 amplification, and MAPK pathway alteration were associated with pCR in our study.
High frequency of somatic PIK3CA mutations was detected in Chinese breast cancer patients and associated with poor prognosis. The prevalence of the PIK3CA mutation was 46.5% (236/507), and 35 patients carried two or three variants of PIK3CA gene.
This overgrowth syndrome is unique and is caused by the somatic PIK3CA mutation c.3140A>G.
The current data show that PIK3CA mutations appear to play an important role in carcinogenesis and tumor aggressiveness in Epstein-Barr virus-associated gastric cancer (EBV-GC), and also support the concept that exon 9 mutation of PIK3CA is a prognostic indicator for predicting patient outcomes and a rationale for therapeutic targeting in EBV-GC.
TRAF6 is a novel PIK3CA regulator whose deregulated overexpression represents a mechanism for PI3K overactivation in tumors.
A high proportion of isolated macrodactyly patients carry a PIK3CA mutation.
This study detected gain-of-function mutations in exon 20 of PI3KCA gene in 11% of gastric cancer patients.
These results suggest that the classical metabolic PI3K pathway and not the canonical proliferation ERK pathway is involved in the insulin/insulin-like growth factor-1-induced increase in crypt proliferation in obese humans, which may contribute to abnormal tissue renewal and function.
The pooled analysis confirmed that the presence of a PIK3CA mutation represents an independent negative prognostic factor (HR = 1.67, 95%CI: 1.15-2.43; P = 0.007) in BC, as previously reported. As PI3K signaling is also a result of other pathways' hyperactivation.
High PIK3CA expression is associated with hepatocellular carcinoma.
PIK3CA silencing inhibited Nalm-6 cell proliferation and invasion, and promoted their apoptosis and sensitivity to chemotherapeutic drugs, potentially through regulation of the PI3K/AKT signaling pathway.
findings provided a comprehensive mutation profiling of AKT1, PIK3CA, PTEN and TP53 genes in Chinese breast cancer patients, which have potential implications in clinical management.
LASP1 may function as an oncogene in glioblastoma and regulate cell proliferation and chemosensitivity in a PI3K/AKT-dependent mechanism.
Targeting activating mutations in PIK3CA assay was used for screening tumor DNA from Metastatic Relapse in Advanced Bladder Cancer patients; at least one mutation was detected in 19 of the 60 patients.
Six mutations located at the BRAF, KRAS, and PIK3CA genes have been detected in colorectal cancer patients using a novel multiplex surface enhanced Raman spectroscopy-multiplex PCR method.
Inflammatory stress displayed by endothelial cells derived from lymphatic malformation is consistent with errors in lipid metabolism that may be linked to PIK3CA acquired mutations.
Results show that activating PIK3CA mutations in lymphatic malformations are specifically localized in lymphatic endothelial cells (LECs); identified a new mutation in exon 10 and a Glu109 deletion of the gene and show that several kinase inhibitors have the potential to block LEC proliferation.
Levels of miR381 were decreased in clear cell and endometrioid carcinoma ovarian cancer. Experimentally induced upregulation of miR381 led to a decrease in the level of PIK3CA in ovarian cancer cells and inhibition of ovarian cancer cells proliferation and migration.
High PIK3CA expression is associated with 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