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抗Mouse (Murine) PIK3CA 抗体:
抗Human PIK3CA 抗体:
抗Rat (Rattus) PIK3CA 抗体:
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 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
Human Polyclonal PIK3CA Primary Antibody for IHC, ELISA - 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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The data establish oncogenic PIK3CA mutations as a cause of glutamine (显示 GFPT1 抗体) 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 (显示 SMAD1 抗体) axis as a central node integrating multiple signaling networks that govern bone formation and homeostasis.
Data suggest a critical role for KDM3A (显示 KDM3A 抗体) in the PI3K/AP-1 (显示 JUN 抗体) oncogenic axis and propose a novel strategy for inhibition of KDM3A (显示 KDM3A 抗体) 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.
The role of PI3K in cancer has been well established, and mutations of PIK3CA, the gene coding for catalytic subunit p110alpha of PI3K, are found in approximately 30% human cancers. we review the structures and activation modes of PI3Ks and its implications in angiogenesis, extracellular matrix remodeling and tumor immunity.
Double mutation of PIK3CA and TP53 (显示 TP53 抗体) is an independent predictive factor for overall survival in stage II/III colorectal cancer patients receiving 5-FU-based chemotherapy.
High PI3K expression is associated with cervical cancer.
High PIK3CA expression is associated with head and neck carcinoma.
pK15-dependent signaling may occur from intracellular vesicles and rely on the endocytotic machinery. Specifically, a class II PI3K, PI3K-C2alpha (显示 PIK3C2A 抗体), is recruited by pK15 and involved in pK15-dependent intracellular signaling and viral reactivation from latency.
The data establish oncogenic PIK3CA mutations as a cause of glutamine (显示 GFPT1 抗体) dependency in colorectal cancer and suggest that targeting glutamine (显示 GFPT1 抗体) metabolism may be an effective approach to treat patients harboring PIK3CA mutations.
High Resolution Melting Analysis can be used as a rapid and sensitive method for mutation screening. Dysregulation of PIK3CA gene in bladder cancer reveals its potentials as a mechanistic link for cancer development, which in turn suggests its special use in interventional studies for targeted therapy
In patients without PIK3CA alteration, TP53 (显示 TP53 抗体) nonfunctional mutations are associated with poor prognosis.
Knowing the mutation status of KRAS, BRAF (显示 BRAF 抗体) or PIK3CA in stage II colorectal cancer can significantly improve the accuracy of prognoses.
Survival analyses revealed that PIK3CA mutation was a significant prognostic factor for poor overall survival [multivariate adjusted hazard ratio (HR), 3.9; 95% confidence interval (95% CI), 1.3-11.8; P = .017] and cancer-specific survival (multivariate adjusted HR, 3.6; 95% CI, 1.2-11.0; P = .024) in stage IIB to IVA cervical cancers treated by concurrent chemoradiotherapy with weekly cisplatin.
There are multiple conformations in equilibrium during the course of PI3K SH3 domain (显示 ITSN1 抗体) unfolding.
PI3K has a role in activation of 5'-AMP (显示 TMPRSS5 抗体)-activated kinase during hypoxia-reoxygenation of bovine aortic endothelial cells
Production of PtdIns3P by PI3K-C2alpha (显示 PIK3C2A 抗体) 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