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anti-Mouse (Murine) PIK3CA Antikörper:
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Human Polyclonal PIK3CA Primary Antibody für 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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Human Polyclonal PIK3CA Primary Antibody für 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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Mouse (Murine) Polyclonal PIK3CA Primary Antibody für 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 für 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 für 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 für 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 für 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
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.
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.
The expression levels of ARID1A and PIK3CA in gastric cancer were significantly associated with the depth of invasion of gastric cancer.
While PIK3CA mutations generally had no impact on survival, and were not associated with clinicopathological variables, patients with exon 9 charge-changing mutations were associated with poor survival in endometrial primary tumors. PIK3CA mRNA levels were increased in metastases compared to the primary tumors, independent of PIK3CA mutation status, which rather associated with reduced PIK3CA mRNA expression.
The ARID1A and PIK3CA were the most frequently mutated genes. Specifically, ARID1A mutations and PIK3CA mutations were detected in 77.8% and 66.7% of ovarian clear cell carcinoma patients, respectively. Mutations in other genes, including MLH1 (6.3%) and CREBBP (6.3%), were detected in the Taiwanese population.
These results suggest that in addition to overgrowth of bone and soft tissue, gain of function variants in PIK3CA may predispose to overgrowth of scar tissue, resulting in the formation of abnormal scars such as keloids or hypertrophic scars.
biomarkers that are predictive of a response, such as PIK3CA mutations for inhibitors of the PI3K catalytic subunit alpha isoform, must be identified and analytically and clinically validated.. we review the current experience with anticancer therapies that target the PI3K-AKT-mTOR pathway.
Authors used six whole-exome-sequenced primary HGSOC/USC cell-lines and three xenografts overexpressing HER2/neu and harboring mutated or wild-type PIK3CA/PIK3R1 genes to evaluate the role of PI3K-mutations as potential mechanism of resistance to afatinib.
These results showed high concordance between detection of PIK3CA mutations in tumor tissue and in corresponding serum circulating tumor DNA.
Increased PIK3CA expression is associated with Colorectal Cancer.
Patients with somatic co-mutation of TP53 and PIK3CA were associated with unfavorable survival compared with non-carriers. Co-mutation of TP53 and PIK3CA could be used as a potential prognosis marker in post-neoadjuvant chemotherapy breast cancer patients.
Letter: PIK3CA mutation, in particular, mutation of exon 9, has a significant positive association with KRAS mutation in colorectal 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.
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