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Here, we describe a role for PI3K/AKT (zeige AKT1 Proteine) in the regulation of TRF1 (zeige TERF1 Proteine), an essential component of the shelterin complex. PI3K and AKT (zeige AKT1 Proteine) chemical inhibitors reduce TRF1 (zeige TERF1 Proteine) telomeric foci and lead to increased telomeric DNA damage and fragility. We identify the PI3Kalpha isoform as responsible for this TRF1 (zeige TERF1 Proteine) inhibition.
The data establish oncogenic PIK3CA mutations as a cause of glutamine (zeige GFPT1 Proteine) 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 (zeige SMAD1 Proteine) axis as a central node integrating multiple signaling networks that govern bone formation and homeostasis.
Data suggest a critical role for KDM3A (zeige KDM3A Proteine) in the PI3K/AP-1 (zeige JUN Proteine) oncogenic axis and propose a novel strategy for inhibition of KDM3A (zeige KDM3A Proteine) against liver tumor development under PI3K pathway activation.
higher frequency of ESR1 and PIK3CA mutations in the plasma than in the serum in 33 MBC patients; therefore, serum samples should not be considered the preferred source of cfDNA.
When considered together (43 cases), 1/25 cases (4%) with a PIK3CA mutation and/or low PTEN expression levels had a pathologic complete response (pCR)compared to 7/18 cases (39%) with wild-type PI3KCA and high PTEN expression levels (p = 0.006).
PI3K is a signal linker between L-selectin (zeige SELL Proteine) and PSGL-1 (zeige SELPLG Proteine) in IL-18 (zeige IL18 Proteine) transcriptional activation at the promoter level.
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 (zeige TP53 Proteine) 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 (zeige PIK3C2A Proteine), 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 (zeige GFPT1 Proteine) dependency in colorectal cancer and suggest that targeting glutamine (zeige GFPT1 Proteine) 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
There are multiple conformations in equilibrium during the course of PI3K SH3 domain (zeige ITSN1 Proteine) unfolding.
PI3K has a role in activation of 5'-AMP (zeige TMPRSS5 Proteine)-activated kinase during hypoxia-reoxygenation of bovine aortic endothelial cells
Production of PtdIns3P by PI3K-C2alpha (zeige PIK3C2A Proteine) 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