anti-PIK3CA (PIK3CA) 抗体产品概述

Mouse (Murine) Phosphoinositide-3-Kinase, Catalytic, alpha Polypeptide (PIK3CA) interaction partners

1. High Pik3ca expression is associated with abdominal aortic aneurysm.

2. 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.

3. PI3K p110alpha plays a significant role in antigen activation and differentiation of CD4(+) and CD8(+) T lymphocytes modulating antitumor immunity.

4. 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).

5. 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.

6. miR152 may have an important role in pancreatic beta cell function, and established an association between miR152 and the PI3Kalpha axis.

7. H1047R mutation of Pik3ca induces centrosome amplification in cultured mouse cells.

8. 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.

9. 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.

10. The data establish oncogenic PIK3CA mutations as a cause of glutamine dependency in colorectal cancer.

11. High PI3k expression is associated with gastrointestinal stromal tumor.

12. High PI3K expression is sensitive to initial injury intensity induced by freeze damage.

13. 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

14. 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.

15. 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.

16. 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.

17. these results identify the PI3K-GSK3-SMAD1 axis as a central node integrating multiple signaling networks that govern bone formation and homeostasis.

18. 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.

19. 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.

20. 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.

Human Phosphoinositide-3-Kinase, Catalytic, alpha Polypeptide (PIK3CA) interaction partners

1. 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.

2. 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.

3. 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.

4. These results showed high concordance between detection of PIK3CA mutations in tumor tissue and in corresponding serum circulating tumor DNA.

5. Increased PIK3CA expression is associated with Colorectal Cancer.

6. 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.

7. Letter: PIK3CA mutation, in particular, mutation of exon 9, has a significant positive association with KRAS mutation in colorectal cancer.

8. PIK3CA mutations are found in benign overgrowth syndromes, collectively known as PIK3CA-related overgrowth spectrum. (Review)

9. Gene alterations, such as TP53 mutation, PIK3CA mutation, ERBB2 amplification and CCND1 amplification, and MAPK pathway alteration were associated with pCR in our study.

10. 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.

11. This overgrowth syndrome is unique and is caused by the somatic PIK3CA mutation c.3140A>G.

12. 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.

13. TRAF6 is a novel PIK3CA regulator whose deregulated overexpression represents a mechanism for PI3K overactivation in tumors.

14. A high proportion of isolated macrodactyly patients carry a PIK3CA mutation.

15. This study detected gain-of-function mutations in exon 20 of PI3KCA gene in 11% of gastric cancer patients.

16. 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.

17. 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.

18. High PIK3CA expression is associated with hepatocellular carcinoma.

19. 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.

20. 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.

Cow (Bovine) Phosphoinositide-3-Kinase, Catalytic, alpha Polypeptide (PIK3CA) interaction partners

1. Data show that both class I and III phosphoinositide 3-kinases (PI3Ks) re present in trafficking vesicles.

2. There are multiple conformations in equilibrium during the course of PI3K SH3 domain unfolding.

3. PI3K has a role in activation of 5'-AMP-activated kinase during hypoxia-reoxygenation of bovine aortic endothelial cells

4. Production of PtdIns3P by PI3K-C2alpha is required for acquisition of fusion competence in neurosecretion.

5. crystallographic and biochemical approaches used to gain insight into activating mutations in two noncatalytic p110alpha domains-the adaptor-binding and the helical domains