anti-PIK3CA (PIK3CA) 抗体产品概述

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

1. The RAS-PI3K interaction is an important signaling node and potential therapeutic target in EGFR-mutant lung cancer.

2. High PI3KCA expression is associated with brain cancer.

3. Despite the induction of oxidative and metabolic stresses, Shp2 deletion in hepatocytes suppressed hepatocarcinogenesis driven by overexpression of oncoproteins MET/CAT or MET/PIK. Shp2 loss inhibited proliferative signaling from c-Met, Wnt/beta-catenin, Ras/Erk and PI3K/Akt pathways, but triggered cell senescence following exogenous expression of the oncogenes.

4. present study highlighted that overexpression of miR-203 may function as a cardioprotective regulator in DCM by targeting PIK3CA via inactivation of PI3K/Akt signaling pathway.

5. The major role in stimulation of the synthesis of granulocytic CSF during stressful stimulation is played by PI3K/Akt signaling cascade.

6. 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]

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

8. 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.

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

10. 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).

11. 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.

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

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

14. 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.

15. 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.

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

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

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

19. 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

20. 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.

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

1. The RAS-PI3K interaction is an important signaling node and potential therapeutic target in EGFR-mutant lung cancer.

2. The data suggest that tumourigenic alterations in the PI3K/AKT-pathway are indispensable in hidradenoma papilliferum (HP) and establish a homogenous morphomolecular entity with a functionally converging and selecting tumourigenic mechanism.

3. PIK3CA mutations might be involved in GC development and might be used as favorable prognostic factor in GC population with low PIK3CA mutations prevalence.

4. Our results indicate that a high proportion of isolated macrodactyly patients carry a pathogenic PIK3CA mutation.

5. Herein, we present a case of PROS that reflects the great variability of cutaneous manifestations associated with this disease spectrum, many of which were found in our patient.

6. there is a difference in PIK3CA mutation, COX-2 expression, and paraneoplastic thromboembolism between ovarian clear cell carcinomas with a different stroma.

7. Linc-ROR is highly expressed in the ectopic endometrium of adenomyosis, and it can promote the proliferative activity of endometrial cells by activating the PI3K-Akt pathway.

8. Taselisib plus fulvestrant had clinical activity irrespective of PIK3CA mutation status, with numerically higher objective response rate and clinical benefit rate in patients with PIK3CA-mutated (vs. -MND) locally advanced or metastatic HER2-negative, HR-positive breast cancer. No new safety signals were reported.

9. 9p21.3 (CDKN2A) loss and PIK3CA mutation characterize a subgroup of metaplastic breast cancers with myoepithelial and spindle cell differentiation.

10. These results demonstrate the dynamical and structural effects induced by the p110alpha E545K mutation in atomic level detail and indicate a possible mechanism for the loss of regulation that E545K confers on PI3Kalpha.

11. IL1B promotes the nuclear translocaiton of S100A4 protein in gastric cancer cells and the cell's stem-like properties through PI3K pathway.

12. This study determined the mutation frequencies and prognostic values of KRAS exon 2, 3 and 4, NRAS exon 2 and 3, PIK3CA exon 9 and 20, and BRAF exon 15 by PCR and direct sequencing in 353 colorectal cancer patients from two Chinese clinical centers.

13. Study shows that ARQ092 counteracts overactivation of PI3K signal pathway in primary fibroblast cells derived from patients with PIK3CA-related overgrowth spectrum.

14. We detected the same PIK3CA mutation in her affected tissue, urine, and tumor, indicating Wilms tumors probably arise from PIK3CA mutant cells in patients with CLOVES. No urine sample from a participant with Klippel-Trenaunay (KTS) had detectable PIK3CA mutations.

15. Expression of Phosphoinositide 3-Kinase p110alpha and p110beta Subunits and PIK3CA Mutation in Patients With Advanced Gastric Carcinoma.

16. To investigate the reasons for which miR-375 holds a special place among circulating miRNAs in Acute myocardial infarction (MI), enrichment and network analyses of miR-375 target genes and their interactions were carried out. PIK3CA and TP53 genes, regulated by miR-375, were identified as the key players of MI disease module.

17. We report the first characterization of clinical acquired resistance to MEKi + CDK4i, identifying a rare preexisting PIK3CA(E545K) subpopulation that expands upon therapy and exhibits drug resistance.

18. Data suggest that receptor-tyrosine kinase HEK2 (EphB3) and phosphatidylinositol 3-kinase catalytic alpha polypeptide (PIK3CA) are cooperating oncogenes that contribute toward its pathogenesis.

19. THE DIAGNOSIS AND RELAPSE PREDICTION OF PATIENTS WITH NON-MUSCLE INVASIVE BLADDER CANCER WITH FGFR3,TP53 AND PIK3CA GENE MUTATION POSSESSED HIGH ACCURACY

20. Results show PIK3CA mutation correlates with poor prostate cancer prognosis and causes prostate cancer in mice. Moreover, PIK3CA mutation and PTEN loss coexist in prostate cancer and can cooperate in vivo to accelerate tumorigenesis and facilitate castration-resistant prostate cancer.

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

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