gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Phosphoinositide-3-kinase, class 2, beta polypeptide

PI3K-C2beta, phosphoinositide 3-kinase C2beta, PIK3C2B
The protein encoded by this gene belongs to the phosphoinositide 3-kinase (PI3K) family. PI3-kinases play roles in signaling pathways involved in cell proliferation, oncogenic transformation, cell survival, cell migration, and intracellular protein trafficking. This protein contains a lipid kinase catalytic domain as well as a C-terminal C2 domain, a characteristic of class II PI3-kinases. C2 domains act as calcium-dependent phospholipid binding motifs that mediate translocation of proteins to membranes, and may also mediate protein-protein interactions. The PI3-kinase activity of this protein is sensitive to low nanomolar levels of the inhibitor wortmanin. The C2 domain of this protein was shown to bind phospholipids but not Ca2+, which suggests that this enzyme may function in a calcium-independent manner. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: PI3K, Akt, CAN, EGFR, V1a
Papers on PI3K-C2beta
Ropinirole alters gene expression profiles in SH-SY5Y cells: a whole genome microarray study.
Jin et al., Shanghai, China. In Braz J Med Biol Res, Dec 2015
Further pathway analysis revealed modulation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway, with prominent upregulation of PIK3C2B.
A seven-gene expression panel distinguishing clonal expansions of pre-leukemic and chronic lymphocytic leukemia B cells from normal B lymphocytes.
Chiorazzi et al., United States. In Immunol Res, Dec 2015
Therefore, we selected FMOD, CKAP4, PIK3C2B, LEF1, PFTK1, BCL-2, and GPM6a from a set of genes significantly differentially expressed in microarray analyses that compared CLL cells with normal B lymphocytes and used these to determine whether we could discriminate CLL and MBL cells from B cells of healthy controls.
Association of Factor V Secretion with Protein Kinase B Signaling in Platelets from Horses with Atypical Equine Thrombasthenia.
Tablin et al., Leesburg, United States. In J Vet Intern Med, Sep 2015
Washed platelets were examined for (1) expression of the αIIb-β3 integrin; (2) fibrinogen binding capacity in response to ADP and thrombin; (3) secretion of dense and α-granules; (4) activation of the mammalian target of rapamycin (mTOR)-protein kinase B (AKT) signaling pathway; and (5) cellular distribution of phosphatidylinositol-4-phosphate-3-kinase, class 2B (PIK3C2B) and SH2 containing inositol-5'-phosphatase 1 (SHIP1).
Gene expression in skeletal muscle after an acute intravenous GH bolus in human subjects: identification of a mechanism regulating ANGPTL4.
Jessen et al., Århus, Denmark. In J Lipid Res, 2013
Four genes involved in the JAK-STAT5 signaling pathway were regulated by GH, including SOCS1-3 and CISH, in addition to three genes associated with insulin action: NFκB1A, PIK3C2B, and PRKAG2.
Polyphyllin I inhibits proliferation and metastasis of ovarian cancer cell line HO-8910PM in vitro.
Su et al., Hangzhou, China. In J Tradit Chin Med, 2013
Real-time PCR (RT-PCR) showed that differential genes PIK3C2B, Caspase 9 and Wnt5A were downregulated with increasing PPI, showing an evident dose-effect relationship.
Identification and Validation of a Putative Polycomb Responsive Element in the Human Genome.
Brahmachari et al., Delhi, India. In Plos One, 2012
In a directed search we identified a potential polycomb responsive element with 25 repeats of YY1 binding motifthatwe designate PRE-PIK3C2B as it occurs in the first intron of human PIK3C2B gene.
Identification of a novel population in high-grade oligodendroglial tumors not deleted on 1p/19q using array CGH.
De Braekeleer et al., Brest, France. In J Neurooncol, 2012
In addition, four recurrent copy number alterations, involving genes that participate to cell growth and cycle, were found to be strongly associated in five tumors not deleted on 1p/19q: gain or amplification at 1q32.1 (MDM4, PIK3C2B genes), 12q14.1 (CDK4 gene), 12q14.3-q15
Identification of somatic mutations in non-small cell lung carcinomas using whole-exome sequencing.
You et al., Milwaukee, United States. In Carcinogenesis, 2012
Of potential immediate clinical relevance, several highly mutated genes identified in our study are promising druggable targets in cancer therapy including ALK, CTNNA3, DCC, MLL3, PCDHIIX, PIK3C2B, PIK3CG and ROCK2.
Tripartite motif containing protein 27 negatively regulates CD4 T cells by ubiquitinating and inhibiting the class II PI3K-C2β.
Skolnik et al., New York City, United States. In Proc Natl Acad Sci U S A, 2012
These findings provide a unique mechanism for regulating class II PI3Ks, and identify TRIM27 as a previously undescribed negative regulator of CD4 T cells.
Gene expression analysis of mammary tissue during fetal bud formation and growth in two pig breeds--indications of prenatal initiation of postnatal phenotypic differences.
Wimmers et al., Germany. In Bmc Dev Biol, 2011
Differential expression was validated by quantitative RT-PCR of five genes (GAB1, MAPK9, PIK3C2B, PIK3C3 and PRKCH) that are involved in several relevant signaling pathways.
Somatic deletions of genes regulating MSH2 protein stability cause DNA mismatch repair deficiency and drug resistance in human leukemia cells.
Evans et al., Memphis, United States. In Nat Med, 2011
Leukemia cells with low levels of MSH2 contained partial or complete somatic deletions of one to four genes that regulate MSH2 degradation (FRAP1 (also known as MTOR), HERC1, PRKCZ and PIK3C2B); we also found these deletions in individuals with adult acute lymphoblastic leukemia (16%) and sporadic colorectal cancer (13.5%).
Myotubularin regulates Akt-dependent survival signaling via phosphatidylinositol 3-phosphate.
Taylor et al., Omaha, United States. In J Biol Chem, 2011
Our data further suggest that inhibition of Akt activation and downstream survival signaling in myotubularin-deficient cells is caused by accumulation of the MTMR substrate lipid phosphatidylinositol 3-phosphate generated from the type II phosphatidylinositol 3-kinase PIK3C2B.
Phosphatidylinositol 3-kinase-C2β inhibits cisplatin-mediated apoptosis via the Akt pathway in oesophageal squamous cell carcinoma.
Yang et al., Zhengzhou, China. In J Int Med Res, 2010
Overexpression of PIK3C2B is associated with esophageal squamous cell carcinoma.
Analysis of human mini-exome sequencing data from Genetic Analysis Workshop 17 using a Bayesian hierarchical mixture model.
Meyers et al., Madison, United States. In Bmc Proc, 2010
One of these 58 genes, PIK3C2B was correctly identified as being associated with affected status based on the simulation process.
Intratumoral patterns of genomic imbalance in glioblastomas.
Ohgaki et al., Lyon, France. In Brain Pathol, 2010
Genetic alterations common to all areas analyzed within a single tumor included gains at 1q32.1 (PIK3C2B, MDM4), 4q11-q12 (KIT, PDGFRA), 7p12.1-11.2
Pooled analysis of phosphatidylinositol 3-kinase pathway variants and risk of prostate cancer.
Berndt et al., Rockville, United States. In Cancer Res, 2010
Pooled data from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium were examined for associations between 89 SNPs in PI3K genes (PIK3C2B, PIK3AP1, PIK3C2A, PIK3CD, and PIK3R3) and prostate cancer risk in 8,309 cases and 9,286 controls.
The class II phosphatidylinositol 3 kinase C2beta is required for the activation of the K+ channel KCa3.1 and CD4 T-cells.
Skolnik et al., New York City, United States. In Mol Biol Cell, 2009
Data show that the class II phosphatidylinositol 3 kinase C2beta (PI3K-C2beta) is activated by the T-cell receptor (TCR) and functions upstream of NDPK-B to activate KCa3.1 channel activity.
Epidermal growth factor stimulates translocation of the class II phosphoinositide 3-kinase PI3K-C2beta to the nucleus.
Domin et al., London, United Kingdom. In Biochem J, 2009
Epidermal growth factor stimulates the appearance of PI3K-C2beta in nuclei.
Phosphoinositide 3-Kinase C2beta regulates cytoskeletal organization and cell migration via Rac-dependent mechanisms.
Arcaro et al., London, United Kingdom. In Mol Biol Cell, 2006
These findings suggest that PI3KC2beta regulates the migration and survival of human tumor cells by distinct molecular mechanisms.
share on facebooktweetadd +1mail to friends