ArticleThe Biochemical journal2005
Specific role for p85/p110beta in GTP-binding-protein-mediated activation of Akt.
Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Class I PI3K Biology.Current topics in microbiology and immunology · 2022Article
- PI3Kβ-A Versatile Transducer for GPCR, RTK, and Small GTPase Signaling.Endocrinology · 2019Review
- TGX-221 inhibits proliferation and induces apoptosis in human glioblastoma cells.Oncology reports · 2017Article
- PI3K in cancer: divergent roles of isoforms, modes of activation and therapeutic targeting.Nature reviews. Cancer · 2015Review
- Review
- PIKfyve regulates the endosomal localization of CpG oligodeoxynucleotides to elicit TLR9-dependent cellular responses.PloS one · 2013Article
- Clinical development of phosphatidylinositol 3-kinase inhibitors for cancer treatment.BMC medicine · 2012Review
- A beta version of life: p110β takes center stage.Oncotarget · 2010Review
- The emerging mechanisms of isoform-specific PI3K signalling.Nature reviews. Molecular cell biology · 2010Review
- The regulation of class IA PI 3-kinases by inter-subunit interactions.Current topics in microbiology and immunology · 2010Review
- PTEN-deficient cancers depend on PIK3CB.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- The p110beta isoform of phosphoinositide 3-kinase signals downstream of G protein-coupled receptors and is functionally redundant with p110gamma.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Evidence for functional redundancy of class IA PI3K isoforms in insulin signalling.The Biochemical journal · 2007Article
- Article
- Oncogenic transformation induced by the p110beta, -gamma, and -delta isoforms of class I phosphoinositide 3-kinase.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We prepared CHO (Chinese hamster ovary) cells expressing both IR (insulin receptor) and A1R (A1 adenosine receptor). Treatment of the cells with insulin or PIA [N6-(2-phenylisopropyl)adenosine], a specific A(1)R agonist increased Akt activity in the cells in a PI3K- (phosphoinositide 3-kinase) dependent manner. Transfection of p110beta into the cells augmented the action of PIA with little effect on insulin. Introduction of a pH1 vector producing shRNA (short hairpin RNA) that targets p110beta abolished PIA-induced Akt activation. By contrast, an shRNA probe targeting p110alpha did not impair the effects of PIA. The effect of PIA in p110alpha-deficient cells was attenuated effectively by both Deltap85 and betaARK-CT (beta-adrenergic receptor kinase-C-terminal peptide). A Deltap85-derived protein possessing point mutations in its two SH2 domains did not impair PIA action. These results suggest that tyrosine-phosphorylated proteins and Gbetagamma (betagamma subunits of GTP-binding protein) are necessary for the specific function of p110beta in intact cells. The p110beta-middle (middle part of p110beta) may play an important role in signal reception from GPCRs (GTP-binding-protein-coupled receptor), because transfection of the middle part impaired PIA sensitivity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.