ArticleCell cycle (Georgetown, Tex.)2011
Addition of N-terminal peptide sequences activates the oncogenic and signaling potentials of the catalytic subunit p110α of phosphoinositide-3-kinase.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Epinephrine inhibits PI3Kα via the Hippo kinases.Cell reports · 2023Article
- Domain analysis reveals striking functional differences between the regulatory subunits of phosphatidylinositol 3-kinase (PI3K), p85α and p85β.Oncotarget · 2017Article
- Insights into the pathological mechanisms of p85α mutations using a yeast-based phosphatidylinositol 3-kinase model.Bioscience reports · 2017Article
- Enzyme activity effects of N-terminal His-tag attached to catalytic sub-unit of phosphoinositide-3-kinase.Bioscience reports · 2013Article
- Oncogenic mutations of p110α isoform of PI 3-kinase upregulate its protein kinase activity.PloS one · 2013Article
- G protein-coupled receptor-mediated activation of p110β by Gβγ is required for cellular transformation and invasiveness.Science signaling · 2012Article
- Retroviral oncogenes: a historical primer.Nature reviews. Cancer · 2012Review
- Functional characterization of an isoform-selective inhibitor of PI3K-p110β as a potential anticancer agent.Cancer discovery · 2012Article
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Authors and funding
5 authors.
Funding
Abstract
Addition of short (6 to 16 amino acids) peptide sequences to the N-terminus of p110α induces a gain of function. Such sequences include the common Flag, His, and VSV tags as well as random sequences. An N-terminal myristylation signal generally believed to activate p110α by providing a constitutive membrane address is also activating, if myristylation is mutationally abolished. The gain of function seen with N-terminally tagged (NTT) p110α constructs extends to signaling, oncogenic transformation and stimulation of cell growth. The activating effect of N-terminal tags requires a functional Ras-binding domain in p110α. Mutations in that domain (T208D and K227A) abolish the gains of function in oncogenicity and signaling. The dominant negative mutant of Ras, RasN17, interferes with transformation induced by NTT p110α. In contrast, binding to p85 activity is not required for cellular transformation and enhanced signaling by NTT p110α.
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