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Literature summary for 2.7.1.137 extracted from

  • Zhao, L.; Vogt, P.K.
    Hot-spot mutations in p110alpha of phosphatidylinositol 3-kinase (PI3K): Differential interactions with the regulatory subunit p85 and with RAS (2010), Cell Cycle, 9, 596-600.
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

Cloned (Comment) Organism
genotyping Homo sapiens

Protein Variants

Protein Variants Comment Organism
additional information identification of hot-spot mutations in gene PIK2CA encoding the catalytic subunit p110alpha of PI3K, gain-of-function mutations allowing the mutant enzyme to constitutvely activate AKT signaling and induce oncogenic transformation in vitro and in vivo, the mutations lead to exchanges in the helical and kinase domains, overview. The gain of function induced by helical domain mutations require RAS-Gtp binding, while the kinase domain mutation is active in absence of RAS-Gtp binding, but depends on the interaction with p85, moleculr mechanisms, overview Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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gene PIK3CA encoding the catalytic subunit p110alpha of PI3K
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Synonyms

Synonyms Comment Organism
PI3K
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Homo sapiens

General Information

General Information Comment Organism
malfunction gene PIK3CA, encoding the catalytic subunit p110alpha of PI3K, is mutated in about 12% of all human cancers, as single point mutations of hot-spot mutation with exchange of three positions, overview Homo sapiens
physiological function the enzyme activates Akt signaling Homo sapiens