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Literature summary for 2.7.1.67 extracted from

  • Alli-Balogun, G.O.; Gewinner, C.A.; Jacobs, R.; Kriston-Vizi, J.; Waugh, M.G.; Minogue, S.
    Phosphatidylinositol 4-kinase IIbeta negatively regulates invadopodia formation and suppresses an invasive cellular phenotype (2016), Mol. Biol. Cell, 27, 4033-4042 .
    View publication on PubMedView publication on EuropePMC
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Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
ATP + 1-phosphatidyl-1D-myo-inositol Homo sapiens
-
 ADP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
-
 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
HeLa cell
-
 Homo sapiens
-
MCF-7 cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
ATP + 1-phosphatidyl-1D-myo-inositol
-
 Homo sapiens ADP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
-
 ?

Synonyms

Synonyms Comment Organism
phosphatidylinositol 4-kinase IIbeta
-
 Homo sapiens
PI4KII
-
 Homo sapiens
type II phosphatidylinositol 4-kinase
-
 Homo sapiens

General Information

General Information Comment Organism
malfunction loss of the PI4K2B allele and underexpression of isoform PI4KIIbeta mRNA are associated with human cancers. Depletion of isoform PI4KIIbeta is sufficient to confer an aggressive invasive phenotype on minimally invasive HeLa and MCF-7 cell lines. Loss of isoform PI4KIIbeta induces the formation of invadopodia and leads to increased exocytic trafficking of membrane type I matrix metalloproteinase Homo sapiens
physiological function isoform PI4KIIbeta synthesizes a pool of 1-phosphatidyl-1D-myo-inositol 4-phosphate that maintains membrane type I matrix metalloproteinase traffic in the degradative pathway and suppresses the formation of invadopodia Homo sapiens