PI3K catalyses the phosphorylation of PIP2 to PIP3 downstream of PDGFRA extracellular domain dimers

Stable Identifier
Reaction [transition]
Homo sapiens
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Gain-of-function extracellular domain mutants of PDGFRA signal through the PI3K/AKT signaling pathway as assessed by the increase in phosphorylated AKT, although all the pathway steps have not been directly demonstrated (Ozawa et al, 2010; Ip et al, 2018).

Literature References
PubMed ID Title Journal Year
20889717 PDGFRA gene rearrangements are frequent genetic events in PDGFRA-amplified glioblastomas

Ozawa, T, Brennan, CW, Wang, L, Squatrito, M, Sasayama, T, Nakada, M, Huse, JT, Pedraza, A, Utsuki, S, Yasui, Y, Tandon, A, Fomchenko, EI, Oka, H, Levine, RL, Fujii, K, Ladanyi, M, Holland, EC

Genes Dev. 2010
30389923 Neomorphic PDGFRA extracellular domain driver mutations are resistant to PDGFRA targeted therapies

Ip, CKM, Ng, PKS, Jeong, KJ, Shao, SH, Ju, Z, Leonard, PG, Hua, X, Vellano, CP, Woessner, R, Sahni, N, Scott, KL, Mills, GB

Nat Commun 2018
Catalyst Activity

phosphatidylinositol-4,5-bisphosphate 3-kinase activity of p-11Y PDGFRA extracellular domain dimers:PI3K [endoplasmic reticulum membrane]

Functional status

Gain of function of p-11Y PDGFRA extracellular domain dimers:PI3K [endoplasmic reticulum membrane]

Disease Entity
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
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