PI3-kinase binds to mutant PDGFR receptor

Stable Identifier
Reaction [binding]
Homo sapiens
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Gain-of-function mutants of PDGFRA bind to phosphatidylinositol-3' kinase (PI3K) to activate AKT signaling, as assessed by the presence of phosphorylated AKT in Western blot analysis (Heinrich et al, 2003; Ohashi et al, 2004; reviewed in Corless et al, 2011). Interaction of PI3K with mutant PDGFRA receptors is assumed to occur through binding to phosphorylated Y731 and Y742 as is the case for the wild-type receptor, although this hasn't been directly demonstrated (reviewed in Roskoski, 2018).

Literature References
PubMed ID Title Journal Year
22089421 Gastrointestinal stromal tumours: origin and molecular oncology

Barnett, CM, Corless, CL, Heinrich, MC

Nat. Rev. Cancer 2011
29408302 The role of small molecule platelet-derived growth factor receptor (PDGFR) inhibitors in the treatment of neoplastic disorders

Roskoski, R

Pharmacol. Res. 2018
15221957 Different inhibitory effect of imatinib on phosphorylation of mitogen-activated protein kinase and Akt and on proliferation in cells expressing different types of mutant platelet-derived growth factor receptor-alpha

Kitamura, Y, Shinomura, Y, Isozaki, K, Nishida, T, Kinoshita, K, Ohashi, A, Hirota, S

Int. J. Cancer 2004
12522257 PDGFRA activating mutations in gastrointestinal stromal tumors

Corless, CL, Heinrich, MC, Singer, S, Griffith, DJ, Town, A, Haley, A, Duensing, A, McGreevey, L, Fletcher, JA, Demetri, GD, Joseph, N, Chen, CJ, Fletcher, CD

Science 2003
Normal reaction
Functional status

Gain of function of p-11Y PDGFR mutant receptor dimers [plasma membrane]

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