SOS-mediated nucleotide exchange on RAS downstream of PDGFRA extracellular domain dimers

Stable Identifier
Reaction [transition]
Homo sapiens
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SOS-mediated nucleotide exchange on RAS is likely promoted by extracellular domain mutants of PDGFRA, as evidenced by the increased levels of phosphorylated MAPK/ERK proteins, although the details have not been fully demonstrated (Ozawa et al, 2010; Ip et al, 2018).

Literature References
PubMed ID Title Journal Year
30389923 Neomorphic PDGFRA extracellular domain driver mutations are resistant to PDGFRA targeted therapies

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

Nat Commun 2018
20889717 PDGFRA gene rearrangements are frequent genetic events in PDGFRA-amplified glioblastomas

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

Genes Dev. 2010
Catalyst Activity

guanyl-nucleotide exchange factor activity of p-11Y PDGFRA extracellular domain dimers:GRB2:SOS1 [endoplasmic reticulum membrane]

Functional status

Gain of function of p-11Y PDGFRA extracellular domain dimers:GRB2:SOS1 [endoplasmic reticulum membrane]

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