Extracellular- , juxtamembrane- and kinase-domain mutants of KIT have been shown to signal through the STAT pathway, although the biological relevance or each STAT isoform varies between tumor types (Brizzi et al, 1999; Ning et al, 2001; Frost et al, 2002; Growney et al, 2005; Hara et al, 2017; Obata et al, 2017; Duensing et al, 2004; Bauer et al, 2007; Deberry et al, 1997; Ronnstrand, 2004). Although the pathway details haven't been examined in all cases, STAT pathway activation likely occurs through the recruitment of JAK2 and SRC family kinases, as is the case for the wild type receptor (reviewed in Lennartsson and Roonstrand, 2012).
Rönnstrand, L, Lennartsson, J
McConarty, B, Medeiros, F, Fletcher, JA, Demetri, GD, Singer, S, Fletcher, CD, Panigrahy, D, Joseph, NE, Duensing, A
Akieda, Y, Abe, R, Obata, Y, Nishida, T, Esumi, H, Fletcher, JA, Takahashi, T, Tsujimoto, M, Horikawa, K
Shiina, I, Murata, T, Abe, R, Tasaki, Y, Obata, Y, Hara, Y, Suzuki, K, Horikawa, K
Frost, MJ, Ferrao, PT, Hughes, TP, Ashman, LK
Yarden, Y, Dentelli, P, Pegoraro, L, Rosso, A, Brizzi, MF
Rönnstrand, L
DeBerry, C, Linnekin, D, Mou, S
Arceci, RJ, Li, J, Ning, ZQ
Demetri, GD, Bauer, S, Fletcher, JA, Duensing, A
Griffin, JD, Gilliland, DG, Adelsperger, J, Fabbro, D, Clark, JJ, Stone, R, Growney, JD
Gain of function of KIT mutant dimers:SFKs:p-JAK2 [plasma membrane]
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