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Details on Person After activation, FGFR point and translocation mutants are p...
| Class:Id | Summation:9753845 |
|---|---|
| _displayName | After activation, FGFR point and translocation mutants are p... |
| _timestamp | 2021-09-15 23:46:04 |
| created | [InstanceEdit:9753846] Rothfels, Karen, 2021-09-15 |
| modified | [InstanceEdit:9753867] Rothfels, Karen, 2021-09-15 |
| text | After activation, FGFR point and translocation mutants are presumed to recruit FRS2 (also known as FRS2alpha). This has been demonstrated in some cases (see for instance Ahmed, 2008; Weiss, 2010; Dutt, 2008; Dutt, 2011; Cha, 2009; Qing, 2009; Bai, 2010 ) and is inferred to occur in others by analogy with the wild-type receptor. Similarly, FGFR3 fusions appear in most cases to promote tumorigenesis and proliferation through the ERK, STAT and AKT pathways suggesting that, as is the case for the wild type receptor, FRS2 is recruited to the phosphorylated receptor (Williams et al, 2013; Parker et al, 2013; Wu et al, 2013; reviewed in Parker et al, 2014; Carter et al, 2015). In contrast, one study reports inhibition of the ERK signaling pathway by FGFR3 fusion proteins. This study supports a model in which the fusion proteins promote chromosomal instability (Singh et al, 2012). |
| (summation) | [Reaction:5655262] Activated FGFR3 point, translocation and fusion mutants bind FRS2 [Homo sapiens] |
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