PTPN11:p-STAT5 dissociates from mutant FLT3

Stable Identifier
R-HSA-9698013
Type
Reaction [dissociation]
Species
Homo sapiens
Compartment
ReviewStatus
5/5
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In the case of FLT3-ITD-dependent BCL2L1 expression, it has been demonstrated that PTPN11 and STAT5 colocalize at the STAT5 binding sites in the promoter, suggesting that this complex dissociates from the receptor and translocates to the nucleus as a unit (Nabinger et al, 2013).
Literature References
PubMed ID Title Journal Year
23103841 The protein tyrosine phosphatase, Shp2, positively contributes to FLT3-ITD-induced hematopoietic progenitor hyperproliferation and malignant disease in vivo

Boswell, HS, Ramdas, B, Feng, GS, Zeng, L, Kapur, R, He, Y, Liu, Z, Zhang, X, Sandusky, GE, Zhang, ZY, Fukuda, S, Li, XJ, Nabinger, SC, Yu, M, Richine, B, Chan, RJ, Goenka, S, Bowling, JD

Leukemia 2013
Participants
Participates
Normal reaction
Functional status

Gain of function of p-6Y FLT3 ITD mutant dimers:GRB2:p-Y GAB2:PTPN11:p-STAT5 [plasma membrane]

Status
Disease
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
Authored
Reviewed
Created
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