p-STAT5 dissociates from FLT3 fusion proteinsp-

Stable Identifier
R-HSA-9703432
Type
Reaction [omitted]
Species
Homo sapiens
Compartment
ReviewStatus
5/5
Locations in the PathwayBrowser
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Phosphorylated STAT5 is released from the receptor to fulfill its role as a nuclear transcription factor (Grand et al, 2007; Vu et al, 2009; Chonabayshi et al, 2013; reviewed in Murphy and Rani, 2015; Kazi and Roonstrand, 2019).
Literature References
PubMed ID Title Journal Year
31066629 FMS-like Tyrosine Kinase 3/FLT3: From Basic Science to Clinical Implications

Kazi, JU, Rönnstrand, L

Physiol. Rev. 2019
19345670 The juxtamembrane domain in ETV6/FLT3 is critical for PIM-1 up-regulation and cell proliferation

Xinh, PT, Vu, HA, Kano, Y, Tokunaga, K, Sato, Y

2009
26716518 STAT5 in Cancer and Immunity

Murphy, JJ, Rani, A

J. Interferon Cytokine Res. 2016
17764812 A constitutively active SPTBN1-FLT3 fusion in atypical chronic myeloid leukemia is sensitive to tyrosine kinase inhibitors and immunotherapy

Grand, FH, Zhang, L, Russell, NH, Cross, NC, Chase, A, Iqbal, S

2007
23168613 Direct binding of Grb2 has an important role in the development of myeloproliferative disease induced by ETV6/FLT3

Ishikawa, T, Kawamata, S, Ohno, T, Chonabayashi, K, Hishizawa, M, Uchiyama, T, Nagai, Y, Takaori-Kondo, A

Leukemia 2013
Participants
Participates
Disease
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
Authored
Reviewed
Created
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