p-STAT5 dissociates from FLT3 fusion proteinsp-

Stable Identifier
Reaction [omitted]
Homo sapiens
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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
19345670 The juxtamembrane domain in ETV6/FLT3 is critical for PIM-1 up-regulation and cell proliferation

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

31066629 FMS-like Tyrosine Kinase 3/FLT3: From Basic Science to Clinical Implications

Kazi, JU, Rönnstrand, L

Physiol. Rev. 2019
26716518 STAT5 in Cancer and Immunity

Rani, A, Murphy, JJ

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

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

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

Leukemia 2013
Participant Of
Name Identifier Synonyms
cancer 162 malignant tumor, malignant neoplasm, primary cancer
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