FLT3 fusions activate STAT5

Stable Identifier
Reaction [omitted]
Homo sapiens
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Active FLT3 fusions promote signaling through the STAT5 pathway as assessed by Western blotting against phosphorylated STAT5 (Grand et al, 2007; Vu et al, 2009; Chonabayashi et al, 2013; reviewed in Kazi and Roonstrand, 2019). In studies with the ETV6-FLT3 fusion EF1, STAT5 activation was shown to depend on tyrosine residues in the juxtamembrane domain and tyrosine kinase domain 1 region of FLT3 (Vu et al, 2009).

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
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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