FLT3 fusions activate STAT5

Stable Identifier
R-HSA-9703435
Type
Reaction [omitted]
Species
Homo sapiens
Compartment
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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

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

2009
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
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, Zhang, L, Russell, NH, Cross, NC, Chase, A, Iqbal, S

2007
Participants
Participates
Disease
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
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