Associated Papers
Discriminating activating, deactivating and resistance variants in protein kinases.
Singh G et al.
Genome Medicine, 2025
41152984 (PubMed )
Supplement: 13073_2025_1564_MOESM2_ESM.xlsx › Table_S5
TET2-mediated mRNA demethylation regulates leukemia stem cell homing and self-renewal.
Li Y et al.
Cell Stem Cell, 2023
Cytoplasmic NEAT1 Suppresses AML Stem Cell Self-Renewal and Leukemogenesis through Inactivation of Wnt Signaling.
Yan H et al.
Advanced Science (weinheim, Baden-wurttemberg, Germany), 2021
Megakaryocytic Expansion in Gilteritinib-Treated Acute Myeloid Leukemia Patients Is Associated With AXL Inhibition.
Suknuntha K et al.
Frontiers in Oncology, 2020
Src-like adaptor protein 2 (SLAP2) binds to and inhibits FLT3 signaling.
Moharram SA et al.
Oncotarget, 2016
Casitas B-lineage lymphoma mutants activate AKT to induce transformation in cooperation with class III receptor tyrosine kinases.
Polzer H et al.
Experimental Hematology, 2013
Src-Like adaptor protein (SLAP) binds to the receptor tyrosine kinase Flt3 and modulates receptor stability and downstream signaling.
Kazi JU et al.
Plos One, 2012
The juxtamembrane domain in ETV6/FLT3 is critical for PIM-1 up-regulation and cell proliferation.
Vu HA et al.
Biochemical and Biophysical Research Communications, 2009
Transformation by oncogenic mutants and ligand-dependent activation of FLT3 wild-type requires the tyrosine residues 589 and 591.
Vempati S et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2008
Src family tyrosine kinases phosphorylate Flt3 on juxtamembrane tyrosines and interfere with receptor maturation in a kinase-dependent manner.
Mitina O et al.
Annals of Hematology, 2007
Internal tandem duplication of the FLT3 gene is a novel modality of elongation mutation which causes constitutive activation of the product.
Kiyoi H et al.
Leukemia, 1998
Select a paper to view details