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Flt3 and cooperating Flt3/Runx1 mutations cause hematopoietic stem cell depletion and myeloid progenitor expansion during adult but not fetal stages of murine development.
Tumor necrosis factor (TNF (show TNF Proteins)), a cell-extrinsic potent negative regulator of hematopoietic stem cells (HSCs), was overexpressed in bone marrow niche cells from FLT3 internal tandem duplications (FLT3 ITDs) mice.
the angiogenic factor (show VEGFA Proteins) Egfl7 (show EGFL7 Proteins) activates the Flt3/Flt3 ligand (show FLT3LG Proteins) pathway and is a key molecular driver enforcing thymus progenitor generation and thereby directly links endothelial cell biology to the production of T cell-based adaptive immunity
the Hoxa9 (show HOXA9 Proteins)- and Meis1 (show MEIS1 Proteins)-associated upregulation of Flt3 is a passive event with regard to leukemia development in mice and with limited relevance to the AML (show RUNX1 Proteins) pathology.
lineage-specific STAT5 (show STAT5A Proteins) activation in hematopoietic progenitor cells predicts the FLT3(+)-mediated leukemic phenotype in mice
DOCK2 is a potential therapeutic target for novel AML (show RUNX1 Proteins) treatments, as this protein regulates the survival of leukemia cells with elevated FLT3 activity and sensitizes FLT3/ITD leukemic cells to conventional antileukemic agents.
Used a genetic model to determine whether miR (show MLXIP Proteins)-155 influences the development of FLT3-ITD-induced myeloproliferative disease. miR (show MLXIP Proteins)-155 promotes FLT3-ITD-induced myeloid expansion in the bone marrow, spleen, and peripheral blood. Mechanistically, miR (show MLXIP Proteins)-155 increases proliferation of the hematopoietic stem and progenitor cell compartments by reducing the growth-inhibitory effects of the interferon (show IFNA Proteins) response.
Overexpression of Abl (show ABL1 Proteins)-related gene tyrosine kinase (show TYRO3 Proteins) ABL2 in pro-B cell line Ba/F3 cells expressing an oncogenic mutant of FLT3 (FLT3-ITD) resulted in partial inhibition of FLT3-ITD-dependent cell proliferation.
Sorafenib-resistant leukemia cells with a FLT3/ITD mutation are sensitive to glycolytic inhibitors.
FLT3-ITD is capable of inhibiting FLT3-ITD+ cell proliferation through the p21/Pbx1 (show PBX1 Proteins) axis
Although transient responses to FLT3 inhibitors are often observed in case of disease relapse, the most promising approach is the use of FLT3 inhibitors either in combination with induction chemotherapy or as consolidation/maintenance therapy after allogeneic hematopoietic cell transplantation.
In this review, we focus on three key areas in acute myeloid leukemia (show BCL11A Proteins) (AML (show RUNX1 Proteins)) developmental therapeutics: FLT3 inhibitors, IDH(IDH1 (show IDH1 Proteins) and IDH2 (show IDH2 Proteins) ) inhibitors, and drugs that may be particularly beneficial in secondary AML (show RUNX1 Proteins)
Concomitant monitoring of WT1 (show WT1 Proteins) and FLT3-ITD expression in FLT3-ITD acute myeloid leukemia (show BCL11A Proteins) patients
FLT3/ITD are present at leukemic stem cells level and may be a primary and not secondary event in leukemogenesis, and the oncogenic events of FLT3/ITD happen at a cell stage possessing CD123 (show IL3RA Proteins)
Sorafenib may enable cure of a proportion of very poor risk FLT3-internal tandem duplication-positive acute emyeloid leukemia relapsing after allogeneic stem cell transplantation.
Results provide evidence that mutations in the tyrosine kinase (show TXK Proteins) domain in FLT3 were found in 7% of Pakistani patients with acute myeloid leukemia (show BCL11A Proteins).
FLT3/ITD increases aerobic glycolysis through AKT (show AKT1 Proteins)-mediated upregulation of mitochondrial hexokinase (HK2 (show HK2 Proteins)). Inhibition of glycolysis preferentially causes severe ATP depletion and massive cell death in FLT3/ITD leukemia cells.
Our results indicate that CD4 (show CD4 Proteins) expression and older age are adverse prognostic factors in wild-type NPM1 (show NPM1 Proteins), FLT3-ITD-negative CN-AML (show RUNX1 Proteins).
FLT3 mutation is associated with Metaplastic Breast Cancer.
Collectively, we have developed a novel targeted therapeutic strategy, using FLT3L (show FLT3LG Proteins)-guided miR (show MLXIP Proteins)-150-based nanoparticles, to treat FLT3-overexpressing AML (show RUNX1 Proteins) with high efficacy and minimal side effects.
This gene encodes a class III receptor tyrosine kinase that regulates hematopoiesis. The receptor consists of an extracellular domain composed of five immunoglobulin-like domains, one transmembrane region, and a cytoplasmic kinase domain split into two parts by a kinase-insert domain. The receptor is activated by binding of the fms-related tyrosine kinase 3 ligand to the extracellular domain, which induces homodimer formation in the plasma membrane leading to autophosphorylation of the receptor. The activated receptor kinase subsequently phosphorylates and activates multiple cytoplasmic effector molecules in pathways involved in apoptosis, proliferation, and differentiation of hematopoietic cells in bone marrow. Mutations that result in the constitutive activation of this receptor result in acute myeloid leukemia and acute lymphoblastic leukemia.
fms-related tyrosine kinase 3
, FL cytokine receptor-like
, FL cytokine receptor
, fetal liver kinase 2
, receptor-type tyrosine-protein kinase FLT3
, tyrosine-protein kinase FLT3
, tyrosine-protein kinase receptor flk-2
, CD135 antigen
, fms-like tyrosine kinase 3
, growth factor receptor tyrosine kinase type III
, stem cell tyrosine kinase 1
, FMS-like tyrosine kinase 3