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Human FLT3 ELISA Kit for Sandwich ELISA - ABIN416723
Feng, Xu, Zhou, Wang, Liu, Wu, Yuan, Che: Alpha-1 Antitrypsin Prevents the Development of Preeclampsia Through Suppression of Oxidative Stress. in Frontiers in physiology 2016
Tumor necrosis factor (TNF (显示 TNF ELISA试剂盒)), 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 (显示 VEGFA ELISA试剂盒) Egfl7 (显示 EGFL7 ELISA试剂盒) activates the Flt3/Flt3 ligand (显示 FLT3LG ELISA试剂盒) 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 (显示 HOXA9 ELISA试剂盒)- and Meis1 (显示 MEIS1 ELISA试剂盒)-associated upregulation of Flt3 is a passive event with regard to leukemia development in mice and with limited relevance to the AML (显示 RUNX1 ELISA试剂盒) pathology.
lineage-specific STAT5 (显示 STAT5A ELISA试剂盒) activation in hematopoietic progenitor cells predicts the FLT3(+)-mediated leukemic phenotype in mice
DOCK2 (显示 DOCK2 ELISA试剂盒) is a potential therapeutic target for novel AML (显示 RUNX1 ELISA试剂盒) 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 (显示 MLXIP ELISA试剂盒)-155 influences the development of FLT3-ITD-induced myeloproliferative disease. miR (显示 MLXIP ELISA试剂盒)-155 promotes FLT3-ITD-induced myeloid expansion in the bone marrow, spleen, and peripheral blood. Mechanistically, miR (显示 MLXIP ELISA试剂盒)-155 increases proliferation of the hematopoietic stem and progenitor cell compartments by reducing the growth-inhibitory effects of the interferon (显示 IFNA ELISA试剂盒) response.
Overexpression of Abl (显示 ABL1 ELISA试剂盒)-related gene tyrosine kinase (显示 TYRO3 ELISA试剂盒) 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 (显示 PBX1 ELISA试剂盒) axis
Data indicate that most Fms-like tyrosine kinase-3 (FLT3) tyrosine kinase (显示 TYRO3 ELISA试剂盒) inhibitors (TKI) effectively target wild-type FLT3 signaling.
FLT3/ITD increases aerobic glycolysis through AKT (显示 AKT1 ELISA试剂盒)-mediated upregulation of mitochondrial hexokinase (HK2 (显示 HK2 ELISA试剂盒)). Inhibition of glycolysis preferentially causes severe ATP depletion and massive cell death in FLT3/ITD leukemia cells.
Our results indicate that CD4 (显示 CD4 ELISA试剂盒) expression and older age are adverse prognostic factors in wild-type NPM1 (显示 NPM1 ELISA试剂盒), FLT3-ITD-negative CN-AML (显示 RUNX1 ELISA试剂盒).
FLT3 mutation is associated with Metaplastic Breast Cancer.
Collectively, we have developed a novel targeted therapeutic strategy, using FLT3L (显示 FLT3LG ELISA试剂盒)-guided miR (显示 MLXIP ELISA试剂盒)-150-based nanoparticles, to treat FLT3-overexpressing AML (显示 RUNX1 ELISA试剂盒) with high efficacy and minimal side effects.
Y842 is critical for FLT3-mediated RAS/ERK (显示 EPHB2 ELISA试剂盒) signaling and cellular transformation.
value of FLT3-ITD allelic ratio in AML (显示 RUNX1 ELISA试剂盒) in risk assessment and evaluating prognosis
Gedatolisib significantly extended survival of mice in a sorafenib-resistant acute myeloid leukemia (显示 BCL11A ELISA试剂盒) (AML (显示 RUNX1 ELISA试剂盒)) patient-derived xenograft model. Taken together, our data suggest that aberrant activation of the PI3K (显示 PIK3CA ELISA试剂盒)/mTOR (显示 FRAP1 ELISA试剂盒) pathway in FLT3-ITD-dependent AML (显示 RUNX1 ELISA试剂盒) results in resistance to drugs targeting FLT3.
HHEX (显示 HHEX ELISA试剂盒) could replace RUNX1 (显示 RUNX1 ELISA试剂盒) in cooperating with FLT3-ITD to induce Acute myeloid leukemia (显示 BCL11A ELISA试剂盒) (AML (显示 RUNX1 ELISA试剂盒)).
mutated FLT3-ITD and JAK2 (显示 JAK2 ELISA试剂盒) augment reactive oxygen species production and homologous recombination, shifting the cellular milieu toward illegitimate recombination.
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