FLT3 (Phospho_Tyr591) Antibody
- Known as:
- FLT3 (Phospho_Tyr591) Antibody
- Catalog number:
- E012078-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- FLT3 (Phospho_Tyr591) Antibody
Related genes to: FLT3 (Phospho_Tyr591) Antibody
- Gene:
- FLT3 NIH gene
- Name:
- fms related tyrosine kinase 3
- Previous symbol:
- -
- Synonyms:
- STK1, FLK2, CD135
- Chromosome:
- 13q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-30
- Date modifiied:
- 2019-04-23
Related products to: FLT3 (Phospho_Tyr591) Antibody
Related articles to: FLT3 (Phospho_Tyr591) Antibody
- Chronic inflammation and aging skew hematopoiesis toward myelopoiesis at the expense of lymphoid output. We screened type 2 and anti-inflammatory cytokines to identify extrinsic signals capable of restoring lymphoid lineage commitment in hematopoietic stem and progenitor cells (HSPCs). Interleukin 4 (IL-4) specifically inhibited inflammation-induced myelopoiesis and shifted multipotent progenitor (MPP) differentiation toward the lymphoid lineage. IL-4 activated a signal transducer and activator of transcription 6 (STAT6)-dependent transcriptional program in MPPs, increasing the expression of lymphoid-specific genes. Mechanistically, the receptor tyrosine kinase FMS-like tyrosine kinase 3 (FLT3), which is highly expressed in MPPs, interacted with IL-4Rα to facilitate STAT6 activation. In vivo, IL-4 reversed inflammation-induced hematopoietic imbalance and accelerated lymphoid recovery. In aged mice, IL-4 administration shifted the MPP composition toward a lymphoid bias and restored B and T lymphocyte output. Long-term IL-4 treatment in aged mice improved immune, metabolic, physical, and cognitive functions; these rejuvenating effects were recapitulated by transplantation of IL-4-treated HSPCs. Promoting IL-4 signaling in MPPs may enable correction of hematopoietic dysregulation in inflammatory and aging-related conditions. - Source: PubMed
Publication date: 2026/05/29
Yao JingfeiWang YutingZhang Yi - In a mouse model of FGFR1-driven leukemia, we demonstrated a role for circulating non-conventional monocyte-derived macrophages in the peripheral blood, which suppressed T-cell function and promoted leukemogenesis. A single cell RNA sequencing (scRNA-Seq) analysis of these leukemia-associated macrophages (LAMs) identified LAM-specific dysregulation of gene expression associated with leukemogenesis. Based on the top markers identified in these LAMs, we generated a LAM score based on the expression levels of a 32 gene signature. This scoring system was then applied to the transcriptomic data from a cohort of 838 newly diagnosed patients treated on Alliance/CALGB protocols, who were similarly treated with intensive cytarabine/daunorubicin-based chemotherapy on the CALGB/Alliance for the Clinical Trials in Oncology protocol. Patients were subclassified as those with high and low LAM scores. Patients with a high LAM score had shorter overall survival, disease-free survival and event-free survival compared to those with a low LAM score. We also noted a strong association of FLT3-ITD, RUNX1 and TP53 mutations with high LAM scores. Applying the LAM score to the current European Leukemia Network risk group criteria, independent prognostic implications and a refined prognostic significance of each subgroup were provided, indicating the value of including immune microenvironment data into AML risk stratification. - Source: PubMed
Publication date: 2026/05/29
Nicolet DeedraZhang TingWalker Christopher JAmeyi JusticeMori Stephanie FFang XuexiuZhang LitaoCortes JorgeHedrick Catherine CCowell John KEisfeld Ann-KathrinHu Tianxiang - B-cell Non-Hodgkin Lymphoma (B-NHL) is a group of lymphoid malignancies characterized by dysregulation of lymphocytes and monocytes. CD135/FLT3 (FMS-like tyrosine kinase 3) and its ligand (FLT3LG) play crucial roles in white blood cell (WBC) proliferation, and their ratios are meaningful indicators of treatment response. - Source: PubMed
Publication date: 2026/05/26
Nandasena C KJayathilake P W D C CDharmarathne H A S GKaluarachchi PSuresh SDe Silva A DPerera I CKottahachchi D U - Not available. - Source: PubMed
Publication date: 2026/05/28
Dobrevski BobanMüller Jörg P - In patients with FLT3-mutated AML who receive frontline azacitidine plus venetoclax, relapses are commonly driven by expansion of the FLT3-mutated clone, providing rationale for "triplet" FLT3 inhibitor-based lower-intensity regimens. Here we report long-term outcomes of a phase II study of azacitidine, venetoclax and gilteritinib in adults with newly diagnosed FLT3-mutated AML who were unfit for intensive chemotherapy. Thirty patients were treated; the median age was 71 years, and 22 (73%) had a FLT3-ITD mutation. The complete remission (CR)/CR with incomplete hematologic recovery rate was 96%, and 14 patients (47%) underwent allogeneic hematopoietic stem cell transplantation (HSCT) in first remission. With a median follow-up of 41.5 months, 11 patients (37%) relapsed; in 67% of evaluable relapses, the FLT3 mutation was not detectable. The median RFS and OS were 23.4 and 29.7 months, respectively, and the 3-year RFS and OS rates were 43% and 46%, respectively. Among patients with FLT3-ITD-mutated AML, the median RFS and OS were 17.0 and 21.8 months, respectively, and the 3-year RFS and OS rates were 32% and 36%, respectively. The presence of a baseline RAS pathway mutation was associated with worse outcomes. Survival rates were similar regardless of HSCT in first remission. Among patients who received at least one consolidation cycle, 68% had a reduction in the dose or duration of at least one of the study drugs. The triplet regimen of azacitidine, venetoclax and gilteritinib is associated with durable remissions and encouraging long-term survival. Randomized studies comparing this regimen to standard of care approaches are warranted. This trial is registered at www.clinicaltrials.gov #NCT04140487. - Source: PubMed
Publication date: 2026/05/27
Short Nicholas JKantarjian Hagop MDaver Naval GAzevedo Roberta SKarrar OmerDiNardo Courtney DKadia Tapan MYilmaz MusaMaroun Manuel MHachem Maria Catherine RitaBorthakur GautamIssa Ghayas CShpall Elizabeth JPopat Uday RHuang XuelinQiao WeiNasr Lewis FadyMacaron WalidAbramova ReginaGarcia-Manero GuillermoKonopleva MarinaRavandi Farhad