FLT3 (Ab_591) Antibody
- Known as:
- FLT3 (Ab_591) Antibody
- Catalog number:
- E021187-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- FLT3 (Ab_591) Antibody
Related genes to: FLT3 (Ab_591) 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 (Ab_591) Antibody
Related articles to: FLT3 (Ab_591) Antibody
- - Source: PubMed
Levis Mark J - The aim of this study was to generate lentiviral vectors carrying an array of AP-1 motifs driving luciferase gene expression as reporters of Mitogen Activated Protein Kinase (MAPK) activity. We created a series of vectors based on LeGO-iG that were used to generate stably transduced leukaemia cell lines. A vector termed LEGO-AP1 × 6-GM55 containing an array of 6 AP-1 sites linked to the minimal CSF2 promoter was sufficient to support high levels of MAPK-inducible luciferase activity in leukaemic cell lines that was suppressed by MAPK inhibitors. The inclusion of a putative chromatin priming element encompassing RUNX and ETS motifs increased the activity of these vectors. The additional inclusion of the full-length mouse CSF2 promoter, or the human DUSP5 promoter further increased the MAPK-dependent activity of these vectors in leukaemic cells. These vectors support moderate levels of constitutive activity in cells carrying mutations that activate the RAS/RAF/MEK MAPK signalling pathway, and high-level activity after direct activation of MAPK signalling. They also respond to T cell receptor activation via MAPK and Ca2+ signalling pathways. This resource will now make it easier to track receptor or oncogene-inducible MAPK activity in cultured cells, and potentially in tumours, in close to real time. TEASER ABSTRACT: Here we developed a series of lentiviral luciferase reporter vectors activated by RAS/RAF/MAPK signalling to AP-1. These vectors are activated in response to signalling driven by most of the signalling mutations detected in cancer cells or by receptors that control cell growth, differentiation and activation. These vectors have been optimised based on pathways known to activate gene expression in acute myeloid leukaemia or in activated T cells. The regulatory elements tested in these vectors includes an array of 6 AP-1 sites, the CSF2 promoter, the DUSP5 promoter and a chromatin priming element that binds RUNX and ETS factors. - Source: PubMed
Publication date: 2026/08/13
Coleman Danial J LAmes LukeAain HurooulGamble JoannaKoscielniak KingaZhang ZijinLau CherisseJoyce AbigailCockerill Peter N - Relapse remains the leading cause of treatment failure after allogeneic hematopoietic cell transplantation (HCT) for acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), and outcomes after relapse are poor. This review summarizes and critically appraises current evidence for post-HCT maintenance therapy aimed at relapse prevention. - Source: PubMed
Publication date: 2026/08/13
Desai NiharPasic Ivan - Dual FLT3/HDAC inhibition represents a promising synergistic strategy to address tumor heterogeneity. Building upon our prior lead , we developed novel 6-ethylpyrazine-2-carboxamide derivatives systematic structural optimization to enhance pharmacokinetic properties and target selectivity. The optimized compound, CF-2-17, demonstrated potent dual inhibition of FLT3 (IC = 1.1 nmol/L) and HDACs (IC = 9.6 nmol/L), and exhibited a 27-fold selectivity for HDAC1 over HDAC6. Its improved physicochemical properties, including enhanced solubility and metabolic stability, translated into favorable plasma exposure . In the MOLM-13 (FLT3-ITD) xenograft model, oral administration of CF-2-17 showed antitumor efficacy comparable to combination therapy, without observable toxicity. CF-2-17 also exhibited antiproliferative activity against non-FLT3-ITD hematological malignancies and solid tumors, outperforming single-target agents. Furthermore, CF-2-17 effectively remodeled the tumor immune microenvironment through CD4 T cell activation and IFN- elevation, achieving 87% tumor growth inhibition in LLC syngeneic models. Mechanistically, CF-2-17 reversed FLT3 blockade-induced DC dysfunction activation of the NF-B pathway, thereby reinstating DC-mediated antitumor immunity. This dual FLT3/HDAC inhibitor demonstrates synergistic epigenetic-immune modulation, offering a promising approach for heterogeneous malignancies. - Source: PubMed
Publication date: 2026/05/26
Chang YingjieLi XueWang HuiruiZhao HuajunZhou YueBi WenchaoCheng RuixueShi YuxinWeng HeYang XinyingZhao WeiFang HaoHou Xuben - Acute myeloid leukemia (AML) is characterized by antigen heterogeneity and poor prognosis. Here, to tackle the heterogeneity of AML, we combined FLT3 with CD33 in a combinatorial OR-gate approach using our split, universal, programmable (SUPRA) chimeric antigen receptor (CAR) platform. The split platform affords tunability over activation levels and multiplexed targeting. We characterized the specificity and sensitivity of different SUPRA CAR adapters for each target across a panel of target cell lines. Our results demonstrate that this CAR system can effectively target two antigens with equivalent efficacy to conventional CARs while reducing the engineering burden of designing CAR T cells against multiple antigens. Furthermore, we can characterize an effective dose range where off-target cytotoxicity against hematopoietic stem and progenitor cells is minimized. Our SUPRA OR gate has the potential to provide an effective and safer solution to treating AML. - Source: PubMed
Publication date: 2026/08/04
Siddiqui Menna YChen JingyaoHuang Joey ZhuoyingLoffredo MadelineLee SeungheeDeng HanLi YongshuaiLeemans NeliaLu TimGarrison Brian SAyala Marcela GuzmánFrankel Nicholas WWong Wilson W