Recombinant Human FLT3 (Y591-V592insVDFREYEYD) Protein

Name: Recombinant Human FLT3 (Y591-V592insVDFREYEYD) Protein
Brand: Beta LifeScience
SKU: BL-0530SG
Availability: InStock

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Product Overview

Tag	GST
Host Species	Human
Accession	NM_004119
Synonym	FLT3-ITD, FLK2, STK1, CD135
Background	Fms-related tyrosine kinase 3 (FLT3) is a gene that encodes for a tyrosine kinase that activates pathways in hematopoietic cells important in cellular proliferation. FLT3 is frequently mutated in acute myeloid leukemia (AML), myelodysplastic syndromes, other hematologic malignancies, and colorectal cancer. FLT3 mutations are observed in 24.3% of AML, of which internal tandem duplications (ITD) are the most frequent. FLT3 ITD occurs when sequences of less than ten to several hundred bases in length are repeated within the juxtamembrane domain are always -€œin-frame-€.
Description	Recombinant human FLT3 (Y591-V592insVDFREYEYD) or FLT3-ITD ((571-993) was produced by baculovirus in Sf9 insect cells, fused with a GST tag at N-terminus. This protein is purified with our unique purification methods.
Source	Sf9 insect cells
AA Sequence	571-993
Molecular Weight	76 kDa
Purity	For specific purity information on a given lot, see related COA.
Endotoxin	< 1.0 EU per μg of the protein as determined by the LAL method
Bioactivity	Active
Formulation	Recombinant protein is supplied in 50mM Tris-HCl, pH 7.5, 50mM NaCl, 10mM Glutathione, 0.25mM DTT, 0.1mM EDTA, 0.1mM PMSF and 25% glycerol.
Stability	The recombinant protein is stable for up to 12 months at -70°C
Usage	For Research Use Only
Storage	Recombinant Human FLT3 (Y591-V592insVDFREYEYD) Protein should be stored should be stored at < -70°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

Target Details

Target Function	Tyrosine-protein kinase that acts as cell-surface receptor for the cytokine FLT3LG and regulates differentiation, proliferation and survival of hematopoietic progenitor cells and of dendritic cells. Promotes phosphorylation of SHC1 and AKT1, and activation of the downstream effector MTOR. Promotes activation of RAS signaling and phosphorylation of downstream kinases, including MAPK1/ERK2 and/or MAPK3/ERK1. Promotes phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A and/or STAT5B. Activation of wild-type FLT3 causes only marginal activation of STAT5A or STAT5B. Mutations that cause constitutive kinase activity promote cell proliferation and resistance to apoptosis via the activation of multiple signaling pathways.
Subcellular Location	Membrane; Single-pass type I membrane protein. Endoplasmic reticulum lumen. Note=Constitutively activated mutant forms with internal tandem duplications are less efficiently transported to the cell surface and a significant proportion is retained in an immature form in the endoplasmic reticulum lumen. The activated kinase is rapidly targeted for degradation.
Protein Families	Protein kinase superfamily, Tyr protein kinase family, CSF-1/PDGF receptor subfamily
Database References	HGNC: 3765 OMIM: 136351 KEGG: hsa:2322 STRING: 9606.ENSP00000241453 UniGene: PMID: 29950146 Results indicate that DNMT3A mutations alone do not affect the clinical outcomes of AML patients undergoing allogeneic HSCT, but when accompanied by FLT3-ITD mutations, the OS was significantly reduced (5-year OS 0% for DNMT3A R882mut/FLT3-ITDpos patients vs. 62% DNMT3A R882wt/FLT3-ITDneg, p=0.025) and the relapse rate increased. PMID: 29786546 RIPK3-dependent cell death and inflammasome activation in FLT3-internal-tandem-duplication-expressing leukemia-initiating cells PMID: 27517160 The results suggested that FLT3 ITD mutations could become an indicator of poor prognosis of APL, and these patients should receive more intensive therapy according to current guidelines. PMID: 29251252 Low FLT3 expression is associated with Pancreatic ductal adenocarcinoma. PMID: 30275197 DNMT3A R882 mutation plays an important role in CN-AML patients' prognosis and clinical outcomes in the presence and absence of NPM1 and FLT3 mutations. PMID: 29079128 the FLT3 inhibitor AC220 inhibited glutamine flux into the antioxidant factor glutathione profoundly due to defective glutamine import. PMID: 28947392 Mutation in FLT3 gene is associated with Acute Myeloid Leukemia. PMID: 29530994 Acute myeloid leukemia harboring internal tandem duplication of FMS-like tyrosine kinase 3 (AML(FLT3-ITD)) is associated with poor prognosis. PMID: 29330746 Impact of FLT3-ITD diversity on response to induction chemotherapy in patients with acute myeloid leukemia has been described. PMID: 28034991 The results of the present study showed that the overexpression of FLT3 is a potential risk factor in leukemia. PMID: 29257272 In this study, FLT3 and NPM1 mutations were evaluated in adult Iranian patients with de novo cytogenetically normal acute myeloid leukemia and its correlations with clinical and laboratory parameters were also assessed. PMID: 28294102 FLT3 and FLT3-ITD can directly bind and selectively phosphorylate p27kip1 on tyrosine residue 88 in acute myeloid leukemia. Inhibition of FLT3-ITD in cell lines strongly reduced p27 tyrosine 88 phosphorylation and resulted in increased p27 levels and cell cycle arrest PMID: 28522571 study showed that FLT3 can be targeted by FLT3-CAR T cells for the treatment FLT3(+) AML. FLT3-CAR T cells may provide a new immunotherapeutic approach for AML patients PMID: 28496177 The high expressions of BCRP mRNA calculated with Pfaffl's rule and FLT3-ITD are independent poor risk factors in adult patients with AML and intermediate or normal karyotype. PMID: 28618074 The new and recurrent FLT3 juxtamembrane deletion mutation shows a dominant negative effect on the wild-type FLT3 receptor. PMID: 27346558 FLT3 cell-surface expression did not vary by FLT3 mutational status, but high FLT3 expression was strongly associated with KMT2A rearrangements. Our study found that there was no prognostic significance of FLT3 cell surface expression in pediatric Acute Myeloid Leukemia PMID: 28108543 DNA mutational analysis in FLT3 in acute myeloid leukemia. PMID: 27071442 data confirm MLL-PTD and, to a lesser extent, FLT3-ITD as common events in +11 AML.6, 7, 8 However, the high mutation frequencies of U2AF1 and genes involved in methylation (DNMT3A, IDH2) have hitherto not been reported in +11 AML PMID: 27435003 The cytokine Fms-like tyrosine kinase 3 ligand is an important regulator of hematopoiesis. Its receptor, Flt3, is expressed on myeloid, lymphoid and dendritic cell progenitors and is considered an important growth and differentiation factor for several hematopoietic lineages. [review] PMID: 28538663 FLT3 amplification in solid cancers is infrequently observed using targeted genomic profile, as yet, FLT3 amplification does not seem to be an actionable target or a proper biomarker for FLT3 inhibitor sensitivity. PMID: 27906677 FLT3 has a role in cytarabine transport by SLC29A1 in pediatric acute leukemia PMID: 27391351 Data indicate a pathway MYSM1/miR-150/FLT3 that inhibits proliferation of B1a cells, which may be involved in the pathogenesis of systemic lupus erythematosus (SLE). PMID: 27590507 findings confirm that FLT3-ITD-location influences disease biology and leads to changes in global gene expression. In our model, ITD-location alters proliferative capacity and sensitivity to FLT3-TKI-treatment in vivo PMID: 26487272 a decision analysis comparing allo-HCT vs chemotherapy in first complete remission for patients with cytogenetically intermediate-risk acute myeloid leukemia, depending on the presence or absence of FLT3-ITD), NPM1, and CEBPA mutations showed that allo-HCT was a favored postremission strategy in patients with FLT3-ITD, and chemotherapy was favored in patients with biallelic CEBPA mutations. PMID: 27040395 ATM/G6PD-driven redox metabolism promotes FLT3 inhibitor resistance in acute myeloid leukemia that can be successfully reversed. PMID: 27791036 Data suggest that there is a place for escalated daunorubicin dosing for fms-like tyrosine kinase 3 (FLT3)-ITD mutated cases. PMID: 27268085 Integrin alphavbeta3 has a role in enhancing beta-catenin signaling in acute myeloid leukemia harboring Fms-like tyrosine kinase-3 internal tandem duplication mutations PMID: 27248172 Review of the role of the most common form of FMS-like tyrosine kinase 3 (FLT3) mutation (internal tandem duplication) in acute myeloid leukemia. PMID: 28470536 the present cohort study demonstrated that FLT3-ITD and DNMT3A R882 double mutation predicts poor prognosis in Chinese AML patients receiving chemotherapy or allo-HSCT treatment. PMID: 28616699 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. PMID: 27775694 In this review, we focus on three key areas in acute myeloid leukemia (AML) developmental therapeutics: FLT3 inhibitors, IDH(IDH1 and IDH2 ) inhibitors, and drugs that may be particularly beneficial in secondary AML PMID: 28561688 Concomitant monitoring of WT1 and FLT3-ITD expression in FLT3-ITD acute myeloid leukemia patients PMID: 28211167 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 PMID: 27465508 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. PMID: 29055209 Results provide evidence that mutations in the tyrosine kinase domain in FLT3 were found in 7% of Pakistani patients with acute myeloid leukemia. PMID: 27735988 FLT3/ITD increases aerobic glycolysis through AKT-mediated upregulation of mitochondrial hexokinase (HK2). Inhibition of glycolysis preferentially causes severe ATP depletion and massive cell death in FLT3/ITD leukemia cells. PMID: 28194038 Our results indicate that CD4 expression and older age are adverse prognostic factors in wild-type NPM1, FLT3-ITD-negative CN-AML. PMID: 28318150 FLT3 mutation is associated with Metaplastic Breast Cancer. PMID: 27568101 Collectively, we have developed a novel targeted therapeutic strategy, using FLT3L-guided miR-150-based nanoparticles, to treat FLT3-overexpressing AML with high efficacy and minimal side effects. PMID: 27280396 Y842 is critical for FLT3-mediated RAS/ERK signaling and cellular transformation. PMID: 28271164 value of FLT3-ITD allelic ratio in AML in risk assessment and evaluating prognosis PMID: 27416910 DOCK2 is a potential therapeutic target for novel AML treatments, as this protein regulates the survival of leukemia cells with elevated FLT3 activity and sensitizes FLT3/ITD leukemic cells to conventional antileukemic agents. PMID: 27748370 Gedatolisib significantly extended survival of mice in a sorafenib-resistant acute myeloid leukemia (AML) patient-derived xenograft model. Taken together, our data suggest that aberrant activation of the PI3K/mTOR pathway in FLT3-ITD-dependent AML results in resistance to drugs targeting FLT3. PMID: 26999641 HHEX could replace RUNX1 in cooperating with FLT3-ITD to induce Acute myeloid leukemia (AML). PMID: 28213513 mutated FLT3-ITD and JAK2 augment reactive oxygen species production and homologous recombination, shifting the cellular milieu toward illegitimate recombination. PMID: 28108507 these data reveal a novel mechanism which regulates acute myeloid leukemia cell death by ceramide-dependent mitophagy in response to FLT3-ITD targeting. PMID: 27540013 MSI2 and FLT3 are significantly co-regulated in human AML PMID: 28107692 Sorafenib-resistant leukemia cells with a FLT3/ITD mutation are sensitive to glycolytic inhibitors. PMID: 27132990 Factors that did not influence the relapse risk included: age, graft type, graft source, type of FLT3 mutation, or conditioning intensity PMID: 28052408

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Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

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