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Flt-3/Flk-2 Protein, Human
Flt-3/Flk-2 Protein, Human
Origin of place Singapore
Model UA040247-10μg
Supplier ANT BIO PTE.LTD.
Price 120
Hits 5
Updated 8/27/2025
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Product Specification


SpeciesHuman
SynonymsFlt-3, Flk-2, STK-1, CD135, FLK2, FLT-3
AccessionP36888-1
Amino Acid SequenceAsn27-Asn541, with C-terminal His Tag
Expression SystemHEK293
Molecular Weight

72-95kDa (Reducing)

Purity>95% by SDS-PAGE
Endotoxin<0.1EU/μg
ConjugationUnconjugated
TagHis Tag
Physical AppearanceLyophilized Powder
Storage BufferPBS, PH7.4
ReconstitutionReconstitute at 0.1-1 mg/ml according to the size in ultrapure water after rapid centrifugation.
Stability & Storage· 12 months from date of receipt, lyophilized powder stored at -20 to -80℃.
· 3 months, -20 to -80℃ under sterile conditions after reconstitution.
· 1 week, 2 to 8℃ under sterile conditions after reconstitution.
· Please avoid repeated freeze-thaw cycles.
Reference

1.Rosnet, O. et al. (1996) Acta. Haemato. 95:218.

Background

The Flt-3 (fms-like tyrosine kinase) receptor, also named Flk-2 (fetal liver kinase) and Stk-1(stem cell tyrosine kinase) is a 130-155 kDa member of the class III subfamily of receptor tyrosine kinases that also includes KIT, the receptor for SCF and FMS, the receptor for M-CSF. The extracellular region of these receptors contains five immunoglobulin-like domains and the intracellular region contains a split kinase domain. FLT3 is a cytokine receptor which belongs to the receptor tyrosine kinase class III. 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. Mutations that cause constitutive kinase activity promote cell proliferation and resistance to apoptosis via the activation of multiple signaling pathways.

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