FLT3 Protein, Human (T227M, HEK293, His)

FLT3, a tyrosine-protein kinase receptor, regulates hematopoietic progenitor cells and dendritic cells' differentiation, proliferation, and survival. It phosphorylates downstream effectors like SHC1 and AKT1, activating signaling cascades involving MTOR, RAS, and MAP kinases. Additionally, it plays a pivotal role in the phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A/B. Wild-type FLT3 activation modestly activates STAT5A or STAT5B, while constitutive kinase mutations heighten cell proliferation and resist apoptosis, highlighting its role in fostering aberrant signaling pathways. FLT3 Protein, Human (T227M, HEK293, His) is the recombinant human-derived FLT3 protein, expressed by HEK293 , with C-His labeled tag and T227M mutation. The total length of FLT3 Protein, Human (T227M, HEK293, His) is 515 a.a., with molecular weight of 85-95 kDa.

FLT3, a tyrosine-protein kinase, functions as a cell-surface receptor for the cytokine FLT3LG, exerting regulatory control over the differentiation, proliferation, and survival of hematopoietic progenitor cells and dendritic cells. This receptor facilitates the phosphorylation of various downstream effectors, including SHC1 and AKT1, and activates signaling cascades involving MTOR, RAS, MAPK1/ERK2, and/or MAPK3/ERK1. Moreover, it plays a pivotal role in the phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A and/or STAT5B. While wild-type FLT3 activation leads to modest STAT5A or STAT5B activation, mutations causing constitutive kinase activity result in heightened cell proliferation and resistance to apoptosis, underscoring its role in fostering aberrant signaling pathways.

Human

HEK293

C-His

P36888-1 (N27-N541, T227M)

2322  [NCBI]

85-95 kDa

Greater than 95% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.