| Overview |
| bs-3150R |
| FLT3 (Tyr842) Polyclonal Antibody |
| WB, ELISA, IHC-P, IHC-F, IF(IHC-P), IF(IHC-F), IF(ICC) |
| Rat |
| Human, Mouse, Rabbit |
| Specifications |
| Unconjugated |
| Rabbit |
| KLH conjugated synthetic phosphopeptide derived from human FLT3 around the phosphorylation site of Tyr842 |
| Tyr842 |
| Polyclonal |
| IgG |
| 1ug/ul |
| Purified by Protein A. |
| 0.01M TBS(pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| Shipped at 4°C. Store at -20°C for one year. Avoid repeated freeze/thaw cycles. |
| Target |
| 2322 |
| P36888 |
| Cytoplasm, Cell membrane |
| FLK2; STK1; CD135; FLK-2; Receptor-type tyrosine-protein kinase FLT3; FL cytokine receptor; Fetal liver kinase-2; Fms-like tyrosine kinase 3; FLT-3; Stem cell tyrosine kinase 1; STK-1; FLT3 |
| 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. |
| Application Dilution |
| WB |
1:300-5000 |
| ELISA |
1:500-1000 |
| IHC-P |
1:200-400 |
| IHC-F |
1:100-500 |
| IF(IHC-P) |
1:50-200 |
| IF(IHC-F) |
1:50-200 |
| IF(ICC) |
1:50-200 |
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