Anti-CD135/FLT3 Antibody Picoband® Fluoro594 Conjugated

Cluster of differentiation antigen 135 (CD135) also known as fms like tyrosine kinase 3 (FLT-3), receptor-type tyrosine-protein kinase FLT3, or fetal liver kinase-2 (Flk2) is a protein that in humans is encoded by the FLT3 gene. This gene encodes a class III receptor tyrosine kinase that regulates hematopoiesis. This receptor is activated by binding of the fms-related tyrosine kinase 3 ligand to the extracellular domain, which induces homodimer formation in the plasma membrane leading to autophosphorylation of the receptor. The activated receptor kinase subsequently phosphorylates and activates multiple cytoplasmic effector molecules in pathways involved in apoptosis, proliferation, and differentiation of hematopoietic cells in bone marrow. Mutations that result in the constitutive activation of this receptor result in acute myeloid leukemia and acute lymphoblastic leukemia.

Receptor-type tyrosine-protein kinase FLT3; 2.7.10.1; FL cytokine receptor; Fetal liver kinase 2; FLK-2; Fms-like tyrosine kinase 3; FLT-3; Tyrosine-protein kinase receptor flk-2; CD135; Flt3; Flk-2, Flt-3

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.

1. Abu-Duhier, F. M., Goodeve, A. C., Wilson, G. A., Care, R. S., Peake, I. R., Reilly, J. T. Identification of novel FLT-3 Asp835 mutations in adult acute myeloid leukaemia. Brit. J. Haemat. 113: 983-988, 2001. 2. Abu-Duhier, F. M., Goodeve, A. C., Wilson, G. A., Gari, M. A., Peake, I. R., Rees, D. C., Vanderberghe, E. A., Winship, P. R., Reilly, J. T. FLT3 internal tandem duplication mutations in adult acute myeloid leukaemia define a high-risk group. Brit. J. Haemat. 111: 190-195, 2000. 3. Ansari-Lari, M. A., Yang, C.-F., Tinawi-Aljundi, R., Cooper, L., Long, P., Allan, R. H., Borowitz, M. J., Berg, K. D., Murphy, K. M. FLT3 mutations in myeloid sarcoma. Brit. J. Haemat. 126: 785-791, 2004.

Membrane; 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 (By similarity) . .