Anti-Cd38 Antibody Fluoro594 Conjugated

The protein encoded by this gene is a non-lineage-restricted, type II transmembrane glycoprotein that synthesizes and hydrolyzes cyclic adenosine 5'-diphosphate-ribose, an intracellular calcium ion mobilizing messenger. The release of soluble protein and the ability of membrane-bound protein to become internalized indicate both extracellular and intracellular functions for the protein. This protein has an N-terminal cytoplasmic tail, a single membrane-spanning domain, and a C-terminal extracellular region with four N-glycosylation sites. Crystal structure analysis demonstrates that the functional molecule is a dimer, with the central portion containing the catalytic site. It is used as a prognostic marker for patients with chronic lymphocytic leukemia. Alternative splicing results in multiple transcript variants.

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

A synthetic peptide corresponding to a sequence at the C-terminus of mouse Cd38, which shares 81.8% and 86.7% amino acid (aa) sequence identity with human and rat Cd38, respectively.

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. Cockayne, D. A., Muchamuel, T., Grimaldi, J. C., Muller-Steffner, H., Randall, T. D., Lund, F. E., Murray, R., Schuber, F., Howard, M. C. Mice deficient for the ecto-nicotinamide adenine dinucleotide glycohydrolase CD38 exhibit altered humoral immune responses. Blood 92: 1324-1333, 1998. 2. Ferrero, E., Malavasi, F. Human CD38, a leukocyte receptor and ectoenzyme, is a member of a novel eukaryotic gene family of nicotinamide adenine dinucleotide +/-converting enzymes: extensive structure homology with the genes for murine bone marrow stromal cell antigen 1 and aplysian ADP-ribosyl cyclase. J. Immun. 159: 3858-3865, 1997. 3. Ferrero, E., Saccucci, F., Malavasi, F. The human CD38 gene: polymorphism, CpG island, and linkage to the CD157 (BST-1) gene. Immunogenetics 49: 597-604, 1999.

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) . .