Synthetic peptide corresponding to a region within N terminal amino acids 2-51 (SSFEGQMAEY PTISIDRFDR ENLRARAYFL SHCHKDHMKG LRAPTLKRRL) of Human Artemis (NP_001029027).
Conjugate
Unconjugated
Applications
Application Notes
WB: 1 μg/ml;Peptide ELISA: 1/62500;
Target
Alternative Names
DCLRE1C; DNA cross-link repair 1C; SCIDA; SNM1C; A-SCID; RS-SCID; DCLREC1C; protein artemis; SNM1 homolog C; SNM1-like protein; severe combined immunodeficiency, type a (Athabascan); DNA cross-link repair 1C (PSO2 homolog, S. cerevisiae);
Required for V(D)J recombination, the process by which exons encoding the antigen-binding domains of immunoglobulins and T-cell receptor proteins are assembled from individual V, (D), and J gene segments. V(D)J recombination is initiated by the lymphoid specific RAG endonuclease complex, which generates site specific DNA double strand breaks (DSBs). These DSBs present two types of DNA end structures: hairpin sealed coding ends and phosphorylated blunt signal ends. These ends are independently repaired by the non homologous end joining (NHEJ) pathway to form coding and signal joints respectively. This protein exhibits single-strand specific 5-3 exonuclease activity in isolation and acquires endonucleolytic activity on 5 and 3 hairpins and overhangs when in a complex with PRKDC. The latter activity is required specifically for the resolution of closed hairpins prior to the formation of the coding joint. May also be required for the repair of complex DSBs induced by ionizing radiation, which require substantial end-processing prior to religation by NHEJ.
We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More
Citations
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Barthels, C; Puchalka, J; et al. Novel Spontaneous Deletion of Artemis Exons 10 and 11 in Mice Leads to T- and B-Cell Deficiency. PLOS ONE 8:-(2013).
Bauer, TR; Adler, RL; et al. Potential Large Animal Models for Gene Therapy of Human Genetic Diseases of Immune and Blood Cell Systems. ILAR JOURNAL 50:168-186(2009).
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COA
Certificate of Analysis
