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Rabbit Polyclonal Phospho-Artemis (S516) antibody (STJ90803)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, IHC, ELISA
Recommended dilution: WB 1:500-1:2000; IHC 1:100-1:300; ELISA 1:5000;
Recommended protocols: check protocols
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Check alternative names for the antibodyExpand
DCLRE1C antibody, ARTEMIS antibody, ASCID antibody, SCIDA antibody, SNM1C antibody,|A SCID antibody|A SCID protein antibody|Artemis protein antibody|ASCID antibody|DCLRE1C antibody|DCLRE1C DNA cross link repair 1C antibody|DCLRE1C protein antibody|DCLREC1C antibody|DCR1C_HUMAN antibody|DNA cross link repair 1C antibody|DNA cross link repair 1C protein antibody|DNA cross-link repair 1C protein antibody|FLJ11360 antibody|FLJ36438 antibody|hSNM1C antibody|OTTHUMP00000045150 antibody|Protein A-SCID antibody|Protein ARTEMIS antibody|PSO2 homolog antibody|RS SCID antibody|SCIDA antibody|Severe combined immunodeficiency type a antibody|SNM1 homolog C antibody|SNM1 like protein antibody|SNM1-like protein antibody|SNM1C antibody|Anti-Artemis antibody (ab35649)
SCBT cat No: sc-368506|sc-23099|
Artemis (phospho Ser516) Polyclonal Antibody
|Catalogue No.|| |
Phospho-Artemis (S516) Polyclonal Antibody detects endogenous levels of Artemis protein only when phosphorylated at S516.
Synthesized phospho-peptide derived from Artemis (phospho Ser516) at AA range 460-540
WB, IHC, ELISA
|Recommended dilution|| |
WB 1:500-1:2000; IHC 1:100-1:300; ELISA 1:5000;
|Molecular weight|| |
Artemis (phospho Ser516) Antibody was tube-contained. Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Artemis (phospho Ser516) Antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
Protein artemis antibody, DNA cross-link repair 1C protein antibody, Protein A-SCID antibody, SNM1 homolog C antibody, hSNM1C antibody, SNM1-like protein antibody
|Protein names|| |
Protein artemis , DNA cross-link repair 1C protein , Protein A-SCID , SNM1 homolog C , hSNM1C , SNM1-like protein
|Protein function|| |
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.
|Protein tissue specificity|| |
Ubiquitously expressed, with highest levels in the kidney, lung, pancreas and placenta (at the mRNA level). Expression is not increased in thymus or bone marrow, sites of V(D)J recombination.
|Involvement in disease|| |
Severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-negative/NK-cell-positive with sensitivity to ionizing radiation (RSSCID) [MIM:602450]: A form of severe combined immunodeficiency, a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy with recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development. Individuals affected by RS-SCID show defects in the DNA repair machinery necessary for coding joint formation and the completion of V(D)J recombination. A subset of cells from such patients show increased radiosensitivity. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Severe combined immunodeficiency Athabaskan type (SCIDA) [MIM:602450]: A variety of SCID with sensitivity to ionizing radiation. A founder mutation has been detected in Athabascan-speaking native Americans, being inherited as an autosomal recessive trait. Affected individuals exhibit clinical symptoms and defects in DNA repair comparable to those seen in RS-SCID. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Omenn syndrome (OS) [MIM:603554]: Severe immunodeficiency characterized by the presence of activated, anergic, oligoclonal T-cells, hypereosinophilia, and high IgE levels. . Note: The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
Belongs to the DNA repair metallo-beta-lactamase (DRMBL) family.
|Protein post-translational modifications|| |
Phosphorylation on undefined residues by PRKDC may stimulate endonucleolytic activity on 5′ and 3′ hairpins and overhangs. PRKDC must remain present, even after phosphorylation, for efficient hairpin opening. Also phosphorylated by ATM in response to ionizing radiation (IR) and by ATR in response to ultraviolet (UV) radiation.
|Protein cellular localization|| |
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St John’s Laboratory Ltd.
|Product type|| |
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