Rabbit Artemis Polyclonal Antibody | anti-S516 antibody

Artemis (Phospho-S516) Polyclonal Antibody

Cat. Num. AAA3005116

• Gene Names: DCLRE1C; SCIDA; SNM1C; A-SCID; RS-SCID; DCLREC1C
• Reactivity: Human, Mouse, Rat
• Applications: Western Blot, Immunohistochemistry
• Purity: The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is >95% (by SDS-PAGE).
• Synonyms: Artemis; Polyclonal Antibody; Artemis (Phospho-S516) Polyclonal Antibody; Protein artemis; DNA cross-link repair 1C protein; Protein A-SCID; SNM1 homolog C; hSNM1C; SNM1-like protein; DCLRE1C; ARTEMIS; ASCID; SCIDA; SNM1C; anti-S516 antibody

• Host: Rabbit
• Reactivity: Human, Mouse, Rat
• Clonality: Polyclonal
• Isotype: IgG
• Specificity: p-Artemis (S516) polyclonal antibody detects endogenous levels of Protein artemis only when phosphorylated at Ser516.
• Purity/Purification: The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is >95% (by SDS-PAGE).
• Form/Format: Rabbit IgG, 1mg/ml in PBS with 0.02% sodium azide, 50% glycerol, pH7.2
• Sequence Length: 692

• Applicable Applications for anti-S516 antibody: Western Blot (WB), Immunohistochemistry (IHC)
• Application Notes: WB: 1:500-1:1000; IHC: 1:50-1:200
• Immunogen: Synthetic phosphopeptide derived from human Artemis around the phosphorylation site of Serine 516.
• Preparation and Storage: Store at 4 degree C short term.; Aliquot and store at -20 degree C long term.; Avoid freeze-thaw cycles.

Western Blot (WB)

(Western Blot (WB) analysis of p-Artemis (S516) polyclonal antibody at 1:500 dilutionLane1:HEK293T cell lysateLane2:Mouse skeletal muscle tissue lysateLane3:Rat skeletal muscle tissue lysate)

Related Product Information for anti-S516 antibody

Distinct DNA repair pathways minimize the consequences of mutagenic events. Reactive oxygen species (ROS) are highly reactive atoms with an unpaired electron that are conducive to double-strand DNA breaking events. Artemis, named after the Greek goddess for the protection of children, is one of the major proteins contributing to the preservation of double-strand breaks in DNA by cutting away the damaged parts of the DNA, which allows the strands to rejoin. Artemis is a single-strand-specific 5' to 3' exonuclease that forms a complex with the 469 kDa DNA-dependent protein kinase (DNA-PKcs). DNA-PKcs phosphorylates Artemis, and Artemis acquires endonucleolytic activity on 5' and 3' overhangs and hairpins. These activities are essential for V(D)J recombination and for the 5' and 3' overhang processing in nonhomologous DNA end joining.

NCBI and Uniprot Product Information

• NCBI GI #: 76496497
• NCBI GeneID: 64421
• NCBI Accession #: NP_001029027.1
• NCBI GenBank Nucleotide #: NP_001029027.1
• UniProt Accession #: Q96SD1
• Molecular Weight: ~ 78kDa
• NCBI Official Full Name: protein artemis isoform a
• NCBI Official Synonym Full Names: DNA cross-link repair 1C
• NCBI Official Symbol: DCLRE1C
• NCBI Official Synonym Symbols: SCIDA; SNM1C; A-SCID; RS-SCID; DCLREC1C
• NCBI Protein Information: protein artemis
• UniProt Protein Name: Protein artemis
• Protein Family: Artemisinic aldehyde Delta(11(13)) reductase
• UniProt Gene Name: DCLRE1C
• UniProt Synonym Gene Names: ARTEMIS; ASCID; SCIDA; SNM1C; hSNM1C
• UniProt Entry Name: DCR1C_HUMAN

NCBI Description

This gene encodes a nuclear protein that is involved in V(D)J recombination and DNA repair. The encoded protein has single-strand-specific 5'-3' exonuclease activity; it also exhibits endonuclease activity on 5' and 3' overhangs and hairpins. The protein also functions in the regulation of the cell cycle in response to DNA damage. Mutations in this gene can cause Athabascan-type severe combined immunodeficiency (SCIDA) and Omenn syndrome. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jan 2014]

Uniprot Description

Artemis: 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. Defects in DCLRE1C are a cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell- negative/NK-cell-positive with sensitivity to ionizing radiation (RSSCID). SCID refers to 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 with SCID 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. Defects in DCLRE1C are the cause of severe combined immunodeficiency Athabaskan type (SCIDA). SCIDA is a variety of RS-SCID caused by a founder mutation in Athabascan- speaking native Americans, being inherited as an autosomal recessive trait with an estimated gene frequency of 2.1% in the Navajo population. Affected individuals exhibit clinical symptoms and defects in DNA repair comparable to those seen in RS-SCID. Defects in DCLRE1C are a cause of Omenn syndrome (OS). OS is characterized by severe combined immunodeficiency associated with erythrodermia, hepatosplenomegaly, lymphadenopathy and alopecia. Affected individuals have elevated T-lymphocyte counts with a restricted T- cell receptor (TCR) repertoire. They also generally lack B- lymphocytes, but have normal natural killer (NK) cell function (T+ B- NK+). Belongs to the DNA repair metallo-beta-lactamase (DRMBL) family. 4 isoforms of the human protein are produced by alternative splicing.

Protein type: DNA repair, damage; EC 3.1.-.-; Deoxyribonuclease

Chromosomal Location of Human Ortholog: 10p13

Cellular Component: nucleus

Molecular Function: 5'-3' exonuclease activity; single-stranded DNA specific endodeoxyribonuclease activity

Biological Process: V(D)J recombination; B cell differentiation; double-strand break repair; response to ionizing radiation; telomere maintenance; DNA catabolic process, endonucleolytic

Disease: Omenn Syndrome; Severe Combined Immunodeficiency With Sensitivity To Ionizing Radiation