Anti-Artemis antibody (ab14289)
- Product nameAnti-Artemis antibodySee all Artemis primary antibodies ...
- DescriptionChicken polyclonal to Artemis
- Tested applicationsWB more details
- Species reactivityReacts with: Human
Recombinant protein: corresponding to C terminal amino acids 316-577 of Human Artemis.
- General notesDuring shipment, small volumes of product will occasionally become entrapped in the seal of the product vial. For products with volumes of 200 µL or less, we recommend gently tapping the vial on a hard surface or briefly centrifuging the vial in a tabletop centrifuge to dislodge any liquid in the container's cap.
- Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
- Storage bufferPreservative: None
- Concentration information loading...
- PurityImmunogen affinity purified
- Clonality Polyclonal
- Research Areas
Our Abpromise guarantee covers the use of ab14289 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||WB: 1/1000 - 1/2000. Predicted molecular weight: 69 kDa.|
- FunctionRequired 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.
- Tissue specificityUbiquitously 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 diseaseDefects 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) [MIM:602450]. 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) [MIM:602450]. 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) [MIM:603554]. 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+).
- Sequence similaritiesBelongs to the DNA repair metallo-beta-lactamase (DRMBL) family.
modificationsPhosphorylation 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.
- Cellular localizationNucleus.
- 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 images
Predicted band size : 69 kDa
Western Blot Test: E coli-derived fusion protein as test antigen. Affinity-purified IgY dilution: 1/2000, Goat anti-IgY-HRP dilution: 1/1000. Colorimetric method for signal development. Arrow points to DCLRE1C fusion protein.
References for Anti-Artemis antibody (ab14289)
This product has been referenced in:
- Mohapatra S et al. Restoration of G1 chemo/radioresistance and double-strand-break repair proficiency by wild-type but not endonuclease-deficient Artemis. Nucleic Acids Res : (2011). WB ; Human . Read more (PubMed: 21531702) »