Overview
- Product nameAnti-Artemis antibodySee all Artemis primary antibodies ...
- DescriptionRabbit polyclonal to Artemis
- Tested applicationsWB, ICC/IF more details
- Species reactivityReacts with: Human
- Immunogen
Synthetic peptide conjugated to KLH derived from within residues 550 - 650 of Human Artemis.
(Peptide available as ab35688.)
- Positive controlThis antibody gave a positive signal in the following whole cell lysates: HepG2 (Human hepatocellular liver carcinoma cell line) U2OS (Human osteosarcoma cell line)
Properties
- FormLiquid
- Storage instructionsStore at +4°C short term (1-2 weeks). Aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
- Storage bufferPreservative: 0.02% Sodium Azide
Constituents: 1% BSA, PBS, pH 7.4 -
Concentration information loading... - PurityImmunogen affinity purified
- Clonality Polyclonal
- IsotypeIgG
- Research Areas
Applications
Our Abpromise guarantee covers the use of ab35649 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
| Application | Notes |
|---|---|
| WB | |
| ICC/IF |
WB: 1/250. Detects a band of approximately 60 kDa. It is thought that this band corresponds to isoforms 2 and 3 which have a predicted molecular weight of 65 kDa (SwissProt data).
Not yet tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
Target
- 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.
- Post-translational
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.
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Database links
- Entrez Gene: 64421 Human
- Entrez Gene: 64421 Human
- Entrez Gene: 64421 Human
- Omim: 605988 Human
- SwissProt: Q96SD1 Human
- SwissProt: Q96SD1 Human
- SwissProt: Q96SD1 Human
- Unigene: 656065 Human
Target information above from: UniProt accession
Q96SD1
The UniProt Consortium
The Universal Protein Resource (UniProt) in 2010
Nucleic Acids Res. 38:D142-D148 (2010)
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Alternative names
- A SCID antibodyA SCID protein antibodyArtemis protein antibody
- ASCID antibodyDCLRE1C antibodyDCLRE1C DNA cross link repair 1C antibodyDCLRE1C protein antibodyDCLREC1C antibodyDCLREC1C antibodyDCR1C_HUMAN antibodyDNA cross link repair 1C antibodyDNA cross link repair 1C protein antibodyDNA cross-link repair 1C protein antibodyFLJ11360 antibodyFLJ11360 antibodyFLJ36438 antibodyhSNM1C antibodyOTTHUMP00000045150 antibodyProtein A-SCID antibodyProtein ARTEMIS antibodyPSO2 homolog antibodyRS SCID antibodySCIDA antibodySCIDA antibodySevere combined immunodeficiency type a antibodySNM1 homolog C antibodySNM1 like protein antibodySNM1-like protein antibodySNM1C antibodySNM1C antibody
see all
Anti-Artemis antibody images
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All lanes : Anti-Artemis antibody (ab35649) at 1/250 dilution
Lane 1 :HepG2 (Human hepatocellular liver carcinoma cell line) Whole Cell Lysate (ab7900)
Lane 2 : MCF-7 (Human breast adenocarcinoma cell line) Whole Cell Lysate
Lane 3 : SHSY-5Y (Human neuroblastoma cell line) Whole Cell Lysate
Lane 4 : U2OS (Human osteosarcoma cell line) Whole Cell Lysate
Lysates/proteins at 10 µg per lane.
Secondary
IRDye 680 Conjugated Goat Anti-Rabbit IgG (H+L) at 1/10000 dilution
Performed under reducing conditions.
Predicted band size : 78 kDa
Observed band size : 60 kDa (why is the actual band size different from the predicted?) -
ICC/IF image of ab35649 stained human HeLa cells. The cells were PFA fixed (10 min), permabilised in TBS-T (20 min) and incubated with the antibody (ab35649, 1µg/ml) for 1h at room temperature. 1%BSA / 10% normal goat serum / 0.3M glycine was used to quench autofluorescence and block non-specific protein-protein interactions. The secondary antibody (green) was Alexa Fluor® 488 goat anti-rabbit IgG (H+L) used at a 1/1000 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red). DAPI was used to stain the cell nuclei (blue).
References for Anti-Artemis antibody (ab35649)
ab35649 has not yet been referenced specifically in any publications.

