Key features and details
- Rabbit polyclonal to Artemis
- Suitable for: WB, IHC-P
- Reacts with: Human
- Isotype: IgG
Product nameAnti-Artemis antibody
See all Artemis primary antibodies
DescriptionRabbit polyclonal to Artemis
Tested applicationsSuitable for: WB, IHC-Pmore details
Species reactivityReacts with: Human
Predicted to work with: Monkey
Recombinant fragment, corresponding to a region within amino acids 306-692 of Human Artemis (Uniprot ID: Q96SD1).
- A549, HeLa, HepG2 and HCT116 whole cell lysates; Human Cal27 xenograft tissue.
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In preparation for this, we have started to update the applications & species that this product is Abpromise guaranteed for.
We are also updating the applications & species that this product has been “predicted to work with,” however this information is not covered by our Abpromise guarantee.
Applications & species from publications and Abreviews that have not been tested in our own labs or in those of our suppliers are not covered by the Abpromise guarantee.
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Storage instructionsShipped at 4°C. Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Storage bufferpH: 7.00
Preservative: 0.01% Thimerosal (merthiolate)
Constituents: 79.99% PBS, 20% Glycerol (glycerin, glycerine)
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab151512 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/500 - 1/3000. Predicted molecular weight: 78 kDa.|
|IHC-P||1/100 - 1/1000. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.|
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.
- Information by UniProt
- A SCID antibody
- A SCID protein antibody
- Artemis protein antibody
All lanes : Anti-Artemis antibody (ab151512) at 1/1000 dilution
Lane 1 : HeLa whole cell lysate
Lane 2 : HepG2 whole cell lysate
Lysates/proteins at 30 µg per lane.
Predicted band size: 78 kDa
Immunohistochemical analysis of paraffin-embedded Human Cal27 xenograft tissue labeling Artemis with ab151512 at 1/100 dilution.
ab151512 has not yet been referenced specifically in any publications.