• Product nameAnti-Artemis antibody
    See all Artemis primary antibodies
  • Description
    Rabbit polyclonal to Artemis
  • Tested applicationsSuitable for: WB, ICC/IFmore details
  • Species reactivity
    Reacts with: Human
  • Immunogen

    Synthetic peptide conjugated to KLH derived from within residues 550 - 650 of Human Artemis.

    (Peptide available as ab35688.)

  • Positive control
    • This antibody gave a positive signal in the following whole cell lysates: HepG2 (Human hepatocellular liver carcinoma cell line) U2OS (Human osteosarcoma cell line)


  • FormLiquid
  • Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
  • Storage bufferPreservative: 0.02% Sodium Azide
    Constituents: 1% BSA, PBS, pH 7.4
  • Concentration information loading...
  • PurityImmunogen affinity purified
  • ClonalityPolyclonal
  • IsotypeIgG
  • Research areas


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 Abreviews Notes
WB Use at an assay dependent concentration. Detects a band of approximately 60 kDa (predicted molecular weight: 78 kDa).

Abcam recommends blocking and incubation using 3% milk.

ICC/IF Use a concentration of 1 µg/ml.


  • 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
    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.
  • Cellular localizationNucleus.
  • Information by UniProt
  • Database links
  • Alternative names
    • 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
    see all

Anti-Artemis antibody images

  • All lanes : Anti-Artemis antibody (ab35649) at 1 µg/ml

    Lane 1 : HepG2 (Human hepatocellular liver carcinoma cell line) Whole Cell Lysate
    Lane 2 : MCF-7 (Human breast adenocarcinoma cell line) Whole Cell Lysate
    Lane 3 : HeLa (Human epithelial carcinoma cell line) Whole Cell Lysate

    Lysates/proteins at 25 µg per lane.

    Goat Anti-Rabbit IgG H&L (HRP) (ab97051) at 1/10000 dilution
    developed using the ECL technique

    Performed under reducing conditions.

    Predicted band size : 78 kDa
    Observed band size : 60 kDa (why is the actual band size different from the predicted?)

    Exposure time : 20 minutes

    Abcam recommends using milk as the blocking agent. ab35649 detects a strong band at 60 kDa in HepG2 whole cell lysate. It is thought that this band corresponds to isoforms 2 and 3 which have a predicted molecular weight of 65 kDa (SwissProt data).

  • 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)

This product has been referenced in:
  • Ho SR  et al. RNF144A, an E3 ubiquitin ligase for DNA-PKcs, promotes apoptosis during DNA damage. Proc Natl Acad Sci U S A 111:E2646-55 (2014). Read more (PubMed: 24979766) »
  • Gole B  et al. Endonuclease G initiates DNA rearrangements at the MLL breakpoint cluster upon replication stress. Oncogene N/A:N/A (2014). Read more (PubMed: 25132265) »

See all 3 Publications for this product

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Abcam guarantees this product to work in the species/application used in this Abreview.
Application Western blot
Sample Human Cell lysate - nuclear (U2OS)
Loading amount 25 µg
Specification U2OS
Gel Running Conditions Reduced Denaturing
Blocking step Milk as blocking agent for 3 hour(s) and 0 minute(s) · Concentration: 5% · Temperature: 21°C

Dr. Andrew Cobb

Verified customer

Submitted Mar 28 2012