Recombinant Human Artemis protein (ab153487)



  • Nature
  • Source
    Wheat germ
  • Amino Acid Sequence
    • Species
    • Sequence
    • Amino acids
      481 to 577
    • Tags
      proprietary tag N-Terminus


Our Abpromise guarantee covers the use of ab153487 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

  • Applications


    Western blot

  • Form
  • Additional notes
    Protein concentration is above or equal to 0.05 mg/ml.
  • Concentration information loading...

Preparation and Storage

  • Stability and Storage

    Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.

    pH: 8.00
    Constituents: 0.31% Glutathione, 0.79% Tris HCl

General Info

  • Alternative names
    • A SCID
    • A SCID protein
    • Artemis protein
    • ASCID
    • DCLRE1C
    • DCLRE1C DNA cross link repair 1C
    • DCLRE1C protein
    • DCLREC1C
    • DNA cross link repair 1C
    • DNA cross link repair 1C protein
    • DNA cross-link repair 1C protein
    • FLJ11360
    • FLJ36438
    • hSNM1C
    • OTTHUMP00000045150
    • Protein A-SCID
    • Protein ARTEMIS
    • PSO2 homolog
    • RS SCID
    • SCIDA
    • Severe combined immunodeficiency type a
    • SNM1 homolog C
    • SNM1 like protein
    • SNM1-like protein
    • SNM1C
    see all
  • Function
    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.
  • Tissue specificity
    Ubiquitously 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 disease
    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) [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 similarities
    Belongs 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 localization
  • Information by UniProt


  • ab153487 on a 12.5% SDS-PAGE stained with Coomassie Blue.


ab153487 has not yet been referenced specifically in any publications.

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