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Anti-Artemis antibody (ab35649)

Overview

  • Product nameAnti-Artemis antibodySee all Artemis primary antibodies ...
  • Description
    Rabbit polyclonal to Artemis
  • Tested applicationsWB, ICC/IF more 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 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
  • Application notesICC/IF: Use at a concentration of 1 µg/ml.
    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
      modifications
      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.
    • Target information above from: UniProt accession Q96SD1 The UniProt Consortium
      The Universal Protein Resource (UniProt) in 2010
      Nucleic Acids Res. 38:D142-D148 (2010) .

      Information by UniProt
    • Database links
    • 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

    • 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.

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    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
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    Submitted Mar 28 2012

    Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"