Home Primary Antibodies Artemis Antibody [H20J21]

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Artemis Antibody [H20J21]

Catalog No.: F1506

    Application: Reactivity:
    • F1506-wb
      Lane 1: Jurkat, Lane 2: HT-29, Lane 3: PC-3, Lane 4: MCF-7

    Usage Information

    Dilution
    1:1000
    1:200
    Application
    WB, IP
    Reactivity
    Human, Monkey
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW
    90 kDa

    Datasheet & SDS

    Biological Description

    Specificity
    Artemis Antibody [H20J21] detects endogenous levels of total Artemis protein.
    Clone
    H20J21
    Synonym(s)
    Protein artemis; DNA cross-link repair 1C protein; Protein A-SCID; SNM1 homolog C; hSNM1C; SNM1-like protein; DCLRE1C; ARTEMIS; ASCID; SCIDA; SNM1C
    Background
    Artemis (DCLRE1C, also known as SNM1C) is a ubiquitously expressed nuclear nuclease belonging to the metallo-β-lactamase (MBL) superfamily, essential for non-homologous end-joining (NHEJ) DNA repair and V(D)J recombination in developing lymphocytes. Artemis is a 692-amino-acid protein with an N-terminal catalytic domain (residues 1-360) comprising a core MBL fold (α/β-β/α sandwich) and embedded β-CASP subdomain containing conserved motifs 1-4 (His33, His35, His115, Asp116 coordinating Zn²⁺ ions M1/M2) and motifs A-C for nucleic acid processing, plus a largely unstructured C-terminal regulatory tail (residues 361-692) that autoinhibits activity and mediates DNA-PKcs tethering. DNA-PKcs phosphorylates Artemis (e.g., at Thr127, Ser251) upon DSB recognition, activating its structure-specific endonuclease activity to open hairpin-sealed coding ends in V(D)J recombination, trim 5'/3' overhangs, flaps, and bubbles in NHEJ for XRCC4/LIG4 ligation, and process IR-induced complex ends while antagonizing HR via 53BP1-PTIP interaction. ATM/ATR further phosphorylate Artemis for G2/M and S-phase checkpoint recovery, promoting Cdk1-cyclin B activation and cyclin E degradation via SCF^{Fbw7}. Biallelic mutations cause radiosensitive severe combined immunodeficiency (RS-SCID) with defective V(D)J joining and genome instability predisposing to malignancy.
    References
    • https://pubmed.ncbi.nlm.nih.gov/14744996/
    • https://pubmed.ncbi.nlm.nih.gov/34387696/

    Tech Support

    Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

    Handling Instructions

    Tel: +1-832-582-8158 Ext:3
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