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Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

HMCES (F4E4Q) Rabbit mAb #65616

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  • WB
  • IP
  • IF

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 40
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100
    Immunofluorescence (Immunocytochemistry) 1:50 - 1:200

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    HMCES (F4E4Q) Rabbit mAb recognizes endogenous levels of total HMCES protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Lys349 of human HMCES protein.

    Background

    HMCES is an abasic site processing protein belonging to the SOS-response associated peptidase (SRAP) family (1,2). In DNA, loss of a base or nucleotide generates an abasic or apurinic/apyrimidinic (AP) site, one of the most common DNA lesions (1,2). HMCES plays a critical role in recognizing these abasic (AP) sites (1,2). HMCES directly binds proliferating cell nuclear antigen (PCNA) and single-stranded DNA (ssDNA) at replication forks, forming covalent cross-links to promote error-free genome repair (1-3). The HMCES DNA-protein cross-link (DPC) prevents translesion DNA synthesis and endonuclease activity, thereby stopping the generation of mutations and double-stranded DNA (dsDNA) breaks (2). Following this action, the HMCES-DPC is degraded by the proteasome or self-reversed (2,3). In dsDNA, AP sites are repaired via the base excision repair (BER) pathway (1-3).

    During somatic hypermutation (SHM) in B cells, HMCES suppresses deletions within immunoglobulin (Ig) genes but allows other types of point mutations to occur, resulting in antigen-specific high-affinity antibodies (4). HMCES deficiency impairs class switch recombination (CSR) in B cells, leading to weakened antibody production (5).

    In APOBEC3A-expressing tumors, disruption of HMCES may increase the tumor’s sensitivity to therapies such as ionizing radiation (IR), oxidative stress, and ATR inhibition (6).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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