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HMCES (F4E4Q) Rabbit Monoclonal Antibody #65616

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    Product Specifications

    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
    Simple Western™ 1:10 - 1:50
    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 Monoclonal Antibody 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).

    Alternate Names

    5-hydroxymethylcytosine (hmC) binding, ES cell-specific; 5-hydroxymethylcytosine binding, ES cell specific; Abasic site processing protein HMCES; C3orf37; DC12; Embryonic stem cell-specific 5-hydroxymethylcytosine-binding protein; ES cell-specific 5hmC-binding protein; HMCES; MGC111075; Peptidase HMCES; putative endonuclease HMCES; putative peptidase SRAPD1; SOS response associated peptidase domain containing 1; SRAP domain-containing protein 1; SRAPD1; UPF0361 protein C3orf37

    For Research Use Only. Not for Use in Diagnostic Procedures.
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