Render Target: STATIC
Render Timestamp: 2025-03-20T10:56:59.449Z
Commit: 779953b12a5930618aae6aca7c87fb286faeb1d7
XML generation date: 2025-03-07 13:20:29.702
Product last modified at: 2025-02-25T20:45:08.560Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

ARID5A (F7T9F) Rabbit mAb #35393

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 75
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    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

    ARID5A (F7T9F) Rabbit mAb recognizes endogenous levels of total ARID5A protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu154 of human ARID5A protein.

    Background

    AT-rich interactive domain-containing protein 5A (ARID5A) is a member of the ARID family, which includes 15 distinct human proteins. ARID is a nucleic acid binding domain that has a helix-turn-helix motif and is conserved in all eukaryotes (1,2). ARID5A expression is seen in many immune cells, including macrophages, CD4+ T cell subsets TH1 and TH17, as well as stromal cells and keratinocytes (2). During inflammation, ARID5A is translocated from the nucleus to the cytoplasm and stabilizes a variety of mRNA transcripts, including IL-6, Stat3, OX40, T-bet, and IL-17, contributing to the inflammatory response and a variety of inflammatory diseases. TLR4-activated NF-kB and MAPK pathways are involved in regulating ARID5A expression (3). ARID5A plays an important role in resistance to chimeric antigen receptor (CAR)-T cell therapy by stabilizing IDO1 mRNA and the upregulation of IDO1 expression. Elevated IDO1 expression levels facilitate the conversion of tryptophan to kynurenine, which contributes to CAR-T cell exhaustion (4).
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