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CSTF2 (F3J2F) Rabbit mAb #60948

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  • WB
  • IP
  • IF

    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 70
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Description

    MW (kDa) 70

    Product Usage Information

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

    CSTF2 (F3J2F) Rabbit mAb recognizes endogenous levels of total CSTF2 protein.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val501 of human CSTF2 protein.

    Background

    The cleavage stimulation factor complex (CSTF) is composed of three subunits: CSTF1, CSTF2, and CSTF3. CSTF binds and recruits the cleavage and polyadenylation specificity factor complex to regulate 3’-untranslated regions (3'-UTRs) of pre-mRNAs (1,2). Within CSTF, CSTF3 forms a bridge that binds to CSTF1 and CSTF2. CSTF2, also known as CSTF64, binds directly to mRNA through G/U- or U-rich sequences via its N-terminal RNA recognition motif (1,2). CSTF1 is capable of binding to the C-terminal domain (CTD) of RNA Pol II, coupling mRNA processing with transcription (3). Additionally, CSTF1 can also bind to BRCA1-associated protein BARD1, which inhibits the polyadenylation machinery during DNA damage and tumor suppression (4,5).

    CSTF2, through its ability to directly bind RNA, has been implicated in many cellular functions and diseases. In embryonic stem cells, CSTF2 controls pluripotency and cell cycle through 3’-end processing of histone mRNAs (6). Widespread shortening of 3’-UTRs has been a phenomenon described in many cancer types. Overexpression of CSTF2 shortens the poly(A) tails of oncogenes, resulting in evasion of miRNA repression and transformation (7).
    For Research Use Only. Not for Use in Diagnostic Procedures.
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