Elav-type RNA-binding protein ETR3 Antibody [M8J19]

Catalog No.: F3634

For research use only.

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000 - 1:10000
    1:50 - 1:70
    1:50 - 1:100
    1:500
    1:270
    Application
    WB, IP, IHC, IF, FCM
    Reactivity
    Human, Mouse, Rat
    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
    54 kDa
    Positive Control Human fetal liver; Human brain; Rat lung; K562 cell; HeLa cell; MCF7 cell; C6 cell; NIH 3T3 cell
    Negative Control

    Datasheet & SDS

    Biological Description

    Specificity
    Elav-type RNA-binding protein ETR3 Antibody [M8J19] detects endogenous levels of total Elav-type RNA-binding protein ETR3 protein.
    Subcellular Location
    Cytoplasm, Nucleus
    Uniprot ID
    O95319
    Clone
    M8J19
    Synonym(s)
    BRUNOL3, CUGBP2, ETR3, NAPOR, CELF2, CUGBP Elav-like family member 2, CELF-2, Bruno-like protein 3, CUG triplet repeat RNA-binding protein 2, CUG-BP- and ETR-3-like factor 2, ELAV-type RNA-binding protein 3
    Background
    Elav-type RNA-binding protein ETR-3 (also known as BRUNOL3, NAPOR, or CUGBP2) is a member of the CELF (CUG-BP and ETR-3-like factor) family of RNA-binding proteins that regulate post-transcriptional gene expression. Structurally, ETR-3 contains three RNA recognition motifs (RRMs)—two near the N-terminus and one at the C-terminus—separated by a divergent central domain (160–230 amino acids) that confers splicing activation potential. ETR-3 is highly expressed in muscle, heart, and brain tissues, where it plays crucial roles in alternative splicing, RNA editing, translation, and mRNA stability. It binds preferentially to UG-rich sequences (UG repeats and UGUU motifs) within pre-mRNAs, regulating exon inclusion or skipping. Through this RNA-binding activity, ETR-3 influences the expression of key genes such as CFTR and MTMR1 and contributes to developmental splicing programs and neuromuscular functions. Dysregulation of ETR-3 and other CELF proteins has been implicated in myotonic dystrophy, where aberrant splicing patterns arise from disrupted CELF and MBNL protein activity.
    References
    • https://pubmed.ncbi.nlm.nih.gov/15657417/

    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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