CELF1
CELF1 (CUGBP Elav-like family member 1, also known as CUGBP1, CUG-BP, BRUNOL2, NAB50, hNab50, NAPOR and EDEN-BP) is an RNA-binding protein that regulates pre-mRNA alternative splicing, mRNA translation and mRNA stability. It belongs to the CELF/BRUNOL family. Browse Assay Genie's current range of CELF1 research reagents below, or read on for the biology behind the target.
CELF1 is an RNA-binding protein implicated in several post-transcriptional events. In the nucleus it mediates exon inclusion or exclusion in pre-mRNAs that undergo tissue-specific and developmentally regulated alternative splicing. It specifically activates inclusion of exon 5 of cardiac TNNT2 isoforms during heart remodelling at the juvenile to adult transition. It can act as both activator and repressor of a coregulated exon pair, promoting the smooth muscle exon and excluding the non-muscle exon in actinin pre-mRNAs, partly by antagonising the repressive effect of PTB. It also promotes exclusion of exon 11 of INSR pre-mRNA and, together with HNRNPH1, inhibits its inclusion in myoblasts.
In the cytoplasm, the CELF1 protein influences translation and mRNA turnover. It increases translation of CEBPB mRNA, controls the choice of translation initiation codon, and raises CEBPB translation in aging liver. It also increases CDKN1A mRNA translation by antagonising CALR3. CELF1 mediates rapid cytoplasmic mRNA deadenylation by recruiting the deadenylase PARN to the poly(A) tail of EDEN-containing mRNAs. It is required for completion of spermatogenesis and may regulate miRNA biogenesis: it binds primary pri-MIR140 and, with CELF2, negatively regulates its processing to mature miRNA.
CELF1 binds (CUG)n triplet repeats in the 3'-UTR of transcripts such as DMPK, Bruno response elements, muscle-specific splicing enhancer sites flanking TNNT2 exon 5, and AU-rich elements in JUN and FOS mRNAs. Family members contain two N-terminal and one C-terminal RNA recognition motif, separated by a divergent segment. The CELF1 gene may play a role in myotonic dystrophy type 1 through interactions with DMPK, and alternative splicing yields multiple isoforms. Mouse and rat orthologs are both named Celf1.
CELF1 controls tissue-specific and developmentally regulated exon choice, including TNNT2, actinin and INSR pre-mRNAs.
CELF1 binds CUG repeats in DMPK transcripts and may contribute to myotonic dystrophy type 1.
CELF1 modulates CEBPB and CDKN1A translation and recruits PARN to promote deadenylation of EDEN-containing mRNAs.
CELF1 acts in heart remodelling and myoblast splicing, and is required for completion of spermatogenesis.
CELF1 is an RNA-binding protein that regulates pre-mRNA alternative splicing, mRNA translation and mRNA stability. It promotes or represses specific exons, increases translation of mRNAs such as CEBPB and CDKN1A, and recruits PARN to drive cytoplasmic deadenylation.
CELF1 is also called CUGBP1, CUG-BP, BRUNOL2, NAB50, hNab50, NAPOR and EDEN-BP. Earlier names included CUG triplet repeat, RNA-binding protein 1. Alternative splicing of the CELF1 gene produces multiple transcript variants encoding different isoforms.
NCBI Gene reports that CELF1 may play a role in myotonic dystrophy type 1 through interactions with DMPK. Orthologs exist in mouse and rat, both named Celf1; check the datasheet of any product for its validated reactivity.
Other CELF family members, splicing partners and mRNA targets of CELF1 with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q92879; product specifications from Assay Genie datasheets.