CELF1 Antibody
- Known as:
- CELF1 Antibody
- Catalog number:
- abx000085
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- CELF1 Antibody
Related genes to: CELF1 Antibody
- Gene:
- CELF1 NIH gene
- Name:
- CUGBP Elav-like family member 1
- Previous symbol:
- CUGBP1
- Synonyms:
- CUG-BP, hNab50, BRUNOL2, NAB50, CUGBP, NAPOR, EDEN-BP
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-25
- Date modifiied:
- 2017-01-20
Related products to: CELF1 Antibody
Related articles to: CELF1 Antibody
- Mounting evidence is revealing an increasing complexity of gene regulation at the level of messenger RNA (mRNA) translation. Within mammalian cells, canonical cap-dependent mRNA translation depends on the eIF4F complex, consisting of the m7G mRNA cap-binding protein eukaryotic initiation factor 4E (eIF4E), the helicase eIF4A (eIF4A), and the eIF4G (eIF4G1) scaffolding protein. eIF4G1 additionally binds poly(A) binding protein (PABPC1) to facilitate mRNA circularization and nucleates pre-translation initiation complex assembly to initiate ribosomal scanning. In breast epithelial cells, the CELF1 RNA-binding protein specifically promotes the translation of select epithelial-to-mesenchymal transition (EMT) effector mRNAs by binding GU-rich elements (GREs) within their 3' untranslated regions (UTRs). Here we show that CELF1 directly binds to both eIF4E and PABPC1 to promote eIF4G1-independent translation of GRE-containing mRNAs in mesenchymal cells. Disruption of this CELF1/eIF4E interaction inhibits both EMT induction in vitro and experimental metastasis in vivo. Our findings define a novel, non-canonical mode of translational regulation underlying cellular de-differentiation, raising the possibility that analogous non-canonical modes of translation impact additional transitional cellular states within development and disease. - Source: PubMed
Chaudhury ArindamKongchan NateeMassey Shebna ASharma RajeshPal RiturajZhao NaTsoi PhoebeZhu YingminOlokpa EmuejevokeMao SufengDel Rincon SoniaReineke Lucas CLloyd Richard ESardiello MarcoRosen Jeffrey MKim ChoelFerreon Josephine CNeilson Joel R - The RNA-binding protein CELF1 is crucial for cardiac development, but its role in cardiomyocyte hypertrophy is unclear. This study investigates the effects of acute knockdown on alternative splicing and hypertrophic growth in cardiomyocytes. - Source: PubMed
Publication date: 2026/01/29
Hu LingjieZhu KailiZeng SiyingLiu YiqiaoZhang ShengqiNi Le - Myogenesis is a stepwise process encompassing myogenic progenitor proliferation, lineage commitment, differentiation, myocyte fusion, and myotube maturation, and it is orchestrated by myogenic regulatory factors (MRFs) together with signaling pathways that coordinate these transitions. Long noncoding RNAs (lncRNAs) have emerged as important regulators of muscle development and regeneration, yet how lncRNAs integrate with canonical signaling networks to shape myogenic progression remains incompletely defined. Here, we identify a novel myocyte-enriched, Notch-repressed myogenic lncRNA ( known as ), as a previously uncharacterized regulator of mouse myogenesis. The expression of is robustly induced during primary myoblast activation and differentiation. Loss-of-function analyses show that knockdown of impairs myogenic differentiation, accompanied by reduced expression of key myogenic genes. In contrast, adenovirus-mediated overexpression of enhances myogenic differentiation and is associated with increased muscle fiber size . Mechanistically, MyoD and MyoG occupy the promoter and promote its transcription during myogenic differentiation. knockdown alerts the transcription of nearby genes, suggesting its function through a cis-regulatory mechanism. RNA pull-down assays further identify an interaction between and the RNA-binding protein CELF1. Together, these findings establish as a novel Notch-associated lncRNA that promotes myogenic differentiation and provide insight into lncRNA-dependent regulation of the myogenic program. - Source: PubMed
Publication date: 2026/02/14
Li YufenZhou YumeiLi Qing YingArrington JustineAbdelhai Mostafa FWang YuboRen JunxiaoCheng Yung-YuXie MingyiTao W AndyKuang ShihuanYue Feng - Precise post-transcriptional regulation of gene expression is essential for vertebrate lens development. Disruption of the gene encoding the RNA-binding protein CELF1 leads to early-onset cataract in mice. Here, using iCLIP-seq in lenses, we mapped transcriptome-wide CELF1 binding sites, revealing interactions with the 3'UTRs of key transcripts involved in lens development and pathology like , , , , or . Integrated analysis with transcriptomic data and luciferase reporter assays demonstrated that binding of CELF1 protein represses its target mRNAs by destabilizing transcripts and/or inhibiting their translation. Indeed, the cataract-linked genes and are upregulated in lenses. In , overexpression of resulted in abnormal lens structure and eye morphology, confirming the developmental relevance of CELF1-mediated repression. Our findings uncover a post-transcriptional network in which CELF1 controls lens morphogenesis by limiting the expression of critical genes at the mRNA level to achive their proper dosage. - Source: PubMed
Publication date: 2026/01/10
Viet JustineDuot MatthieuMéreau AgnèsAudic YannJan IwanReboutier DavidLe Goff-Gaillard CatherineCoomson Sarah YLachke Salil AGautier-Courteille CarolePaillard Luc - RNA-binding proteins (RBPs) shape post-transcriptional programs in cancer, yet subtype-specific roles in breast cancer remain unclear. We evaluated whether CUGBP Elav-like family member 1 (CELF1), an RBPs with prognostic relevance in luminal A (ER-positive) breast cancer, drives malignant phenotypes via glycolytic reprogramming through glucose transporter 1 (GLUT1). - Source: PubMed
Publication date: 2025/11/12
Li JinyuWang NingBi JianleiGuo MeihuaXu BingbingHuang Gena