CUGBP1 Blocking Peptide
- Known as:
- CUGBP1 Blocking Peptide
- Catalog number:
- 33r-1032
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- CUGBP1 Blocking Peptide
Related genes to: CUGBP1 Blocking Peptide
- 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: CUGBP1 Blocking Peptide
Related articles to: CUGBP1 Blocking Peptide
- The CUG-BP and Elav-like (CELF) family of RNA-binding proteins are key regulators of post-transcriptional gene expression, coordinating alternative splicing, mRNA stability, and translation. Although individual members, particularly CELF1 and CELF2, have been extensively characterized, a systematic, paralog-resolved integration of structural determinants, regulatory mechanisms, and disease relevance across all six CELF proteins remains limited. Here, we establish an integrative framework linking conserved RNA recognition motifs and divergent linker domains to context-dependent regulatory outputs, mediated by phosphorylation, nucleocytoplasmic dynamics, and RNA network interactions. We further highlight the neuron-enriched CELF3-CELF6 subfamily, consolidating emerging evidence that extends their roles beyond neural splicing into cancer-associated regulatory programs. Notably, we delineate functional divergence within the family, with CELF1 frequently acting as an oncogenic driver in contrast to the tumor-suppressive role of CELF2, while positioning less-characterized paralogs within this regulatory spectrum. Together, this work defines a unified structure-function-disease axis for CELF proteins and provides a conceptual framework for their prognostic and therapeutic exploitation. However, current CELF-targeted strategies remain largely preclinical and face key translational challenges, including paralog selectivity, off-target effects, and delivery barriers such as limited blood-brain barrier penetration. Accordingly, the most immediate clinical utility of CELF biology is likely to lie in biomarker development and patient stratification, rather than direct therapeutic intervention. - Source: PubMed
Publication date: 2026/05/09
Ma YukangMa ChiYang AoboChen YimingGao JiajunWang QunshuWei ZhixiGao MeilingXing XianglingLiu Wancheng - 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