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
- 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 Gja8, , Maf, Pax6, or Prox1. 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 -cKO lenses. In , overexpression of maf 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 achieve their proper dosage. - Source: PubMed
Publication date: 2026/08/05
Viet JustineDuot MatthieuMéreau AgnèsAudic YannJan IwanReboutier DavidGoff-Gaillard Catherine LeCoomson Sarah YLachke Salil AGautier-Courteille CarolePaillard Luc - RNA-binding motif protein 20 (RBM20) is a splicing factor that forms discrete nuclear speckles. Certain pathogenic RBM20 variants disrupt its nuclear localization, leading to cytoplasmic granules formation. The composition of RBM20 nuclear speckles and cytoplasmic granules, how these compartments differ from one another, and how they contribute to splicing regulation remain unclear. Here, we employed in situ proximity labeling proteomics and identified 25 and 12 proteins associated with RBM20 nuclear speckles and cytoplasmic granules, respectively. RBM20 nuclear speckles were enriched in proteins involved in splicing and transcriptional regulation, whereas cytoplasmic granules contained proteins commonly found in other cytoplasmic granule populations. Among these, CELF1 and MBNL2 were detected in both RBM20 nuclear speckles and cytoplasmic granules, as confirmed by co-localization and immunoprecipitation experiments. We further showed that CELF1- and MBNL2-regulated splicing events were disrupted in the hearts of mice carrying pathogenic Rbm20 variants but not in animals with Rbm20 loss-of-function that lack cytoplasmic granules. Moreover, reducing cytoplasmic granule burden through RBM20 knockdown in pathogenic variant knock-in mice showed a trend toward partial restoration of MBNL2-mediated splicing defects. Collectively, these findings define the distinct protein compositions of RBM20 nuclear speckles and cytoplasmic granules and suggest that cytoplasmic RBM20 granules affect the splicing of non-RBM20 target genes. - Source: PubMed
Zhang YanghaiGregorich Zachery RLiu ChunlingLarson Eli JGe YingGuo Wei - Myotonic Dystrophy Type 1 (DM1) is a multisystemic neuromuscular disease characterized by severe skeletal muscle dysfunction. The etiology of DM1 is primarily driven by RNA toxicity resulting from a gain-of-function mutation in DMPK mRNAs. Beyond this hallmark, DM1 is also characterized by the repression of the AMP-activated protein kinase (AMPK) pathway. Previous work has shown that targeting AMPK represents a novel therapeutic avenue for DM1. In this study, we investigated the therapeutic potential of novel AMPK activators derived from Momordica charantia (bitter melon). A screen of 26 bitter melon-derived compounds (BMCs) in C2C12 myotubes identified BMC-25 as a potent AMPK activator. Acute treatment of DM1 (HSA) mice with BMC-25 induced an expected activation of AMPK in DM1 mice, while chronic treatment restored several DM1 histopathological features, including toxic ribonuclear foci. Interestingly, BMC-25 treatment induced distinct, sex-dependent molecular benefits. In female DM1 mice, BMC-25 treatment corrected the pattern of expression of RNA-binding proteins including CELF1, MBNL1, and Staufen1 in skeletal muscle and achieved a much greater correction of alternative splicing of multiple transcripts relative to their respective controls. In contrast, male DM1 mice exhibited very limited improvements in these parameters. Collectively, our findings indicate that sustained AMPK activation with BMC-25 confers multifaceted benefits to DM1 skeletal muscle by improving core DM1 pathogenic features in a sex-dependent manner. Finally, these results highlight the potential of natural compounds like BMCs as novel, promising and accessible therapeutics for the DM1 muscle pathology. - Source: PubMed
Publication date: 2026/08/03
Atieh Shatha AFahmi ChimèneLiu JiaTang ChunpingYe YangRavel-Chapuis AymericJasmin Bernard J - Diabetic cardiomyopathy (DCM) is a prevalent diabetes-related cardiac complication. miR-671-5p has been shown to mitigate ischemia-reperfusion-induced cardiomyocyte injury. This study investigated the role and underlying mechanisms of miR-671-5p in a DCM cell model established by exposing AC16 cardiomyocytes to high glucose (HG). The miRNA expression dataset GSE210036 from diabetic mouse hearts was analyzed. Cell injury was evaluated by assessing cell viability, apoptosis, and ferroptosis-related alterations. The expression levels and interactions of miR-671-5p, circHUWE1, and CELF1 were examined in the cell model. p38 MAPK activation was further assessed following modulation of the circHUWE1/miR-671-5p/CELF1 axis. Additionally, the m6A modification of circHUWE1 was evaluated. Bioinformatics analysis revealed decreased miR-671-5p expression in diabetic mouse hearts compared to healthy controls. HG treatment downregulated miR-671-5p expression and upregulated the levels of circHUWE1 and CELF1. circHUWE1 upregulation resulted from diminished METTL3-dependent m6A modification. Both miR-671-5p mimic and circHUWE1 knockdown attenuated HG-induced apoptosis and ferroptosis-related alterations. Mechanistically, circHUWE1 elevated CELF1 expression and subsequently activated p38 MAPK by sponging miR-671-5p. The cardioprotective effects of dexmedetomidine (Dex) are associated with the circHUWE1/miR-671-5p/CELF1 axis. In conclusion, the circHUWE1/miR-671-5p/CELF1 axis regulates HG-induced cardiomyocyte apoptosis and ferroptosis-related alterations and represents a novel mechanism underlying Dex-mediated cardioprotection. - Source: PubMed
Publication date: 2026/07/16
Yu YeMa ZihanShi LeiDing Li - Despite the promise of immune checkpoint blockade (ICB), only a minority of non-small-cell lung cancer (NSCLC) patients achieve long-term benefits. In this study, we present a single-cell spatial transcriptomic landscape of NSCLC, revealing a previously uncharacterized link between elevated glutathione peroxidase 8 (Gpx8) and resistance to PD-1 blockade. Through CyTOF, CODEX, and ATAC-sequencing analyses, we demonstrate that Gpx8 knockout in both immunocompetent and humanized mouse models suppress tumor growth. This suppression is accompanied by increased infiltration of antitumor T lymphocytes, reduced enrichment of pro-tumorigenic myeloid cells, and the formation of tertiary lymphoid structures (TLS). Mechanistically, Gpx8 inhibits the activity of the RNA-binding protein Celf1(CUGBP Elav-like family member 1) through disulfide bonding between cysteine 79 of Gpx8 and cysteine 177 of Celf1. This interaction stabilizes CCAAT-enhancer-binding protein β (C/EBPβ) mRNA, promotes CSF1 secretion, and drives the recruitment of myeloid-derived suppressor cells (MDSCs) into the tumor microenvironment. Notably, resistance to anti-PD-1 treatment in Gpx8-expressing NSCLCs can be overcome through enforced expression of Celf1, CSF1R blockade, or a mimic peptide designed to disrupt the Gpx8-Celf1 interaction. Furthermore, anti-PD-1 or rCSF1 treatment activates C/EBPβ and upregulates Gpx8 transcription, establishing a Gpx8-C/EBPβ-CSF1 feedback loop that contributes to immune evasion. These findings provide new insights into the role of Gpx8 in modulating the tumor microenvironment and offer a potential framework for enhancing the sensitivity of NSCLC to PD-1 blockade therapy. - Source: PubMed
Publication date: 2026/07/14
Zhang HengMa JialinShi MengChen LiangZhang Yu-FeiGao ZhiWang Zhuo-RanLiu BiaoLuo WenwuPei HuadongWang BinChen LingLi Zhi-GangFeng XingZhou Wen-Yong