Ask about this productRelated genes to: RBM24 Blocking Peptide
- Gene:
- RBM24 NIH gene
- Name:
- RNA binding motif protein 24
- Previous symbol:
- RNPC6
- Synonyms:
- FLJ30829, dJ259A10.1
- Chromosome:
- 6p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-24
- Date modifiied:
- 2015-08-26
Related products to: RBM24 Blocking Peptide
Related articles to: RBM24 Blocking Peptide
- Cochlear hair cells are the mechanosensitive receptor cells responsible for detecting sound information. They are characterized by their apical F-actin-filled stereocilia that are essential for mechano-electrical transduction. Previously, we and other groups reported that RNA Binding Motif Protein 24 (RBM24) plays pivotal roles in stereocilia development and maintenance by regulating pre-mRNA alternative splicing and mRNA stability. In the present work, we show that exon 4 of the mouse gene is subjected to alternative splicing. Inclusion of exon 4 in mRNA results in premature translational stop, giving rise to a short isoform of RBM24 (RBM24-S). Notably, while sharing the same RNA-recognition motif, the canonical RBM24 long isoform (RBM24-L) and RBM24-S can bind different mRNA targets to affect their splicing and/or stability. Deletion of exon 4 in mice abolishes the expression of transcripts that encode for RBM24-S, and both homozygote and heterozygote mice suffer from severe hearing loss. Further investigations revealed that exon 4 deletion leads to stereocilia disorganization and eventually hair cell loss. Moreover, overexpression of RBM24-L in the hair cells leads to significant stereocilia deficits as well as profound hearing loss. Finally, we identified several RBM24 targets such as , whose dysregulation contributes to stereocilia disorganization as well as hearing loss in deficient mice. Taken together, our present data suggest that is subjected to alternative splicing and appropriate RBM24 expression levels are important for stereocilia integrity and hearing function. - Source: PubMed
Publication date: 2026/04/13
Sun ChunjiaoZhao JingshuangLi NanaYao XueboWang YanfeiKim Chul HoonBok JinwoongPeng Anthony WXu Zhigang - The inactivation of Rbm24, an RNA-binding protein, leads to cell death and hair bundle defects in cochlear outer hair cells (OHCs). However, the underlying molecular mechanisms remain unclear. To address this, we have performed comprehensive transcriptomic profiling of purified wild-type and Rbm24-/- mouse OHCs at postnatal day 7 (P7). Loss of Rbm24 perturbs numerous genes associated with hair bundle morphogenesis and delays the overall OHC differentiation program. Insm1, a key transcription factor normally downregulated by P2, remains aberrantly and persistently expressed in Rbm24-/- OHCs. Overexpression of Insm1 alone induces OHC death, whereas simultaneous inactivation of Rbm24 and Insm1 largely rescues OHC survival but only partially restores hair bundle morphology. It demonstrates that Rbm24 promotes OHC survival independently of its role in regulating hair bundle morphogenesis. Collectively, our findings establish Rbm24 as a dual-function regulator that ensures OHC survival by acting as a critical repressor of Insm1 expression, while independently orchestrating hair bundle assembly. These results highlight the central role of Rbm24 in coordinating OHC differentiation and structural maturation, and provide insights into potential molecular targets for hair cell regeneration. - Source: PubMed
Publication date: 2026/04/14
Li ChaoZhao YishuWang LuyueLi ShutingLi JieGu YunpengHe ShunjiWang GuangqinLei FangLu YingGu LiqinXu ShengjinXiong WeiLi BinLiu Zhiyong - As the mechanosensitive sensory cells in the inner ear, hair cells are characterized by their apical, F-actin-filled stereocilia. The stereocilia are organized into a staircase-like pattern with rows of increasing height. The development and maintenance of stereocilia are tightly regulated, and deficits in this process usually lead to hearing loss. Recently, our group reported that RNA-binding proteins (RBPs), such as RBM24 and ESRP1, play essential roles in the inner ear hair cells. In the present work, we show that nucleolin (NCL), a highly conserved RBP, is required for stereocilia maintenance in inner ear hair cells. Ncl knockout leads to progressive stereocilia degeneration in the outer hair cells in a basal-to-apical gradient. Meanwhile, Ncl knockout results in progressive stereocilia fusion in the inner hair cells in an apical-to-basal gradient. As a result, these stereocilia deficits lead to hair cell loss and eventually cause hearing loss in Ncl conditional knockout mice. RNA-sequencing analysis identified several genes for which the mRNA level is affected by Ncl knockout. Among them are Espnl and Ptprq, which have been shown to play essential roles in stereocilia development and/or maintenance. Further investigations confirmed that NCL could directly bind to Espnl and Ptprq mRNAs, and that NCL could increase the stability of Espnl and Ptprq mRNAs. Together, our data demonstrate that NCL plays essential roles in stereocilia maintenance by regulating the stability of its target mRNAs. - Source: PubMed
Publication date: 2026/04/16
Zong WenYan KejiXing HaiyueZhang HaoqingZhang WenGao RuiPeng XiaonaLi TangliangWang ZhaoqiXu Zhigang - Papillary thyroid carcinoma (PTC), the most common thyroid malignancy, is characterized by a high incidence rate and unfavorable outcomes. The competing endogenous RNA (ceRNA) network is systemic and intricate, incorporating various non-coding RNAs, and offers new insights into the cancer pathogenesis. This study explored ceRNA-mediated pathways contributing to PTC pathogenesis. Datasets from GEO were analyzed to detect differentially expressed mRNAs (DEmRNAs) and lncRNAs (DElncRNAs) in PTC, which identified 49 DElncRNAs and two key genes, RBM24 and LIPI. Then a total of 119 shared microRNAs (miRNAs) of them were predicted, leading to the construction of a comprehensive ceRNA regulatory network. Among these, lncRNA CASC2/miR-193a-3p/RBM24 was identified as the core regulatory axis, by using the cytoHubba plugin in Cytoscape. Expression analysis using public datasets and clinical tissue samples revealed significant downregulation of CASC2 and RBM24, alongside upregulation of miR-193a-3p in PTC. Dual-luciferase assays verified CASC2-miR-193a-3p and miR-193a-3p-RBM24 binding. In IHH4 cells, CASC2 knockdown promoted proliferation, migration, and invasion, whereas miR-193a-3p inhibition partly reversed the effects. The RBM24 effect experiments demonstrated that reduced RBM24 facilitated IHH4 progression. Xenograft models validated the expression patterns of CASC2, miR-193a-3p, and RBM24 in vivo, showing that CASC2 knockdown promoted tumor growth. This study is the first to identifies lncRNA CASC2/miR-193a-3p/RBM24 as a critical modulator of PTC progression. By influencing proliferation, apoptosis, and motility, this axis sheds light on the molecular mechanisms of PTC and highlights the targets for therapeutic intervention. - Source: PubMed
Publication date: 2026/02/23
Ou DongWu YanGuo YoumingHu XiaochiLiu WeiHuo Jinlong - Cuproptosis is an emerging form of programmed cell death that has been implicated in tumor progression. Nevertheless, the relationship between cuproptosis and the metastatic process in colorectal cancer (CRC) remains obscure, as are the underlying molecular mechanisms that drive CRC progression in this process. - Source: PubMed
Publication date: 2025/04/20
Huang TianchenBai DongxiaoZhang YongLi KanGuo ZhipengLi LeiHan XiaodongWu YachaoXin YanshanWang Weijie