Ask about this productRelated genes to: RBM47 antibody
- Gene:
- RBM47 NIH gene
- Name:
- RNA binding motif protein 47
- Previous symbol:
- -
- Synonyms:
- FLJ20273, NET18
- Chromosome:
- 4p14
- Locus Type:
- gene with protein product
- Date approved:
- 2007-10-25
- Date modifiied:
- 2014-11-18
Related products to: RBM47 antibody
Related articles to: RBM47 antibody
- Neonatal hypoxic-ischemic encephalopathy (NHIE) is a leading cause of morbidity and mortality in term infants. The anesthetic dexmedetomidine (Dex) has been shown to reduce brain damage. In this study, hypoxia-ischemia (HI) in neonatal rats caused significant cerebral infarction, neurological deficits, learning and cognitive impairments, inflammatory responses, and microglia polarization. Dex treatment mitigated HI-induced brain injury in rats. Lipopolysaccharide (LPS) increased inflammation in BV2 cells, elevated M1 polarization markers, and raised the proportion of M1 cells. Dex reduced inflammation and M1 polarization in BV2 cells. Rbm47 was identified as a target of Dex, being downregulated in NHIE rat brain tissues and upregulated by Dex. Rbm47 co-localized with microglia and was decreased as the microglia marker Iba-1 increased. Adenovirus-mediated overexpression of Rbm47 alleviated brain injury in NHIE rats and reduced microglial inflammation and M1 activation, both in vitro and in vivo. Conversely, knockdown of Rbm47 hindered the protective effects of Dex against BV2 cell inflammation and M1 polarization. This study indicates that Rbm47 mediates the protective effects of Dex against NHIE brain injury. - Source: PubMed
Feng Shan-ShanZhang Sen-YuLi Yu-CanZhang TaoYang Yu-Hang - Macrophages play central roles in the initiation and growth of atherosclerosis (AS). This study aimed to investigate the role of ENC1 in macrophage oxidative stress during AS and its mechanism. An animal model of AS was constructed by feeding ApoE KO mice with a high-cholesterol diet, and an in vitro AS model was induced on mouse macrophages RAW 264.7 using oxLDL. Macrophage-specific adeno-associated viruses containing the F4/80 promoter were used to interfere with RBM47 and ENC1 expression in vivo, and lentiviral infection of RAW 264.7 was applied in vitro. RBM47 improved the stability of ENC1 by binding to the AU-rich elements, which curbed NRF2 synthesis and nuclear translocation. Exogenous inhibition of ENC1 or RBM47 suppressed aortic oxidative stress in mice with AS, reduced lipid and cholesterol uptake, and strengthened cellular scavenging activity against oxidative stress in RAW 264.7 cells. The NRF2 inhibitor ML385 reversed the above benefits from the knockdown of ENC1 in RAW 264.7 cells, and combined overexpression of ENC1 reversed these benefits from the knockdown of RBM47 in vitro and in vivo. This study provides new evidence that ENC1 is a contributor to AS progression, and targeting ENC1 in macrophages may serve as a potential therapy. - Source: PubMed
Publication date: 2026/04/08
Li YangxueShi HengheLu YangWu Junduo - Breast cancer (BC) remains a leading cause of cancer-related mortality, in part due to the lack of effective therapeutic targets. In this study, we report that Coiled-Coil Domain Containing 12 (CCDC12), a relatively uncharacterized member of the CCDC protein family, is upregulated in BC tissues. Functional assays in vitro and in vivo indicate that CCDC12 contributes to malignant phenotypes, including enhanced proliferation and metastatic potential. Transcriptomic analysis is associated with widespread alterations in alternative splicing programs. Among the affected events, RNA Binding Motif Protein 47 (RBM47) was identified as a splicing-related target exhibiting increased exon 5 skipping following CCDC12 knockdown. This splicing change produces a truncated RBM47 isoform with reduced tumor-suppressive activity, while reintroduction of full-length RBM47 partially restores impaired cellular phenotypes. These findings support the existence of a CCDC12-RBM47 regulatory relationship that may participate in breast cancer progression, although the upstream signals and detailed molecular mechanisms remain to be clarified. Collectively, the study provides insight into a previously underappreciated role of CCDC12 in breast cancer biology and highlights the need for future work to establish its mechanistic and translational significance. - Source: PubMed
Publication date: 2026/02/12
Ye ZhoujieZhu LipingChen LuYu HaileFan XiaoluSun PengmingWang Xinrui - Down-regulation of the RNA-binding motif protein 47 (RBM47) frequently occurs in colorectal cancer (CRC) and is associated with poor prognosis. However, the downstream effectors of RBM47 have remained unknown. Therefore, we performed a comprehensive RNA-Seq analysis after inactivation or ectopic expression of RBM47. /, a poorly characterized member of the gasdermin family highly expressed in gastrointestinal epithelium, was identified as the most differentially regulated transcript. RBM47 directly bound to the 3'-untranslated region of mRNA and stabilized it. Consistently, ectopic increased GSDMA mRNA and protein expression, whereas knockdown had the opposite effect. GSDMA was necessary for the RBM47-induced mesenchymal-to-epithelial transition (MET) and suppression of migration and invasion by RBM47 in CRC cells. Moreover, activation of the RBM47/GSDMA axis triggered pyroptosis, a form of cell death characterized by cell swelling, plasma membrane rupture, and, therefore, immunogenic effects. Both RBM47 and GSDMA enhanced sensitivity to Oxaliplatin through the induction of MET and pyroptosis. Knockdown of GSDMA abolished RBM47-mediated pyroptosis and chemo-sensitization. Analysis of CRC patient cohorts revealed that expression correlates with response to FOLFOX chemotherapy. Therefore, our results establish GSDMA as a critical downstream mediator of RBM47-induced tumor suppression that links epithelial differentiation and pyroptosis to chemotherapy sensitivity. Finally, these findings identify the RBM47/GSDMA axis as a potential predictive biomarker for the response to Oxaliplatin in CRC patients. - Source: PubMed
Publication date: 2026/02/03
Du YuyunRokavec MatjazHermeking Heiko - Intermittent hypoxia (IH) is a hallmark pathological feature of obstructive sleep apnea and a critical risk factor for neurodegenerative diseases such as Alzheimer's disease. Transcription factors (TFs) and splicing factors (SFs) serve as pivotal regulators orchestrating cellular adaptations to hypoxia. This study aimed to elucidate the dynamic changes and identify candidate key TFs and SFs in the mouse hippocampus under IH. By establishing an IH mouse model (7% O, 1/3/5/7 weeks) and integrating multi-time points RNA-seq with bioinformatic analysis and experimental validation, we systematically identified putative core TFs and SFs involved in hippocampal hypoxia response and inferred their potential functions. Our study revealed that the TFs Lef1 and Foxj1, along with the SF Rbm47, emerge as candidate key regulators. Lef1 may modulate apoptosis-related genes such as Il31ra, while Foxj1 could be linked to ciliary function and neural development by regulating genes like Rsph1. The SF Rbm47 potentially contributes to hippocampal hypoxic adaptation by modulating alternative splicing of genes such as Apc and Hnrnpa2b1. The Lef1 gene itself undergoes alterations in exon retention rates during intermittent hypoxia. These findings provide critical data to decipher hippocampal IH adaptation and offer theoretical insights into the mechanisms of AD and related neurodegenerative disorders. - Source: PubMed
Publication date: 2026/02/09
Liu ChunchengLi XiaoyuPu WenhuaJing JingCui WenjiaLiu GuojunCai Lu