RBM15B

Last update 08 May 2025

Basic Info

Synonyms

HsOTT3, HUMAGCGB, HuOTT3

+ [6]

Introduction

RNA-binding protein that acts as a key regulator of N6-methyladenosine (m6A) methylation of RNAs, thereby regulating different processes, such as alternative splicing of mRNAs and X chromosome inactivation mediated by Xist RNA (PubMed:16129689, PubMed:27602518). Associated component of the WMM complex, a complex that mediates N6-methyladenosine (m6A) methylation of RNAs, a modification that plays a role in the efficiency of mRNA splicing and RNA processing (PubMed:27602518). Plays a key role in m6A methylation, possibly by binding target RNAs and recruiting the WMM complex (PubMed:27602518). Involved in random X inactivation mediated by Xist RNA: acts by binding Xist RNA and recruiting the WMM complex, which mediates m6A methylation, leading to target YTHDC1 reader on Xist RNA and promoting transcription repression activity of Xist (PubMed:27602518). Functions in the regulation of alternative or illicit splicing, possibly by regulating m6A methylation (PubMed:16129689). Inhibits pre-mRNA splicing (PubMed:21044963). Also functions as a mRNA export factor by acting as a cofactor for the nuclear export receptor NXF1 (PubMed:19586903).

100 Clinical Results associated with RBM15B

100 Translational Medicine associated with RBM15B

0 Patents (Medical) associated with RBM15B

Literatures (Medical) associated with RBM15B

01 Jul 2025·Cellular Signalling

LncRNA FOXD3-AS1 modulates ER stress and epithelial barrier dysfunction in allergic rhinitis by destabilizing CHOP mRNA

Article

Author: Zhang, Hao ; Huang, Xinyi ; Fu, Li ; Yang, Chunping ; Zhu, Yaqiong

BACKGROUNDAllergic rhinitis (AR) is an allergic disease of nasal mucosa. LncRNAs are key modulators affecting AR development. Nevertheless, the impact of LncRNA FOXD3-AS1 in AR is not clear.METHODSHuman nasal epithelial cells (hNECs) were exposed to ovalbumin (OVA) to establish AR cell model, AR mice model was also constructed by OVA treatment. RIP assay was conducted to verify the association between FOXD3-AS1 and RBM15B. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analyses were performed to detect the expression of ER stress markers: Autophagy Related Gene 4 (ATG4), phosphorylated Protein kinase R-like endoplasmic reticulum kinase (p-PERK), and phosphorylated eukaryotic initiation factor 2α (p-eIF2α) in hNECs after overexpression of FOXD3-AS1. HNECs were treated with ER stress inhibitor 4-phenylbutyric acid (4-PBA).RESULTSThe expressions of LncRNA FOXD3-AS1 were downregulated in AR model. Moreover, overexpression FOXD3-AS1 reversed the effect of AR on ER stress markers. RBM15B was found to be bound with FOXD3-AS1. After 4-PBA treatment, the protein expression of ATG4, CHOP, p-PERK, and p-eIF2α was significantly reduced in cultured AR cell model.CONCLUSIONThis study illustrated that FOXD3-AS1 acted as an inhibitor in AR induced ER stress and epithelial barrier dysfunction by destabilizing CHOP mRNA via RBM15B.

31 Dec 2024·Epigenetics

Expression patterns and clinical value of key m6A RNA modification regulators in smoking patients with coronary artery disease

Article

Author: Ouyang, Hua ; Peng, Yangfei ; Xiang, Kun ; Zhuang, Huanwei ; Gong, Shuji ; Chen, Jinlan ; Chen, Le

Even though N6-methyladenosine (m6A) RNA modifications are increasingly being implicated in human disease, their mechanisms are not fully understood in smokers with coronary artery disease (CAD). Thirty m6A-related regulators' expression (MRRE) in CAD individuals (smokers and non-smokers) were analyzed from GEO. Support Vector Machine, random forest, and nomogram models were constructed to assess its clinical value. Consensus clustering, principal component analysis, and ssGSEA were used to construct a full picture of m6A-related regulators in smokers with CAD. Oxygen-glucose deprivation (OGD) and qRT-PCR were used to validate hypoxia's effect on MRRE. A comparison between smokers with CAD and controls revealed lower expression levels of RBM15B, YTHDC2, and ZC3H13. Based on three key MRREs, all models showed good clinical value, and smokers with CAD were divided into two distinct molecular subgroups. The correlations were found between key MRRE and the degree of immune infiltration. Three key MRREs in HUVECs and FMC84 mouse cardiomyocytes were reduced in the OGD group. Through hypoxia, smoking might reduce the expression levels of RBM15B, YTHDC2, and ZC3H13 in smokers with CAD. Our findings provide an important theoretical basis for the treatment of smokers with CAD.

12 Jul 2024·Technology and Health Care

NME6 as a potential biomarker and therapeutic target involved in immune infiltration for lung adenocarcinoma

Article

Author: Yang, Lijie ; Luo, Linjie ; Zhang, Lin ; Li, Ying

BACKGROUND: Lung adenocarcinoma (LUAD), a prevalent form of lung cancer, is characterized by its high global mortality rate. Previous studies have demonstrated the significance of Nucleoside diphosphate kinase (NME) in various cancers; however, the specific role of NME6 in LUAD remains inadequately understood. OBJECTIVE: This research aims to enhance our understanding of LUAD by investigating the expression level, epigenetic mechanism, signaling activities, and immune infiltrating characteristic immune cells of NME6 in patients. METHODS: The NME6 expression was explored between LUAD and normal tissue samples using GEPIA, UALCAN and HPA databases. The survival analysis was performed by Kaplan-Meier plotter. The Shiny Methylation Analysis Resource Tool was employed to examine the methylation characteristics of NME6. The Tumor Immune Single-cell Hub (TISCH) and CIBERSORT algorithm were utilized to analyze immune infiltrating characteristic immune cells between NME6 high- and low-expression group in LUAD. RESULTS: According to GEPIA, UALCAN, and HPA databases, NME6 is highly expressed in LUAD compared to normal tissues. At the same time, elevated levels of NME6 were found to be significantly correlated with inferior overall survival outcomes in LUAD patients. Subsequently, the top 10 genes interacted with NME6 were mainly involved in seven pathways, such as p53 signaling pathway, glutathione metabolism, thiamine metabolism, metabolic pathways, and drug metabolism. Notably, NME6 methylation in LUAD samples was lower than in normal samples. The methylation of cg04625862 has a significant impact on the regulation of NME6 expression in LUAD. Furthermore, high NME6 expression in LUAD was associated with tumor stages and relative abundance of tumor infiltrating immune cells, such as Macrophage M2, activated mast cell, and neutrophil. Moreover, NME6 regulated the expression of m6A modification of genes related to LUAD, including METTL3, WTAP, RBM15B, METTL14, RBMX, VIRMA, YTHDC1, RBM15, ZC3H13, YTHDF1, YTHDC2, IGF2BP2, YTHDF3, HNRNPA2B1, YTHDF2, HNRNPC, FTO, and ALKBH5. CONCLUSION: The analysis showed that NME6 is a crucial prognostic factor for LUAD patients. NME6 regulates genes related to m6A modification and immune cells infiltration. Furthermore, NME6 could sever as a potential therapeutic target for LUAD.

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