Ask about this productRelated genes to: Mettl4 antibody
- Gene:
- METTL4 NIH gene
- Name:
- methyltransferase like 4
- Previous symbol:
- -
- Synonyms:
- FLJ23017, HsT661
- Chromosome:
- 18p11.32
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-08
- Date modifiied:
- 2019-04-16
Related products to: Mettl4 antibody
Related articles to: Mettl4 antibody
- This study investigates the role of N6-methyladenosine (m6A) regulators in osteoporosis (OP) and their interplay with the immune microenvironment, aiming to identify potential m6A-related biomarkers for OP risk assessment and treatment. - Source: PubMed
Publication date: 2026/04/14
Wang ZhenyangChen YongqinYang YuxuanXu BitengJiao XiejiaQi Lei - -methyladenosine (mA) RNA methylation, regulated by writer, eraser, and reader proteins, modulates mRNA stability, splicing, and translation, thereby influencing key cellular processes. Environmental stressors, such as alcohol, may disrupt this epitranscriptomic machinery and contribute to disease vulnerability. In this study, we investigated how chronic exposure to ethanol, its toxic metabolite acetaldehyde, and subsequent withdrawal affect the expression of mA regulatory genes. Neuron-like (SH-SY5Y) and non-neuronal (SW620) cells were exposed for 3 weeks to ethanol (40 mM) or acetaldehyde (30 μM) (concentrations comparable to blood levels after heavy drinking), followed by a 24-h withdrawal period. Gene expression of seven writers (, and ), two erasers (, FTO), and nine readers (, and ) was quantified by RT-qPCR. Concurrently, RNA-seq data from eight reward-related brain regions of 24 individuals of European ancestry (12 with alcohol use disorder [AUD] and 12 controls) were analyzed for AUD-associated expression changes in mA regulatory genes. In cell models, ethanol broadly suppressed the expression of most mA regulatory genes, whereas withdrawal largely restored their levels. Acetaldehyde induced subtler gene expression changes, likely reflecting its lower exposure concentration and rapid metabolism. Postmortem brain analysis revealed trends toward altered expression of mA regulatory genes across multiple brain regions in individuals with AUD. Collectively, these findings suggest that chronic alcohol exposure dysregulates mA regulatory gene expression and may impact downstream RNA regulatory pathways involved in AUD pathophysiology. Further studies are warranted to elucidate the mechanisms by which alcohol-induced dysregulation of mA regulators influences AUD risk. - Source: PubMed
Publication date: 2026/03/26
Koo Ji SunZhan QianshengZhang Huiping - Vascular cognitive impairment (VCI) is strongly associated with mitochondrial dysfunction, yet the underlying molecular mechanisms connecting mitochondrial impairment to neuroinflammation remain elusive. While mitochondrial epigenetic modifications are emerging as key regulators of cellular metabolism, the role of mitochondrial DNA (mtDNA) N-methyladenine (6 mA) modification and its writer enzyme METTL4 in VCI pathogenesis has not been established. - Source: PubMed
Publication date: 2026/01/12
Gong ZheChen ZiyiSang ShuixianYang LingfeiQin HongzhuoLi QingshengJia Yanjie - Hepatocellular carcinoma (HCC) is a major cause of cancer-related mortality. Epigenetic dysregulation, particularly through methyltransferase METTL4, plays a critical role in HCC progression. METTL4 is known to catalyze mAm methylation of mRNA, yet its pathological significance in liver cancer remains unclear. - Source: PubMed
Publication date: 2026/01/07
Sun WeijieDai WeiqiChen ChaoboQiu QianChen JianqingChen JiaojiaoLi YueyueLiu YuqiHan DengyuMo WenhuiWang ZishuYuan YihangXu Xuanfu - Epitranscriptomics modifications play an important role in sex-dependent biological phenomena. N6-adenosine methylation (m6A), the most prevalent epitranscriptomics modification in eukaryotic mRNA, participates in regulating various sex-specific physiological processes. Here, we generated METTL4 knockout mice lacking methyltransferase-like 4, which mediates m6A. Behavioral analyses revealed that only female METTL4 mice exhibited pain hypersensitivity, with subsequent experiments showing the involvement of METTL4-mediated m6A in this sex-differentiated biological phenotype. Further exploration demonstrated that this sex-specific pain hypersensitivity is closely associated with sex-dependent expression of uncoupling protein 2 (UCP2) in synapses. Specifically, elevated UCP2 expression in METTL4 female mice enhances the efficiency of synaptic transmission by modulating mitochondrial energy metabolism at synapses. Collectively, this study identifies a distinct pathway mediated by METTL4-driven m6A modification, providing critical insights into the molecular basis of sex-specific differences in pain transmission. These findings also highlight the potential of targeting METTL4 for sex-differentiated pain management strategies in clinical settings. - Source: PubMed
Publication date: 2025/12/27
Wu YanqiongLuo YifanXiao QinXu XueqinJin WenjiaoLi LonghuiLiu ChengHe ZhigangLi ZhixiaoLi JuanYang XuesongJiang FanYang ZeyongMa DaqingKe ChangbinXiang Hongbing