Water DEPC
- Known as:
- Water DEPC
- Catalog number:
- 003-075
- Product Quantity:
- 5x1.5 ml
- Category:
- -
- Supplier:
- A&A
- Gene target:
- Water DEPC
Related genes to: Water DEPC
- Gene:
- ALKBH3 NIH gene
- Name:
- alkB homolog 3, alpha-ketoglutaratedependent dioxygenase
- Previous symbol:
- -
- Synonyms:
- DEPC-1
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-09
- Date modifiied:
- 2018-05-03
Related products to: Water DEPC
Related articles to: Water DEPC
- Liver cancer remains one of the leading causes of cancer-related mortality worldwide, with its progression driven by uncontrolled cell proliferation and evasion of apoptosis. N1-methyladenosine (mA) is a prevalent RNA modification implicated in cancer progression, yet its role in liver cancer remains unclear. Here, we report a significant reduction in mA levels in liver cancer tissues, which contributes to apoptosis evasion in liver cancer cells. We demonstrate that ALKBH3, an mA demethylase, regulates apoptosis by modulating BIRC2 expression. Specifically, ALKBH3 depletion destabilizes BIRC2 mRNA by promoting its degradation, facilitated by mA modifications at positions A98/99/100 in the 5'-UTR of BIRC2. These modifications enhance the interaction between BIRC2 mRNA and the YTHDF3/CNOT1-XRN2 complex, thereby driving mRNA degradation. In vitro, in vivo, and clinical analyses validate the critical role of the mA/BIRC2 axis in regulating apoptosis and tumor progression in liver cancer. Our findings underscore the therapeutic potential of targeting the mA/BIRC2 axis to overcome apoptosis resistance in liver cancer, offering new avenues for intervention in this malignancy. - Source: PubMed
Publication date: 2026/04/16
Wu YingminZhang ShenjieZhang ShilongLu JieyuYang YuntaoZeng ZhiruiLei ShanMi RuiZhang YeweiGe LichenChen TengxiangLi Haiyang - : Metabolic dysfunction-associated steatotic liver disease (MASLD) is a globally prevalent condition with a complex pathogenesis. While both m6A RNA methylation regulators and gut microbiota have been independently implicated in MASLD, their potential causal interplay remains unexplored. This study aimed to investigate the causal relationships among m6A regulatory genes, gut microbiota, and MASLD, and to assess the mediating role of gut microbiota. : We performed a two-sample Mendelian randomization (MR) analysis using publicly available genome-wide association study (GWAS) data. Genetic instruments for m6A regulators were derived from blood expression quantitative trait loci (eQTL) data. Gut microbiota and MASLD data were obtained from large-scale metagenomic and disease GWAS, respectively. The inverse-variance weighted method was the primary analysis, supplemented by sensitivity and mediation analyses to evaluate potential mediating pathways. : Genetically predicted levels of four m6A regulators showed significant causal associations with MASLD risk: ALKBH3 increased risk (OR = 1.17), whereas ALKBH5 (OR = 0.89), CBLL1 (OR = 0.76), and RBM15B (OR = 0.83) were protective. Nineteen gut microbial taxa were causally linked to MASLD. Among these, seven taxa were influenced by the four identified m6A genes. Although no mediation effects reached strict statistical significance, the pathway from ALKBH5 to MASLD via Parabacteroides abundance showed a suggestive indirect effect accounting for 21.9% of the total effect ( = 0.068). Given the limited statistical power of mediation analyses in MR settings, this observation should be interpreted with caution and requires validation in larger, well-powered studies. : This MR study provides genetic evidence supporting causal roles of specific m6A regulators in MASLD and suggests that gut microbiota may partially mediate these relationships. The findings highlight a potential "m6A-gut microbiota-liver" axis in MASLD pathogenesis. - Source: PubMed
Publication date: 2026/03/11
Qiu DongmeiSuo LiweiWei TaoLu ZhenweiWeng QixinXiao JianxingWang XinchiXu QinyuWu Jingtong - Amyloid-beta (Aβ) aggregation, mitochondrial dysfunction, and cognitive decline are hallmarks of Alzheimer's disease (AD), but its initiating molecular events remain unknown. Given that RNA modifications regulate neurodevelopment and neurodegeneration, we explore their functional role in 5xFAD mice, an Aβ AD model. We discover that N1-methyladenosine (m1A) is the most altered RNA modification, and that its regulator demethylase, ALKBH3 is upregulated. Strikingly, Alkbh3 reduction decreases Aβ plaques and restores cognition. Conversely, elevated ALKBH3 levels, observed in AD patients, compromise neuronal morphology and mitochondrial function by impairing mitophagy (degradation of dysfunctional mitochondria), a known driver of neuronal dysfunction. Mechanistically, we reveal that ALKBH3 removes m1A from PINK1 mRNA, the mitophagy master regulator. Given that ALKBH3 is elevated in human AD, causally linked to mitophagy impairment, and confers neuroprotection when depleted, we present ALKBH3 as a mechanistically validated therapeutic target in AD. - Source: PubMed
Publication date: 2026/03/12
Li YueyangYu SifeiLu KaidongZhang YujieDong MingjiePeng YanXue LiangAlam WaleedShui YuxuanZhou YiMa WuyunhanBao MengLi PeimingLuo PeiyiLu TiezhanLi JiajiaZhang KangWang YuyingYang ShuchenYin NuoyaFaiola FrancescoGao ZilongZhou JingfengZhao FeiHe YaliKoziol Magdalena J - Myocardial ischemia/reperfusion (I/R) injury induces an intense inflammatory response and involves multiple cell death pathways. PANoptosis, an integrated cell death process involving pyroptosis, apoptosis and necroptosis, is a major driver of cardiomyocyte loss during I/R injury. However, the epitranscriptomic control of PANoptosis is poorly understood. - Source: PubMed
Diao HongtaoWang ChunleiXiong YutingZhao QiaoyueZhang XinyueQi XiaohuiZou YuanLi JiaxuanZeng LinghuaSi WeiZhang FengPang PingWang NingBian YuYang Baofeng - Nucleotide repeat expansions contribute to a number of neurological disorders. Mutations and augmented expression in fused in sarcoma (FUS) can result in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Here we reveal that FUS is an N1- and N6-methyladenosine (m1A- and m6A)-binding protein, where the protein interacts with the methylated adenosines in CAG repeat expansion RNA, thereby leading to the protein's cytoplasmic redistribution in SH-SY5Y cells. We also found that ectopically expressed FUS co-localizes with CAG repeat RNA in the cytosol. This co-localization is diminished upon genetic depletion of m6A and m1A writer proteins (i.e. METTL3 and TRMT61A), pharmacological inhibition of METTL3, and ectopic overexpression of m1A and m6A eraser proteins (i.e. ALKBH3 and FTO). Moreover, binding to methylated CAG repeat RNA renders the ectopically expressed FUS protein less dynamic in cells. Together, our study underscores a critical role for m1A and m6A in enhancing FUS-RNA interaction, which results in aberrant subcellular distribution and attenuated mobility of the protein in cells. These findings unveil a novel mechanism underlying neurodegenerative disorders emanating from elevated expression of FUS and suggest targeting FUS-methylated adenosine interactions as a potential therapeutic strategy for FUS proteinopathy. - Source: PubMed
Liang XiaochenZhao TingDai XiaoxiaSun YuxiangYuan JunAfzalpurkar SanatDuong ConnorYu AlbertTang FengHe XiaomeiLiu XiaochuanChen XingyuanCao ZhongwenWang Yinsheng