Ask about this productRelated genes to: WTAP antibody
- Gene:
- WTAP NIH gene
- Name:
- WT1 associated protein
- Previous symbol:
- -
- Synonyms:
- KIAA0105, MGC3925, Mum2
- Chromosome:
- 6q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-19
- Date modifiied:
- 2017-02-28
Related products to: WTAP antibody
Related articles to: WTAP antibody
- Diabetic nephropathy (DN) is a severe microvascular complication of diabetes mellitus. The specific role of M1 macrophage-derived exosomes in DN progression remains largely unexplored. - Source: PubMed
Publication date: 2026/09/26
Li LeiLiu HongmeiMao YuWang HuanhuanSong LigeKang Zhiqiang - Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by thrombotic and inflammatory manifestations whose molecular regulatory mechanisms remain incompletely understood. Long non-coding RNAs (lncRNAs) and N6-methyladenosine (m6A)-related regulation are increasingly recognized as components of immune gene regulation, but their involvement in APS remains poorly characterized. This study investigated BRD3OS (LINC00094) expression in APS and explored its molecular and predicted structural context in relation to m6A-associated regulation. An exploratory case-control study was conducted using an initial lncRNA PCR-array discovery cohort followed by targeted RT-qPCR validation in an independent cohort. Candidate prioritization incorporated multiple expression and technical features and was evaluated through sensitivity analyses. BRD3OS expression, selected m6A regulators (METTL3, METTL14, WTAP, and FTO), inflammatory mediators, and global m6A abundance in total peripheral blood mononuclear cell (PBMC) RNA were evaluated. Bioinformatic network analysis was used to contextualize BRD3OS within APS- and m6A-related molecular systems. RNAfold and RNAplfold were used to characterize the predicted structural context and accessibility of DRACH consensus motifs, with additional analyses evaluating fragment-boundary and composite-score robustness. BRD3OS was significantly downregulated in PBMCs from patients with APS in the independent validation cohort. METTL3, METTL14, and WTAP expression was also reduced, whereas global m6A levels in total PBMC RNA were increased. These observations indicate concurrent alterations in BRD3OS expression and the broader m6A-related molecular environment but do not establish transcript-specific methylation of BRD3OS. Bioinformatic network analysis placed BRD3OS within predicted RNA-centered regulatory relationships relevant to APS. DRACH motifs exhibited heterogeneous predicted structural accessibility, with unpaired structural environments showing greater RNAplfold-derived accessibility than paired regions. Quantitative accessibility estimates were highly concordant across overlapping transcript fragments, although sensitivity analyses indicated that the identity of individual highest-ranked candidates depended on the weighting scheme. BRD3OS downregulation represents a reproducible molecular finding in APS. Concurrent alterations in global m6A abundance and selected m6A regulators suggest broader epitranscriptomic dysregulation; however, these measurements cannot establish m6A modification of BRD3OS or a causal relationship between these observations. Structural and network analyses therefore provide a hypothesis-generating framework for prioritizing candidate regions and interactions for future transcript-specific methylation mapping and functional validation. - Source: PubMed
Publication date: 2026/09/01
Guzmán-Martín Carlos AJuárez-Vicuña YaneliBojalil RafaelAranda-Cano EvelynPeña-Peña MarioAlvarez-Alvarez Yamnia QHuang FengyangGonzález-Ramírez JavierMartínez-Martínez Laura AlineSánchez-Muñoz Fausto - This study established a rat model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) to evaluate pathological damage, collagen deposition, inflammatory cytokine levels, and key gene/protein expression following water extract (HDWE) intervention. Combined with ultra-high-performance liquid chromatography-quadrupole Orbitrap high-resolution mass spectrometry (UHPLC-Q-Orbitrap HRMS), transcriptomic analysis, and molecular simulation, this study identified the bioactive components of HDWE, evaluated their potential interactions with ALI-related targets, and explored the multi-omics-based protective mechanisms of HDWE. - Source: PubMed
Publication date: 2026/09/04
Lu ChenyiYang XinyiYang Xin - Depression, anxiety, cognitive impairment, fatigue, and sleep disturbance are clinically important sequelae of intracerebral hemorrhage (ICH), but the molecular events linking acute hemorrhagic injury to delayed neuropsychiatric vulnerability remain incompletely defined. This narrative review synthesizes evidence identified through targeted PubMed/MEDLINE and Europe PMC searches updated through 31 August 2026, supplemented by citation chaining. Evidence was categorized as direct ICH evidence, supportive evidence from other stroke or central nervous system models, or hypothesis-generating evidence from other disease contexts. Acute hematoma-derived hemin, iron, thrombin, hypoxia, mitochondrial dysfunction, and altered glycolysis create a perihematomal metabolic-inflammatory environment characterized by oxidative stress and altered lactate handling. Direct preclinical ICH studies support site-specific H3K14la-PMCA2 and H3K18la-METTL3-LCN2 mechanisms, together with separate m6A-related pathways involving METTL3-TFRC, METTL3-YTHDF1-BCL-3, WTAP-UQCRQ, m6A-modified miR-873-RIPK3, and FTO-BCLW. These studies primarily address acute cell death, mitochondrial stress, and glial activation. Direct lactylation-m6A crosstalk evidence in ICH is currently limited to the H3K18la-METTL3-LCN2 axis, and no study has yet shown that this axis causes persistent depression, anxiety, cognitive impairment, or circuit dysfunction after ICH. We therefore present a hypothesis-generating metabolic-glial-circuit framework that separates demonstrated acute ICH mechanisms from proposed downstream neuropsychiatric links. Cell-specific, longitudinal, behavioral, circuit-level, and human validation is required before biomarker or therapeutic translation. - Source: PubMed
Publication date: 2026/09/12
Chen WeihuaTeng HongweiYang XudongGao FengHan ChaoyuYang ShengkaiZhou HaiYang Ziwei - Oral squamous cell carcinoma (OSCC) is a malignant tumor arising from the oral mucosa and is highly prevalent in Southeast Asia and the Pacific region. Recurrence and metastasis significantly contribute to poor clinical outcomes, highlighting the importance of understanding the underlying molecular mechanisms. Circular RNAs (circRNAs), a class of covalently closed non-coding RNAs, have emerged as key regulators of tumor development and progression. However, their roles in OSCC remain largely unexplored. In this study, we identified for the first time that circRHBDD1(4,5) (hsa_circ_0058493, a 656-nt circRNA generated by back-splicing of exons 4 and 5 of the RHBDD1 gene) is markedly upregulated in OSCC and promotes tumor cell proliferation, invasion, and metastasis. Mechanistically, circRHBDD1(4,5) functions as a molecular scaffold that brings IGF2BP2 and DKK1 mRNA into close proximity, thereby facilitating the mA-dependent recognition of DKK1 mRNA by IGF2BP2, which is mediated by WTAP. This interaction enhances DKK1 mRNA stability, leading to increased DKK1 expression and subsequent activation of the PI3K-AKT signaling pathway, thereby driving the malignant progression in OSCC. Collectively, our findings highlight the critical role of the circRHBDD1(4,5)/IGF2BP2/DKK1 axis in OSCC pathogenesis and provide a potential foundation for developing novel targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/09/11
Ren DaixiZhang JiarongHuang MaoWu JieYang MeiLiu YixuanXiang PingjuanQu HongkeWang DanGe JunshangYan QijiaShi LeiXiang BoXiong WeiLi GuiyuanFan ChunmeiZeng Zhaoyang