WTAP Antibody
- Known as:
- WTAP Antibody
- Catalog number:
- XW-7324
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- WTAP Antibody
Related 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
- Osteoarthritis (OA) arises from impaired epigenetic coordination of inflammatory and metabolic cues, leading to compromised cartilage homeostasis. Such coordination is partly governed by ribonucleic acid (RNA) epigenetic mechanisms, however, the role of the predominant RNA modification N-methyladenosine (mA) in this process remains unclear. Herein, we identify an epigenetic-metabolic pathway in which Wilms' Tumor 1-Associating Protein (WTAP)-mediated mA modification stabilizes low-density lipoprotein receptor-related protein 1 (LRP1) and redirects lipid metabolism toward chondrogenesis. Loss-of-function assays demonstrate that WTAP is required for the chondrogenic differentiation of BMSCs, as its depletion suppresses the expression of multiple cartilage-associated genes. Mechanistically, WTAP enhances mA methylation and stabilizes Lrp1 transcripts, a key regulator of cholesterol metabolism and matrix synthesis, thereby driving lipid metabolic reprogramming toward chondrogenesis. Structure-based screening identified silibinin and estradiol benzoate as LRP1-specific agonists that activate the WTAP-LRP1 pathway to promote cartilage repair in vivo. Collectively, our findings establish mA-dependent metabolic reprogramming as a pivotal epigenetic mechanism of cartilage regeneration with therapeutic potential for promoting chondrogenesis. - Source: PubMed
Publication date: 2026/05/06
Huang ChenyanDeng ChenyuGao ZhengrongChen ChenZheng HuiminYang YueWei Yan - This review aims to synthesize and evaluate the evidence on the role of N-methyladenosine (mA) modification in pathogenesis, progression, and tissue repair of endodontic diseases, focusing on its regulatory functions in dental stem cells. - Source: PubMed
Publication date: 2026/05/04
Liao SupingGuo JihuaJia Rong - The lncRNA SH3PXD2A-AS1 drives therapy resistance in non-small cell lung cancer (NSCLC) through mA-mediated PD-L1 overexpression, representing a novel molecular toxicology paradigm. In the present work, the functional significance of SH3PXD2A-AS1 in orchestrating immune escape and malignant progression of NSCLC was systematically examined. Integrating TCGA analyses with cell and mouse studies, we found that SH3PXD2A-AS1 was elevated in NSCLC and associated with features of an immunosuppressive tumor microenvironment. Multi-omics profiling, RNA pull-down/RIP, and promoter-reporter assays revealed that SH3PXD2A-AS1 interacts with the transcription factor MYBL2 to drive transcriptional activation of WTAP, a core component of the mA writer complex. This axis enhanced mA modification of PD-L1 mRNA, stabilizing PD-L1 and dampening CD8 T-cell responses. Silencing SH3PXD2A-AS1 reduced MYBL2/WTAP/PD-L1 signaling, decreased malignant phenotypes in vitro, and restored antitumor T-cell activity in humanized mouse models, whereas enforced MYBL2 or WTAP expression counteracted these effects. Collectively, these findings define an lncRNA-transcription factor-epitranscriptomic checkpoint that sustains PD-L1-mediated immune escape in NSCLC, and nominate SH3PXD2A-AS1 and its MYBL2/WTAP partners as potential biomarkers and therapeutic targets to improve responses to immune checkpoint inhibition. - Source: PubMed
Wu SiyanChen JuanHan YuDong YuanShi HaiLiu PingchuangChen YunfengYuan JieqingCui Wenjie - Castration-resistant prostate cancer (CRPC) is one of the most prevalent cancers in men. The new generation androgen receptor (AR) inhibitor enzalutamide can improve the therapeutic effectiveness of patients with CRPC. However, these patients eventually develop acquired enzalutamide resistance (ENZR), and the mechanisms underlying resistance are not well understood. Wilms' tumor 1-associating protein (WTAP) plays an important role in mA modification and has been reported as an oncogene in various cancers. Here, we utilized a tissue microarray and collected tissues from prostate cancer (PCa) patients to detect WTAP expression, and found that WTAP is upregulated in PCa. Meanwhile, WTAP overexpression promotes cell proliferation and accelerates tumor growth through colony formation assays and the establishment of a subcutaneous xenograft model in vivo. These findings establish the tumor promoter role of WTAP in prostatic tumorigenesis. Furthermore, we verified that WTAP is a novel responsive gene of AR via promoter activity and chromatin immunoprecipitation (ChIP) assays. Importantly, we uncovered that WTAP is upregulated in ENZR cells, and WTAP knockdown inhibited the proliferation of ENZR cells. Mechanistically, ubiquitin-specific protease (USP7) enhanced the stability of WTAP by the ubiquitin-proteasome pathway in ENZR cells, thereby WTAP increases promote AKT signaling through an mA-mediated way, and an AKT inhibitor can abolish the pro-resistance phenotype mediated by WTAP. Together, these findings suggest that WTAP plays a key role in ENZR development of PCa cells, and WTAP may be a potential treatment target for ENZR tumors. In this manuscript, we utilized a tissue microarray and collected tissues from prostate cancer (PCa) patients to detect WTAP expression, and found that WTAP is upregulated in PCa. Meanwhile, WTAP overexpression promotes cell proliferation and accelerates tumor growth through colony formation assays and the establishment of a subcutaneous xenograft model in vivo. These findings establish the tumor promoter role of WTAP in prostatic tumorigenesis. Furthermore, we verified that WTAP is a novel responsive gene of AR via promoter activity and chromatin immunoprecipitation (ChIP) assays. Importantly, we uncovered that WTAP is upregulated in ENZR cells, and WTAP knockdown inhibited the proliferation of ENZR cells. Mechanistically, ubiquitin-specific protease (USP7) enhanced the stability of WTAP by the ubiquitin-proteasome pathway in ENZR cells, thereby WTAP increases promote AKT signaling through an mA-mediated way, and an AKT inhibitor can abolish the pro-resistance phenotype mediated by WTAP. Together, these findings suggest that WTAP plays a key role in ENZR development of PCa cells, and WTAP may be a potential treatment target for ENZR tumors. - Source: PubMed
Publication date: 2026/04/14
Shi RuxueGu KaiLi HaichuanSun QingweiWu XinyuHuang ShuhongHu Qingxia - - Source: PubMed
Publication date: 2026/04/13
Tang YingYi ZhaoquanHuang BoWu JingxinTian BiaoLong Guoliang