METT10D Blocking Peptide
- Known as:
- METT10D Blocking Peptide
- Catalog number:
- 33r-1370
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- METT10D Blocking Peptide
Related genes to: METT10D Blocking Peptide
- Gene:
- METTL16 NIH gene
- Name:
- methyltransferase like 16
- Previous symbol:
- METT10D
- Synonyms:
- MGC3329
- Chromosome:
- 17p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-12-19
- Date modifiied:
- 2017-11-02
Related products to: METT10D Blocking Peptide
Related articles to: METT10D Blocking Peptide
- Dysfunction of vascular endothelial cells is recognized as a critical driver in pulmonary vascular remodeling of pulmonary hypertension (PH). Although interleukin-6 (IL-6) has been firmly established as an indispensable factor leading to pulmonary vascular remodeling, its downstream molecular mechanisms remain incompletely elucidated. Here, we discover that ubiquitin-specific protease 2a (USP2a) is upregulated in lung tissues of PH patients and preclinical PH models, and in IL-6-stimulated endothelial cells. Both the endothelial cell-specific Usp2a genetic deletion and the pharmacological inhibition of USP2a with the inhibitor ML364 alleviate experimental PH manifestations. Mechanistically, USP2a attenuates the degradation of methyltransferase-like 16 (METTL16) by deubiquitination. Notably, METTL16 reciprocally enhances USP2a expression via interactions with eIF3a and eIF3b in a methyltransferase activity-independent manner, establishing a self-reinforcing USP2a-METTL16 regulatory loop. Subsequent investigations reveal that METTL16 enhances N6-methyladenosine (mA)-mediated IL-6 receptor (IL-6R) mRNA stabilization, thereby promoting the expression of IL-6R. This study demonstrates that endothelial USP2a-METTL16 loop potentiates IL-6 signaling via IL-6R and represents a promising therapeutic target for PH. - Source: PubMed
Publication date: 2026/04/25
Zhu HanqingYuan PingWu XiangyangHuang YuxiaZhang WentianSun XingxingXu JianhuaZhou TianranXu JunfangChen LiYang WenlanLiu JinmingLiu HaipengGao FenghouGuo Jian - Ischemic stroke leads to severe cerebral ischemia/reperfusion (I/R) injury, resulting in neuronal death and neurological deficits. The N-methyladenosine (mA) methyltransferase METTL16 has emerged as a key regulator of RNA metabolism, but its specific role and mechanism in ischemic stroke remain unclear. - Source: PubMed
Publication date: 2026/04/12
Xiang MeilingHan JiemiYe ZaiChen BimengWang Hongbo - Lung cancer is the leading cause of cancer-related death and has the second-highest incidence worldwide. For patients with advanced EGFR-mutated non-small cell lung cancer, EGFR tyrosine kinase inhibitors (EGFR-TKIs) are the preferred treatment option; however, acquired resistance to TKIs is inevitable. Gefitinib and osimertinib, the first-generation and third-generation EGFR-TKI, have shown promising results in patients with EGFR-mutated lung cancer in clinical treatment. Here, we identified that pyruvate dehydrogenase kinase 1 (PDK1) was up-regulated in gefitinib- and osimertinib-resistant cell lines, and PDK1 knockdown rendered cells more sensitive to TKI treatment. PDK1 expression levels were significantly increased in lung, colon, liver, and breast cancer tissues compared with those in normal tissues. Histone demethylase KDM3A was also induced in TKI-resistant cell lines, and demethylated histone H3 lysine 9 to facilitate PDK1 expression to regulate TKI resistance. Further study demonstrated that METTL16 promoted the mA modification of PDK1 mRNA, and the mA reader IGF2BP1 directly recognized and enhanced PDK1 mRNA stability. Interestingly, KDM3A also induced METTL16 expression. Moreover, PDK1 inhibitor JX06 rendered cancer cells more sensitive to gefitinib treatment , and JX06 and gefitinib combination treatments have a synergic effect to inhibit tumor growth. In conclusion, the KDM3A/METTL16/PDK1 axis plays an important role in cancer development and TKI resistance, which may offer new prognostic biomarkers and therapeutic targets for TKI resistance in the future. - Source: PubMed
Publication date: 2025/11/25
Zhou ZhihaoZhang RuikeZhang ZhaoyangZhang LiyuanWang WeiLiu WenjingZhang ChunyangLin GenYu WeimiaoXu BoWang LinJiang Bing-Hua - Premature ovarian failure (POF) and insufficiency induced by cisplatin are common complications associated with gynecological diseases. This study aims to investigate the role of N-methyladenosine (mA) methyltransferase METTL16 in cisplatin-induced ovarian granulosa cells ferroptosis. In cisplatin-treated ovarian tissue, the level of METTL16 was significantly elevated. Furthermore, METTL16 was also upregulated in cisplatin-stimulated granulosa cells. Functionally, silencing METTL16 inhibited iron accumulation and lipid peroxidation, while alleviating mitochondrial injury. Mechanistically, METTL16 was found to target NRF2, negatively regulating its RNA stability, and YTHDF2 facilitated the degradation of NRF2 mRNA. In summary, the METTL16/YTHDF2/NRF2 axis regulates ferroptosis in cisplatin-stimulated granulosa cells in POF. This study suggests that METTL16 may serve as a promising immunotherapeutic target for POF. - Source: PubMed
Publication date: 2026/04/19
Xiong JingHe LingZhang YongjingLi Lifang - -methyladenosine (mA) RNA modification regulates diverse biological process. The mA writers and downstream readers collaboratively undertake mA-mediated RNA metabolism, yet the functional specificity among different writers and readers remains poorly understood. Using limb organogenesis as a development model, we uncover a critical and specific functional axis between the mA reader YTHDC1 and writer METTL16. Depletion of either YTHDC1 or METTL16-but not METTL3-causes severe limb malformations, revealing unexpected functional selectivity. Mechanistically, we demonstrate that YTHDC1 specifically recognizes METTL16-deposited mA marks on chromatin-associated RNAs, orchestrating cotranscriptional splicing of genes vital for cell cycle progression and DNA repair. Loss of YTHDC1 triggers genome-wide transcription arrest and dysregulates key developmental gene expression programs. Importantly, chromatin-bound YTHDC1 recruits splicing factors to transcriptional complex through liquid-liquid phase separation (LLPS), with alkalic arginine residues in its C-terminal region being molecular determinants. Our findings identified a selective and specific METTL16-mA-YTHDC1 axis that couples RNA modification with cotranscriptional splicing during mammalian organogenesis, providing molecular insights into how epitranscriptomic regulation governs developmental decisions. - Source: PubMed
Publication date: 2026/04/14
Zhang ZhongYin QiLin WeiminLi QiwenSheng RuiJiang ShuangLei KexinLiu LinfengZhang LanxinQian ChunlinWen JunruWang ZiruiChen ChongYuan Quan