Ask about this productRelated genes to: MYH9 antibody
- Gene:
- MYH9 NIH gene
- Name:
- myosin heavy chain 9
- Previous symbol:
- DFNA17
- Synonyms:
- NMMHCA, NMHC-II-A, MHA, FTNS, EPSTS
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-12
- Date modifiied:
- 2019-04-23
Related products to: MYH9 antibody
Related articles to: MYH9 antibody
- As a major global health threat, tumors present significant clinical challenges due to their heterogeneity, metastatic potential, and therapy resistance. In recent years, non-coding RNAs, particularly microRNAs (miRNAs), have emerged as crucial players in cancer research. Among them, let-7f, a key member of the let-7 family, exhibits significant dysregulation and biological functions in various cancers. This review systematically summarizes the differential expression patterns of let-7f in common malignancies, revealing its prevalent downregulation in cancers such as lung, gastric, colorectal, breast, and glioblastoma. This downregulation is closely associated with tumor size, stage, metastatic potential, and patient prognosis. The expression of let-7f is regulated by multiple molecular mechanisms, including transcription factors (e.g., C/EBPβ), RNA-binding proteins (e.g., LIN28), ceRNA networks (e.g., FAM222A-AS1, LINC00106), and genetic polymorphisms. Regarding biological functions, let-7f inhibits tumor cell proliferation, invasion, metastasis, stemness maintenance, and metabolic reprogramming by targeting multiple oncogenes (e.g., MYH9, HMGA2, ADAMTS1, Periostin) and key signaling pathways (e.g., MAPK, Wnt, PI3K/AKT). Furthermore, let-7f is involved in modulating the tumor microenvironment, including angiogenesis, stromal cell function, and the immune milieu. At the therapeutic level, let-7f not only serves as a predictive biomarker for the efficacy of chemotherapy, radiotherapy, and endocrine therapy but also holds potential for reversing drug resistance and enhancing drug sensitivity. For diagnosis, its stable presence in body fluids like plasma and stool offers a non-invasive detection advantage, positioning it as a promising novel biomarker for various cancers. However, challenges remain, including the standardization of detection methods, optimization of delivery systems, and insufficient clinical validation. Future efforts should integrate multi-omics analyses, artificial intelligence-assisted modeling, and novel nanodelivery technologies to advance the translation of let-7f from basic research to clinical application, thereby providing new strategies for the precise diagnosis and treatment of cancer. - Source: PubMed
Publication date: 2026/05/29
Deng JianhuaLi DaoshengLi ZhiqiPan YuanmingZeng Xiangsheng - Fetal growth restriction (FGR) remains a major contributor to neonatal morbidity and mortality worldwide, with limited effective diagnostic and therapeutic options. To better understand its molecular mechanism, we performed integrated multi-omics analyses of placental tissues from FGR pregnancies and normal controls, identifying Ring Finger Protein 126 (RNF126), an E3 ubiquitin ligase, as a key regulator of FGR and a potential biomarker distinguishing FGR from small-for-gestational-age (SGA) fetuses. Placenta-specific RNF126 conditional knockout (cKO) mice demonstrated a causal role of elevated placental RNF126 in FGR development . Functional studies revealed that RNF126 induced endoplasmic reticulum (ER) stress and apoptosis in trophoblasts. Mechanistically, RNF126 promoted a ubiquitin-proteasome-mediated degradation of the MYH9/MYH10 complex, thereby exacerbating ER stress and impairing trophoblast function, with lysine 833 (K833) of MYH9 identified as a critical ubiquitination site. Collectively, these findings elucidate an RNF126-mediated pathogenic mechanism in FGR and highlight RNF126 as a promising biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/06/08
Lu LilinYe XiaomeiLan JiawenXu ShuxiuCheng ManyuLv ChenlinZhou JunLi Jing - Epstein-Barr virus (EBV) lytic reactivation contributes to the pathogenesis of EBV-associated epithelial malignancies, including nasopharyngeal carcinoma and gastric carcinoma, highlighting the need for therapeutic strategies targeting viral reactivation. Capsaicin exhibits anticancer and antiviral activities; however, its effects on EBV lytic reactivation remain unclear. This study investigated the effects of capsaicin on EBV lytic reactivation in EBV-positive epithelial cancer models. Capsaicin significantly suppressed the expression of lytic genes, including , , , and , and reduced EBV virion production. Proteomic analysis revealed alterations in host cellular pathways associated with metabolism, chromatin organization, and cytoskeletal regulation, whereas metabolomic profiling demonstrated perturbations in nucleotide, amino acid, and polyamine metabolism processes involved in viral DNA replication and protein synthesis. Protein-protein interaction network analysis identified key host proteins, including HSP90AB1, MYH9, and ANXA2, implicated in metabolic reprogramming, cytoskeletal organization, and stress responses. Moreover, upstream regulators associated with EBV lytic activation, including p65, AP-1, HIF-1α, and SP1, were down-regulated following capsaicin treatment. Collectively, these findings demonstrate a multitarget inhibitory effect of capsaicin on EBV lytic reactivation and support its therapeutic potential against EBV-associated epithelial malignancies. - Source: PubMed
Publication date: 2026/06/05
Chatchawankanpanich NutchanatPiyapittayanun ChanitchotePientong ChamsaiHeawchaiyaphum Chukkris - Zika virus (ZIKV) infection represents an emerging cause of cardiovascular pathology, yet the molecular mechanisms driving virus-induced vascular injury remain incompletely defined. This investigation identifies a crotonylation pathway underlying ZIKV-induced vascular disease. We demonstrate that ZIKV infection upregulates the metabolic regulator ACSS2, consequently elevating intracellular crotonyl-CoA levels. This metabolic shift drives lysine crotonylation of the cytoskeletal protein MYH9 at the critical K82 residue, triggering a pathological transition of vascular smooth muscle cells from contractile to synthetic phenotypes. This cellular reprogramming promotes aortic injury across multiple animal models, including northern pig-tailed macaques and A129 mice. Genetic ablation of ACSS2 substantially attenuated both the phenotypic switching and disease progression. Furthermore, we developed a targeted therapeutic peptide that effectively inhibits MYH9-K82 crotonylation and mitigates pathological vascular remodeling. These findings not only elucidate ACSS2-mediated protein crotonylation as a fundamental mechanism in ZIKV-induced vasculopathy but also present a promising precision therapeutic strategy for treating virus-induced proliferative vascular diseases. - Source: PubMed
Publication date: 2026/05/28
Gao Wen-CongWang Bin-BaoYang Ren-HuaMa LiangWang PengMa XinYang Tie-HuaTan Jia-XiangQiao Guan-RongZhang Ding-ChengYu He-MinJiang Ying-JieZhang Hong-YeZheng Yong-TangChen PengZheng Chang-Bo - MYH9-related disease (MYH9-RD) is an autosomal dominant disorder characterized by thrombocytopenia, giant platelets, and variable systemic manifestations including nephropathy. While most pathogenic MYH9 variants are missense substitutions causing dominant-negative effects, the pathogenic potential of non-missense variants, particularly those affecting splicing, remains unclear. - Source: PubMed
Publication date: 2026/05/26
Inoue SeiyaNagano ChinaMatsuo MasafumiAoyama ShuheiKimura YukaInoki YutaSakakibara NanaHorinouchi TomokoYamamura TomohikoIshimori ShingoNozu Kandai