Ask about this productRelated genes to: MYL9 Blocking Peptide
- Gene:
- MYL9 NIH gene
- Name:
- myosin light chain 9
- Previous symbol:
- -
- Synonyms:
- MYRL2, MLC2, LC20, MRLC1
- Chromosome:
- 20q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-17
- Date modifiied:
- 2015-11-13
Related products to: MYL9 Blocking Peptide
Related articles to: MYL9 Blocking Peptide
- Idiopathic pulmonary arterial hypertension (IPAH) is characterized by irreversible pulmonary vascular remodeling. This pathological remodeling is mainly driven by the aberrant proliferation and migration of pulmonary artery smooth muscle cells (PASMCs). However, the molecular mechanisms underlying these dysfunctions remain incompletely understood. In this study, we integrated single-cell RNA sequencing (scRNA-seq) analysis with in vivo and in vitro validation to identify key driver genes implicated in IPAH. The GSE169471 dataset was acquired from the Gene Expression Omnibus and processed via quality control, clustering, and cell subtype annotation. Further analyses identified dominant cell subtypes, cell-cell communication networks, and differentially expressed genes (DEGs). Hub genes were then screened using multiple bioinformatic algorithms. The selected hub genes were validated in pulmonary arteries from a monocrotaline (MCT)-induced PAH rat model via qPCR and Western blotting. Furthermore, siRNA-mediated knockdown was conducted to investigate the effects of hub gene silencing on HMGB1-induced PASMC proliferation and migration. Our results revealed that SMCs were the dominant communicating cell subtype and were significantly increased in IPAH. A total of 63 upregulated DEGs were identified, primarily enriched in biological processes such as extracellular matrix organization and signaling pathways, including the focal adhesion pathway. Four hub genes (COL1A1, MYL9, COL1A2, and TPM2) were identified, with significantly increased expression observed in the pulmonary arteries of PAH rats. Subsequently, silencing these genes notably reduced HMGB1-induced PASMC proliferation and migration. These findings provide novel insights into the molecular mechanisms of IPAH and highlight these hub genes as potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/30
Li BinbinZhu EnpengWang YijieHu YatingZhang QiLi Fangwei - Airborne microplastic polyethylene terephthalate (PET) accumulates in human lungs and is linked to respiratory pathologies; however, its molecular role in lung adenocarcinoma (LUAD) remains unclear. This study aims to explore the potential carcinogenic mechanisms of PET exposure in LUAD. - Source: PubMed
Publication date: 2026/02/27
Su QianGuo JuanjuanGu YilinXu WangCao HaihongLu YongbinSu FeiHou XiaomingZhang Tao - Colorectal cancer liver metastasis (CRLM) and chemotherapy resistance remain major clinical challenges, with the underlying molecular mechanisms yet to be fully elucidated. In this study, based on analyses of five initial clinical cohorts from FUSCC, the E3 ubiquitin ligase COP1 was identified as a critical driver of CRLM and resistance to oxaliplatin-based chemotherapy. Using an organoid biobank derived from paired primary colorectal tumors and liver metastases, integrated multi-omics analyses (WES, bulk RNA-seq, scRNA-seq) of patient-derived organoids (PDOs) from CRLM revealed significantly elevated COP1 expression in liver metastases compared to primary tumors. High COP1 levels were associated with poor prognosis, increased liver metastatic burden, and resistance to oxaliplatin-based chemotherapy. In vitro and in vivo functional experiments demonstrated that COP1 facilitates CRLM progression by ubiquitinating and degrading LUZP1, thereby releasing DAPK3 from LUZP1-mediated suppression. This process leads to enhanced MYL9 phosphorylation and activation of epithelial-mesenchymal transition (EMT) as well as the JAK2-STAT3-CCND2 signaling axis-pathways crucial for liver metastasis and resistance to oxaliplatin-based chemotherapy. These findings establish the COP1-LUZP1-MYL9 axis as a therapeutic target for CRLM and oxaliplatin-based chemoresistance. Clinically, COP1 expression profiling in PDOs from postoperative specimens enables a precision strategy for managing oxaliplatin-based chemoresistance, especially in the context of FOLFOX. - Source: PubMed
Publication date: 2026/04/05
Zhang RuijiaLuo WenqinZhou QikaiLiang DongguoHao YuankaiChen FanQiu YulinCao YixianShan ZezhiZhang YuLi QingguoCai SanjunLuo DakuiMo ShaoboMa BinLi Xinxiang - The twospot puffer (Takifugu bimaculatus) is a species of significant aquacultural value in East Asia, yet its production is constrained by slow growth rates and suboptimal body morphology. To advance genetic enhancement via marker-assisted selection, we conducted a genome-wide association study (GWAS) focusing on traits related to body shape. Utilizing a full-sib family comprising 167 individuals to reduce genetic variability, we employed whole-genome resequencing to identify 122,553 high-quality (SNPs) for association analysis. Our study identified 17 significant and suggestive SNP loci correlated with torso length (TL), body depth (BD), body width (BWI), head length (HL) and tail length (TAL). Functional annotation of surrounding genomic regions revealed 26 candidate genes associated with these traits, including lrp8, kank4 for TL; tfrc, dab1 for BD; pgm1, cp, rala, and cdh7 for BWI; gli3, sox17a, and zip12 for HL; myl9, smurf2 for TAL. These genes were implicated in skeletal development, cell migration, metabolism, and BMP/TGF-β signaling pathways. Our findings offered the first genetic insights into body shape in T. bimaculatus and provided valuable SNP markers for future genetic mapping of body shape related traits in multi-line famlies and marker-assisted selection breeding programs. - Source: PubMed
Publication date: 2026/04/01
Zhao HongbinWang LingzheChang YanwenLiang ShuangLiang JianLiu HuiruSong AnranLi LeibinGuo YongjunZhou Zhixiong - Rosacea, an inflammatory skin disorder, poses a dilemma owing to limited effectiveness of treatments for pathological vasodilation-mediated erythema. Here, we identify oxoglutaric acid (α-KG) as a rosacea-associated metabolite elevated in patients and correlated with erythema severity. Exogenous α-KG administration ameliorates rosacea-like manifestations in murine models. Mechanistically, α-KG activates OXGR1, a vascular smooth muscle cell (VSMC)-enriched G protein-coupled receptor (GPCR) to induce Gq signaling and enhance MYL9 phosphorylation, promoting VSMC contraction and limiting vasodilation. Cryo-electron microscopy (cryo-EM) structures of OXGR1-Gq complexes bound to α-KG or itaconate reveal a specific bipartite-acid pocket recognizing its endogenous agonist and an activation mechanism distinct from classical GPCRs. Building on these structures, we developed A-1, a synthetic selective OXGR1 agonist that mitigates erythema and inflammation with efficacy comparable to first-line therapy while offering enhanced safety in rosacea-like models. These findings link a metabolite to vascular dysfunction and nominate OXGR1 agonism for precision treatment of erythema and vascular disorders. - Source: PubMed
Publication date: 2026/03/05
Xiao WenqinZhu YanTang XinjieZhu KongkaiZhang WeifengChen MengtingCai KuiXu SanWu ZhengWang MeiLiu JiayiLong LinglongTan ZixinWu AikeZhou SongqiZhao ZhixiangTang YanHuang YingxueWang BenLiu FangfenWang QianYang FanJian DanShi WeiXie HongfuChen XiangGuo LuluDeng ZhiliSun JinpengLi Ji