Ask about this productRelated genes to: MYL3 antibody
- Gene:
- MYL3 NIH gene
- Name:
- myosin light chain 3
- Previous symbol:
- -
- Synonyms:
- CMH8, VLC1, MLC1V, MLC1SB
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: MYL3 antibody
Related articles to: MYL3 antibody
- Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are X-linked dystrophinopathies caused by mutations in the dystrophin (DMD) gene. A common DMD-causing mutation in humans is exon 52 deletion (DMDΔ52), which disrupts the reading frame and abolishes dystrophin expression. Therapeutic skipping of exon 51 or 53 can restore the reading frame, producing a truncated but functional protein and generating a BMD-like phenotype. Porcine models recapitulating DMDΔ52 (DMD) and DMDΔ51-52 (BMD-like) were used to identify molecular differences and condition-specific miRNA-mRNA networks. - Source: PubMed
Reschke SarahGraf AlexanderHadlich FriederJaudas FlorianFröhlich ThomasStirm MichaelKlymiuk NikolaiKrebs StefanWolf EckhardAli Asghar - Amyotrophic lateral sclerosis (ALS) likely has a prolonged presymptomatic phase. Identifying blood biomarkers that predict phenoconversion is critical for early intervention. - Source: PubMed
Publication date: 2026/09/03
Lehrer StevenRheinstein Peter H - Feed scarcity constrains livestock production, particularly on the Qinghai-Tibet Plateau. The effects of green alfalfa (GA) on Diqing Tibetan pig performance remain unclear. This study aimed to evaluate GA effects on Diqing Tibetan pig performance and to explore the potential underlying mechanisms through integrated metagenomic, transcriptomic, and metabolomic analyses. Thirty-six Diqing Tibetan pigs were randomly assigned to two groups and fed either a basal diet or a diet containing 90% basal diet and 10% GA. GA did not adversely affect growth performance but reduced 6-7 rib backfat thickness and muscle water loss rate by 19.79% (FDR = 0.027) and 17.80% (FDR = 0.036), while increasing muscle moisture content by 3.51% (FDR = 0.036). GA increased cecal microbial alpha diversity, Bacteroidota-related taxa, and functional genes related to lipid and vitamin metabolism, while decreasing Bacillota and . In the longissimus dorsi, , and were upregulated, whereas and were downregulated; GA increased vanillyl alcohol, L-histidine, LPE (0:0/22:5), and licochalcone B, but decreased glyceryl monostearate, benzaldehyde, cortisol, tryptamine, 4-ethyloctanoic acid, 8-methylnonanoic acid, and purine. Overall, 10% GA reshaped gut microbial, muscle transcriptomic, metabolomic profiles and collectively influenced 6-7 rib backfat thickness and muscle water-holding capacity in Diqing Tibetan pigs. - Source: PubMed
Publication date: 2026/07/17
Huang HeteLi XinpengZhang KangLiang BingkunBai SiyaDong XinxingYan Dawei - Apolipoprotein A-IV (apoA-IV) plays key roles in lipid metabolism, reverse cholesterol transport, and kidney function, yet its genetic determinants remain poorly defined. We conduct a genome-wide association study (GWAS) meta-analysis of apoA-IV concentrations measured by ELISA in 25,181 individuals and combine these with proteomic data from 33,995 UK Biobank participants (Olink platform), yielding a total sample of 59,176. We perform genetic correlations and colocalization analyses to explore links with lipid, renal, and other complex traits. - Source: PubMed
Publication date: 2026/07/14
Koller AdrianaSchnitzer FlorianKollerits BarbaraLamina ClaudiaMoix SamuelClaringbould AnniqueMishra Binisha HLu HaojieSchachtl-Riess Johanna FForer LukasGieger ChristianKheirkhah AzinLehtimäki TerhoMarques-Vidal PedroSchönherr SebastianStark Klaus JWürzner ReinhardEckardt Kai-UweHeid Iris MKavousi MaryamKöttgen AnnaRaitakari OlliSijbrands Eric J GPeters AnnetteVollenweider PeterKronenberg Florian - Hypertrophic cardiomyopathy (HCM) variants in genes encoding the myosin heavy chain (MHC) (), myosin light chains ( and ), and cardiac myosin binding protein-C (cMyBP-C, ) lead to cardiac hypertrophy, with abnormal contractility, relaxation, and energy consumption. Here, we defined the structural consequences of pathogenic and benign missense variants in these genes by mapping 233 variants (, n = 175; , n = 41; , n = 12; , n = 5) onto a cryo-EM-based atomic model of the human cardiac thick filament. We identified HCM variants residing in 30 molecular interfaces of the complex thick filament interactome, including the two main interfaces of the myosin interacting-heads motif (IHM), and interfaces involving the MHC, essential and regulatory light chains, and cMyBP-C. None of the 21 variants classified as benign were within interfaces. We demonstrated earlier disease onset and adverse outcomes in HCM patients with pathogenic variants within vs. outside of molecular interfaces, emphasizing their importance in normal thick filament function and improving risk stratification of patients. - Source: PubMed
Publication date: 2026/06/29
Dutta DebabrataKim YuriHo Carolyn YSeidman Jonathan GSeidman Christine ECraig RogerPadrón Raúl