Ask about this productRelated genes to: MYOZ1 antibody
- Gene:
- MYOZ1 NIH gene
- Name:
- myozenin 1
- Previous symbol:
- MYOZ
- Synonyms:
- FATZ, CS-2
- Chromosome:
- 10q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-10-23
- Date modifiied:
- 2016-10-05
Related products to: MYOZ1 antibody
Related articles to: MYOZ1 antibody
- BackgroundThe extent and biological relevance of shared genetic architecture between myocardial infarction (MI) and heart failure (HF) remain incompletely understood.MethodsWe analyzed large-scale European-ancestry genome-wide association studies summary statistics for MI and HF. Genome-wide genetic correlation was estimated using linkage disequilibrium score regression, and polygenic overlap was quantified using MiXeR. Shared loci were identified via conditional and conjunctional false discovery rate (condFDR/conjFDR) approaches. Functional prioritization incorporated Functional Mapping and Annotation-based annotation, Bayesian fine-mapping, transcriptome-wide association studies (TWAS), FOCUS gene fine-mapping, and summary-level Mendelian randomization (SMR) integrating UKB-PPP proteomic data.ResultsLinkage disequilibrium score regression revealed a robust positive genetic correlation between MI and HF (rg = 0.494, = 1.12 × 10). MiXeR demonstrated substantial polygenic overlap, with approximately 90% of MI-associated variants shared with HF and strong concordance in effect direction. The cond/conjFDR analyses identified multiple pleiotropic loci, including novel HF-associated regions. Fine-mapping prioritized rs544366796 within the SLC22A2/SLC22A3 locus as a high-confidence candidate variant for MI based on posterior probability. The TWAS and FOCUS highlighted canonical MI genes (CDKN2B, CELSR2, BRAP, NBEAL1) and identified MYOZ1 as an HF-specific candidate gene. Proteome-wide SMR analysis provided statistical evidence consistent with apolipoprotein E being a shared protein influenced by variants associated with both MI and HF.ConclusionThe MI and HF share substantial genetic liability characterized by strong polygenic overlap and pleiotropic loci. Our integrative analyses suggest a potential 2-stage genetic framework linking ischemic susceptibility to myocardial remodeling and HF progression, which should be interpreted as a hypothesis-generating conceptual model rather than direct evidence of temporal progression. - Source: PubMed
Publication date: 2026/05/16
Liu RuikangSun ChiyunJiang NanLiu YangLi JunZhang FuyuanChen CongLiu YiyingQi XiaodiGuo BingtingYang Kai - Heart failure (HF) is a leading global cause of morbidity and mortality, yet the regulatory molecular mechanisms that link genetic variation to cardiac dysfunction remain elusive. To bridge this gap, we created the Trans-Omics for Precision Medicine in Congestive Heart Failure (TOPCHeF) resource, a multi-omics dataset comprising >700 human left-ventricular tissue samples, including dilated cardiomyopathy (DCM), ischemic cardiomyopathy (ICM), and non-failing controls, with paired whole-genome and RNA sequencing. By mapping expression- (eQTL) and splicing- (sQTL) quantitative trait loci directly in diseased human hearts, we identified over 10,000 transcripts with significant eQTL and 8,600 isoforms with significant sQTL, across both coding and non-coding genes, many of which overlap loci previously associated with HF and emerging novel gene associations. Single-locus colocalization with a largescale DCM genome-wide association study revealed 21 expression and 17 splicing-QTL that share causal variants with disease risk. These include known Mendelian cardiomyopathy risk genes such as and , and novel regulatory candidates like , , , , , and . Several loci also showed coordinated effects on both gene expression and RNA splicing, implicating calcium signaling, cytoskeletal organization, and metabolic pathways in HF pathogenesis. Together, these results help define the regulatory landscape of the failing human heart and establish TOPCHeF as a foundational resource for connecting genetic variation to transcriptional and splicing molecular mechanisms in HF research. - Source: PubMed
Publication date: 2026/01/13
Murray Connor SYang ChaojieChen Suet NeeGraw SharonKarimpour-Fard AnisCleveland JosephGao ShanshanIm Hae KyungWheeler Heather EAmbardekar Amrut VHoffman Jordan R HGabriel StaceyGupta NamrataArdlie KristinRotter Jerome ITaylor Kent DRich Stephen SMestroni LuisaManichaikul AniTaylor Matthew R G - This study applied shotgun proteomics to investigate the temporal changes in goat meat exudate and elucidate the biochemical mechanisms underlying postmortem aging. Exudates were collected from vacuum packaged goat Longissimus thoracis muscles at 24, 48 and 72 h postmortem. A total of 823 proteins were identified and quantified, of which 188 were differentially abundant: n = 60 between 24 h vs. 48 h, n = 56 between 48 h vs. 72 h and n = 168 between 24 h vs. 72 h. Comparative analyses revealed distinct temporal release patterns, with catalytic and ATP-metabolic proteins predominating early postmortem (17%), structural and contraction-related proteins peaking between 48 h and 72 h (39%), and binding, transport, and calcium homeostasis proteins (27%), as well as extracellular matrix (ECM) and matrisome components (14%), accumulating later. Chaperones including heat shock proteins and proteolytic and related enzymes were consistently released from 24 h to 72 h, but in lower percentages (5% and 4%, respectively). Overlap analysis identified 14 core proteins including FLNC, TNNI2, TNNC2, PDLIM7, TMOD4, MYOZ1, MYBPC1, MYOM2 (muscle contraction and structure), DYSF, EIF4G2, PPARGC1A (binding, transport and calcium homeostasis), DCN, OGN, and IGFALS (matrisome and ECM associated proteins), shared across all time points, which mapped to five significantly enriched pathways, primarily myofibril assembly and muscle system processes. These findings provide the first comprehensive proteomic profile of goat meat exudate, demonstrating its potential as a non-invasive source for monitoring postmortem biochemical changes and meat tenderization dynamics, ultimately offering insights to improve meat quality. - Source: PubMed
Publication date: 2026/01/22
Gagaoua MohammedAlbenzio MarziaDella Malva Antonella - Myozenin 1 (MYOZ1) is expressed in fast-twitch muscle fibers and functions as a calcineurin (CaN)-interacting protein. The deletion of MYOZ1 was reported to enhance the exercise capacity of mice. It would be prospective to explore the exact role of MYOZ1 in Duchenne muscular dystrophy pathology. The transfection of an adenoviral MYOZ1 shRNA in mdx mice was used to knock down MYOZ1 expression. Forelimb grip strength test, hanging wire test, and run-to-exhaustion test were conducted for assessing muscle strength and exercise ability of mice. Muscle tissue pathology was detected by HE and Masson staining. In addition, the myofiber composition of tibialis anterior muscle relied on detecting the markers of slow- fast-twitch muscle fibers. Then, the indicators of mitochondrial function, autophagy, and fission were also investigated. According to the results, in the tibialis anterior muscle of mdx mice, MYOZ1 inhibition facilitated CaN signal transduction and ameliorated muscle atrophy, also upregulated slow-twitch muscle fiber markers and downregulated fast-twitch muscle fiber markers. Besides, mitochondrial DNA and ATP content and mitochondrial membrane potential were increased in the MYOZ1 silenced group. The inhibition of MYOZ1 also promoted the expressions of mitochondrial autophagy and fission-associated proteins, including LC3I, LC3II, and p-DRP1 (Ser637). Cyclosporin A, a CaN signaling inhibitor, reversed the effect of MYOZ1 inhibition described above. In conclusion, MYOZ1 inhibition mitigated the pathological progression of tibialis anterior muscle in mdx mice, presenting as the improved mitochondrial function and increased slow-twitch muscle fibers. - Source: PubMed
Cai NaZhai WenZhang RuixueSun Siyuan - Stress urinary incontinence (SUI) remains a significant clinical challenge due to the lack of strategies that simultaneously address muscle degeneration, neurogenic atrophy, and vascular deficits. Here, we report an innovative injectable system that combines a thermo-responsive poly(N-isopropylacrylamide)-COOH/leucine/decellularized extracellular matrix hydrogel with adipose-derived stem cells (ADSCs) pre-programmed by zeolitic imidazolate framework-8/polyethylene glycol 200@magnesium (ZIF-8/PEG200@Mg) nanoparticles. In vitro, programmed ADSCs exhibit enhanced neurogenic differentiation, while the hydrogels support robust myogenic activity and cell viability. In a female rat model of SUI-chosen to reflect the higher prevalence of SUI in women-the composite system leads to a marked improvement in leak point pressure (LPP) and restores urethral sphincter function. Mechanistic analyses reveals upregulation of muscle regeneration (e.g., Myoz1, Smyd1) and neurogenesis/neuromuscular junction stabilization (NMJ) stabilization genes (e.g., Dok7, Musk), highlighting a coordinated multi-lineage regenerative process. This work establishes an integrated regeneration-plus-support injectable strategy, offering a regenerative medicine-based approach that surpasses conventional bulking or sling therapies for SUI. - Source: PubMed
Publication date: 2025/09/25
Fang WenzhuoDu XuanYang RanxingLiu MengYang MingJin YangwangGao GuoFu QiangWang Ying