Ask about this productRelated genes to: MYL7 antibody
- Gene:
- MYL7 NIH gene
- Name:
- myosin light chain 7
- Previous symbol:
- -
- Synonyms:
- MYLC2A, MYL2A
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-14
- Date modifiied:
- 2016-10-05
Related products to: MYL7 antibody
Related articles to: MYL7 antibody
- Abnormal cardiac valve development may lead to functional impairment in adulthood. , a highly conserved receptor of the BMP family, exists in two subtypes ( and ) in zebrafish. However, the roles of and in valve development remain unclear. In this study, we generated three mutant zebrafish strains, namely, - and -knockout zebrafish ( and , respectively) using CRISPR/Cas9 and and double-knockout zebrafish ( ) according to and hybridization. Using cardiac function assessment (M-mode), we characterized the cardiac developmental phenotypes of the three zebrafish mutant strains. Transcriptomic profiling (RNA-seq) was combined with whole-mount hybridization (WISH) and qRT-PCR to validate gene-expression changes. The results indicated that , , and mutant zebrafish strains exhibited valve developmental defects at 52 hours post-fertilization (hpf), followed by cardiac contractile dysfunction. RNA-seq revealed upregulation of cardiac markers (, , , , , and ) and valve-related genes (, , and ), along with the downregulation of , as validated by WISH and qRT-PCR. Pathway analysis identified the ECM-receptor interaction as a key regulatory axis of -mediated valve development. In this study, we demonstrate that and cooperatively regulate cardiac contractile function and valve development in zebrafish, providing insights into BMPR2-mediated cardiovascular morphogenesis in humans. - Source: PubMed
Publication date: 2026/03/23
Shi YanHuang YanliXia YuLi YongqingWang YuequnYuan WuzhouLi FangJiang ZhigangChen YuZhu PingZhuang JianWu XiushanFan Xiongwei - Myocardial infarction (MI), a significant complication of coronary artery disease (CAD), results from prolonged myocardial ischemia. Generally, MI is caused by the rupture of an atherosclerotic plaque and thrombus formation. Among various pharmaceutical therapies and interventions, percutaneous coronary intervention (PCI) restores blood flow to the heart through reperfusion. These therapies do not target any of the signaling pathways involved in cardiac tissue repair post-MI. Specifically, the JAK2/STAT3 pathway is a key mediator of cardiac repair and defence mechanisms. This study investigated the cardioprotective efficacy of a novel fluorinated benzothiazole derivative, AS09. The in silico studies preliminarily revealed the potential interactions of AS09 with MI targets (JAK2, GSK3B, and PIK3CA). Behavioural Assays determined that AS09 significantly improved anxiety and increased locomotion. Biochemical assay showed that AS09 significantly increased the levels of antioxidant enzymes (SOD and CAT) and reduced oxidative stress (MDA) and cell death (LDH). Gene expression analyses further exhibited the decreased expression in inflammation and apoptosis (tnf-α, nf-κb, and Caspase-3). Whereas, increased expression of the antiapoptosis (bcl-2) and cardiac function (myl7, vmhc) associated genes suggests the potential for regeneration by AS09. The reduced myocardial fibrosis and increased structural repair observed at 28 days post-treatment (confirmed by histological analysis with H&E and MTS staining) indicate that AS09 has cardioprotective and regenerative properties. Additionally, these data preliminarily support the cardio-protective and regenerative potential of AS09, with in silico predictions suggesting involvement of the JAK2/STAT3 signaling pathway. - Source: PubMed
Publication date: 2026/02/14
Dharshan Santhanam SanjaiRao Shreya MadhankumarRanjan Nayak S P RamyaRamamurthy KarthikeyanMurali PradeepPalaniappan SenthilkumarRajagopal RajakrishnanAlfarhan AhmedChoi Ki ChoonKumaradoss Kathiravan MuthuRaja Namasivayam S KarthickArockiaraj Jesu - Aromatase, the key enzyme for estrogen biosynthesis, is present in zebrafish as two isoforms: the ovarian form (cyp19a1a; Aromatase A (AroA)) and the brain form (cyp19a1b; Aromatase B (AroB)). Here, we investigated the role of AroA in early cardiac development. RT-PCR and immunostaining demonstrated that only AroA, and not AroB, is expressed in the zebrafish heart, specifically in atrial and ventricular cardiomyocytes and smooth muscle cells of the bulbus arteriosus. Dot blot analysis and whole-mount immunostaining confirmed the reduction of AroA expression in AroA morphants at 2 days post-fertilization (dpf). Phenotypic analysis revealed impaired yolk sac extension and reduced heart size, accompanied by significant downregulation of yolk-associated mRNA expression (vitellogenin 1 (vtg1), ribonuclease-like 2 (rnasel2)) and cardiac development genes (myosin light chain 7 (myl7), natriuretic peptide A (nppa), leucine-rich repeat-containing protein 10 (lrrc10)). Moreover, AroA knockdown suppressed dopamine β-hydroxylase (DBH) protein expression in catecholaminergic cells and significantly reduced heart rate. Morphological assessment using cardiac myosin light chain 2 (cmlc2):GFP and histological staining showed normal cardiac looping but smaller ventricular chambers. Additionally, morphants exhibited reduced end-systolic volume (ESV) and end-diastolic volume (EDV), accompanied by decreases in stroke volume (SV), cardiac output (CO), and ventricular fractional shortening (FS%). Altogether, these findings demonstrate that AroA is an essential regulator of zebrafish heart morphogenesis and function. - Source: PubMed
Publication date: 2026/01/21
Ulhaq Zulvikar SyambaniKishida Mitsuyo - Activating transcription factor 3 (ATF3) is a crucial regulator of gene expression in response to physiological stress across various tissues. Abnormal ATF3 expression is associated with cardiac dysfunction; however, the mechanisms by which it affects cardiac pathology remain unclear. In this study, we developed a cardiac-specific ATF3-expressing zebrafish line, Tg(myl7:ATF3), using a well-established vertebrate model for cardiovascular research to investigate the role of human ATF3 in the zebrafish heart. We conducted morphological assessments, immunofluorescence staining, electrocardiography, and transcriptome analysis on transgenic and wild-type zebrafish. Compared to wild-type siblings, Tg(myl7:ATF3) zebrafish exhibited significant pathophysiological changes, including cardiac hypertrophy and features resembling hypertrophic cardiomyopathy. Histological analysis revealed increased fibrotic scarring and disorganized sarcomeres. Electrocardiogram measurements indicated that ATF3 overexpression induced symptoms resembling long QT syndrome, suggesting electrical dysfunction. Transcriptome analysis demonstrated downregulation of apoptosis-related genes and upregulation of proliferation-related genes in the hearts of transgenic zebrafish. These findings suggest that ATF3 expression is associated with cardiac hypertrophy accompanied by increased proliferation of cardiac cells, including cardiomyocytes. The findings of this study provide novel insights into the role of ATF3 in cardiovascular disease progression. - Source: PubMed
Publication date: 2025/12/26
Kim EunmiKim JinhoMoon Hyun-YiKim Ji YeonJeong Myong-HoKim Geun-YoungLee Seung HeeKim Chul-HongKim Jung-WoongKim Won-Ho - Paediatric heart transplantation requires lifelong immunosuppression, highlighting the need for recovery-oriented strategies. A subset of children with dilated cardiomyopathy (DCM) recovers left ventricular (LV) function after LV assist device (LVAD) implantation, allowing for device explantation. We aimed to identify factors associated with LV functional recovery using single-nucleus multiomics analysis of LV tissue collected at LVAD implantation. - Source: PubMed
Publication date: 2025/10/20
Kugo YosukeKawamura TakujiHarada AkimaTominaga YujiMiki KenjiIshida HidekazuUeno TakayoshiMiyagawa Shigeru