Ask about this productRelated genes to: SMCR7L antibody
- Gene:
- MIEF1 NIH gene
- Name:
- mitochondrial elongation factor 1
- Previous symbol:
- SMCR7L
- Synonyms:
- FLJ20232, MiD51
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-06-26
- Date modifiied:
- 2014-11-19
Related products to: SMCR7L antibody
Related articles to: SMCR7L antibody
- To investigate the regulatory role of epigenetic regulator disruptor of telomeric silencing 1-like (DOT1L) and its mediated histone H3 lysine 79 (H3K79) methylation in modulating neuronal amyloid precursor protein (APP) expression, and to elucidate the underlying mechanisms involving mitochondrial homeostasis and the upstream p38 kinase. - Source: PubMed
Publication date: 2026/06/29
Zhang YuminZhu FeiyuWu XiaotianLi ZhansongHuang PengGao YanpanZeng Linghui - Post-intensive care syndrome (PICS) is defined by persistent psychological, cognitive and physical impairments after critical illness, yet its shared genetic basis remains unknown. We applied genomic structural equation modeling (Genomic SEM) to large-scale GWAS summary statistics for major depressive disorder (N = 217,584), post-traumatic stress disorder (N = 199,213), cognitive function (N = 257,841), memory performance (N = 152,605) and hand grip strength (N = 461,089) to construct a latent genetic factor related to PICS component phenotypes. We then performed multivariate GWAS, Bayesian fine-mapping, MAGMA, sCCA-TWAS with FOCUS, pathway enrichment, cell-type analysis and spatial transcriptomic mapping. A single factor Genomic SEM showed good fit (CFI = 0.981; SRMR = 0.168). The factor GWAS identified 1,301 genome-wide significant SNPs and 590 largely independent lead variants, including 574 novel signals not genome-wide significant in any input trait. Fine-mapping and TWAS convergently prioritised loci and genes such as NTRK1, CACNA1C, SPG11, MLKL, TRIB3, WNT5B, C2orf88, TRIM38, MIEF1, MSTN, implicating neuronal plasticity, programmed cell death, immune-inflammatory regulation, metabolic stress and muscle wasting. Heritability was enriched in conserved coding regions, non-myeloid neurons, and embryonic brain, spinal cord, dorsal root ganglion, muscle and barrier organs. These findings provide empirical support for a shared polygenic architecture underlying PICS-related traits and offer a multilevel map of variants, genes, pathways, cell types and tissues that may shape long-term psychological, cognitive and physical vulnerability after critical illness. - Source: PubMed
Publication date: 2026/04/01
Lv QuankunWu GuoxinHuang ZihaoHuo JiaxianHuang XinmingYang BinYe YiCai YanglinChen ShenganChen LongGuan ZiyunLiu Zhiyu - - Source: PubMed
Publication date: 2026/03/18
Zhou JiayuZhang ShizhenLi ZhijunChen ZhoumiaoXu YongYe WeiwenHe Zhengfu - Cell motility is critical for physiological processes including wound healing. However, high concentrations of motility-promoting agents may suppress cellular migration; this newly observed phenomenon warrants further characterization. - Source: PubMed
Publication date: 2026/02/04
Li Chang-ZhiZhou Hong-JuanChen Jin-DongHuang JieLiu Yi-XiuQian Chao-Nan - Glaucoma remains the leading cause of irreversible blindness worldwide. Trabecular meshwork (TM) dysfunction, particularly fibrosis, is a major driver of elevated intraocular pressure (IOP). Although steroid-induced glaucoma is well established, the impact of chronic stress-related endogenous steroids on TM pathology remains unclear. This study established a corticosterone induced chronic stress mouse model and a cortisol treated human TM cells (HTMCs) model that demonstrated that sustained steroid elevation promotes TM fibrosis and mitochondrial dysfunction. RNA sequencing of HTMCs after cortisol treatment revealed monoamine oxidase A (MAOA) upregulation and enrichment of profibrotic pathways. Cortisol increased mitochondrial elongation factor 1 (MIEF1) and dynamin-related protein 1 (DRP1) phosphorylation at Ser616 (p-DRP1), driving excessive fission. Knockdown of MAOA or MIEF1 reduced oxidative stress, mitochondrial fragmentation, and extracellular matrix remodeling, whereas overexpression of MAOA and MIEF1 produced the opposite effect. Molecular docking, molecular dynamics simulations, and co-immunoprecipitation confirmed that MAOA interacts with MIEF1 and enhances MIEF1-DRP1 coupling. This study identified the MIEF1-MAOA-DRP1 pathway as a mediator of stress-induced TM fibrosis. It provides new insight into the pathogenesis of glaucoma and identifies MAOA as a potential intervention target for treating glaucoma. - Source: PubMed
Publication date: 2026/01/22
Sun YilinSun YingjianWang MingxuanSi ZhiboZhang ZhaoyingZheng Yajuan