Ask about this productRelated genes to: MTRF1 antibody
- Gene:
- MTRF1 NIH gene
- Name:
- mitochondrial translation release factor 1
- Previous symbol:
- -
- Synonyms:
- RF1, MTTRF1, MGC47721
- Chromosome:
- 13q14.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-03
- Date modifiied:
- 2016-10-05
Related products to: MTRF1 antibody
Related articles to: MTRF1 antibody
- The gut microbiome (GM) has been reported to play a role in traumatic brain injury (TBI). To investigate the causal relationship between GMs, inflammatory mediators, and TBI, a comprehensive Mendelian randomization (MR) analysis was conducted. We utilized Genome-Wide Association Study (GWAS) summary statistics to examine the causal relationships between GM and TBI. To assess the potential causal associations between GM and TBI, we employed the inverse-variance-weighted, MR-Egger, and weighted median methods. Mediation analysis was used to assess the possible mediating factors. Several sensitivity analyses methods were implemented to verify the stability of the results. Additionally, we utilized FUMA GWAS to map single-nucleotide polymorphisms to genes and conduct transcriptomic MR analysis. We identified potential causal relationships between nine bacterial taxa and TBI. Notably, class , family , and order ( = 0.0003) maintained a robust positive correlation with TBI. This causal association passed false discovery rate (FDR) correction (FDR < 0.05). Genetically determined 1 inflammatory protein, 30 immune cells and 3 inflammatory factors were significantly causally related to TBI. None of them mediated the relationship between GMs and TBI. The outcome of the sensitivity analysis corroborated the findings. Regarding the mapped genes of significant GMs, genes such as , , , , and in class showed a significant causal correlation with TBI. Our study reveals the potential causal effects of nine GMs, especially on TBI, and there was no link between TBI and GM through inflammatory protein, immune cells, and inflammatory factors, which may offer fresh insights into TBI biomarkers and therapeutic targets through specific GMs. - Source: PubMed
Publication date: 2025/03/20
Song BingyiQiu YoujiaWang ZilanTao YuchenWang MenghanDuan AojieXie MinjiaYin ZiqianChen ZhouqingMa ChaoWang Zhong - Mitochondrial translation is a complex process responsible for the synthesis of essential proteins involved in oxidative phosphorylation, a fundamental pathway for cellular energy production. Central to this process is the termination phase, where dedicated factors play a pivotal role in ensuring accurate and timely protein production. This review provides a comprehensive overview of the current understanding of translation termination in human mitochondria, emphasizing structural features and molecular functions of two mitochondrial termination factors mtRF1 and mtRF1a. - Source: PubMed
Krüger AnnikaKovalchuk DariaShiriaev DmitriiRorbach Joanna - Aging is a well-known factor that accelerates brain deterioration, resulting in impaired learning and memory functions. This current study evaluated the potential of an extract of (AP), an edible flavonoid-rich plant, to ameliorate D-galactose-induced brain aging in male mice. Chronic administration of D-galactose (150 mg/kg/day) in mice mimicked the characteristics of aging by accelerating senescence via downregulation of the following telomere-regulating factors: mouse telomerase reverse transcriptase (mTERT) and mouse telomeric repeat-binding factors 1 (mTRF1) and 2 (mTRF2). D-galactose also decreased the activities of the antioxidant enzymes catalase (CAT) and superoxide dismutase (SOD), while increasing expression of neuroinflammatory cytokines in the frontal cortex and hippocampus. Daily treatment of D-galactose-induced aging mice with AP at 250 and 500 mg/kg/day or vitamin E (100 mg/kg/day) significantly increased the activities of SOD and CAT, as well as expression of mTERT, mTRF1, and mTRF2, which are involved in telomere stabilization, but decreased the levels of proinflammatory cytokines IL-1β, IL-6, and TNF-α. In the behavioral portion of the study, AP improved aging-related cognitive deficits in short-term memory as shown by the Y-maze task and the novel object recognition test (NORT) and long-term memory as shown by the Morris water maze test (MWMT). The flavones kaempferol--glucoside (), quercetin (), alternanthin B (), demethyltorosaflavone D (), and chrysoeriol-7--rhamnoside (), which could be responsible for the observed effects of AP in the D-galactose-induced aging mice, were identified by HPLC analysis. - Source: PubMed
Publication date: 2024/01/19
Aon-Im PossatornMonthakantirat OrawanDaodee SupawadeeChulikhit YaowaredSriya NattapatsornBoonyarat ChantanaChumwangwapee ThanutKhamphukdee CharinyaKijjoa Anake - Mitochondria are the essential players in eukaryotic ATP production by oxidative phosphorylation, which relies on the maintenance and accurate expression of the mitochondrial genome. Even though the basic principles of translation are conserved due to the descendance from a bacterial ancestor, some deviations regarding translation factors as well as mRNA characteristics and the applied genetic code are present in human mitochondria. Together, these features are certain challenges during translation the mitochondrion has to handle. Here, we discuss the current knowledge regarding mitochondrial translation focusing on the termination process and the associated quality control mechanisms. We describe how mtRF1a resembles bacterial RF1 mechanistically and summarize and recent data leading to the conclusion of mtRF1a being the major mitochondrial release factor. On the other hand, we discuss the ongoing debate about the function of the second codon-dependent mitochondrial release factor mtRF1 regarding its role as a specialized termination factor. Finally, we link defects in mitochondrial translation termination to the activation of mitochondrial rescue mechanisms highlighting the importance of ribosome-associated quality control for sufficient respiratory function and therefore for human health. - Source: PubMed
Publication date: 2023/06/29
Nadler FranziskaRichter-Dennerlein Ricarda - The genetic code that specifies the identity of amino acids incorporated into proteins during protein synthesis is almost universally conserved. Mitochondrial genomes feature deviations from the standard genetic code, including the reassignment of two arginine codons to stop codons. The protein required for translation termination at these noncanonical stop codons to release the newly synthesized polypeptides is not currently known. In this study, we used gene editing and ribosomal profiling in combination with cryo-electron microscopy to establish that mitochondrial release factor 1 (mtRF1) detects noncanonical stop codons in human mitochondria by a previously unknown mechanism of codon recognition. We discovered that binding of mtRF1 to the decoding center of the ribosome stabilizes a highly unusual conformation in the messenger RNA in which the ribosomal RNA participates in specific recognition of the noncanonical stop codons. - Source: PubMed
Publication date: 2023/05/04
Saurer MartinLeibundgut MarcNadimpalli Hima PriyankaScaiola AlainSchönhut TanjaLee Richard GSiira Stefan JRackham OliverDreos RenéLenarčič TeaKummer EvaGatfield DavidFilipovska AleksandraBan Nenad