ArticleNucleic acids research2011
TEFM (c17orf42) is necessary for transcription of human mtDNA.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.
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Who cites it
115 citing papers in PubMed, 181 citations in OpenAlex.
- ABHD11-Mediated mtDNA Transcription Restored Mitochondrial Function to Attenuate Cardiomyocyte Ferroptosis After Myocardial Infarction.Circulation · 2026Article
- USP15-mediated deubiquitination of FIS1 impairs mitochondrial function and sensitizes bladder cancer cells to radiotherapy.Oncogene · 2026Article
- Distinct Mitochondrial Central Dogma Gene Expression in the Buffalo Brain: A Comparative Transcriptomic Study with Metabolically Active Organs.Molecular neurobiology · 2026Article
- TEFM drives cartilage degeneration in osteoarthritis via the ROS-AKT/NF-κB signaling axis.Frontiers in immunology · 2026Article
- POLRMT overexpression increases mtDNA transcription without affecting steady-state mRNA levels.Life science alliance · 2025Article
- Nucleic Acid Sequence Determinants of Transcriptional Pausing by the Human Mitochondrial RNA Polymerase (POLRMT).Biochemistry · 2025Article
- Structural basis for promoter recognition and transcription factor binding and release in human mitochondria.Molecular cell · 2025Article
- Guanine quadruplexes mediate mitochondrial RNA polymerase pausing.BMC biology · 2025Article
- TEFM facilitates transition from RNA synthesis to DNA synthesis at H-strand replication origin of mtDNA.Communications biology · 2025Article
- TEFM facilitates uterine corpus endometrial carcinoma progression by activating ROS-NFκB pathway.Journal of translational medicine · 2024Article
- Mitochondrial transcription elongation factor TEFM promotes malignant progression of gliomas.Cancer cell international · 2024Article
- Exploring potential causal genetic variants and genes for endometrial cancer: Open Targets Genetics, Mendelian randomization, and multi-tissue transcriptome-wide association analysis.Translational cancer research · 2024Article
- Identification of TEFM as a potential therapeutic target for LUAD treatment.Journal of translational medicine · 2024Article
- GTPBP8 plays a role in mitoribosome formation in human mitochondria.Nature communications · 2024Article
- The initiation of mitochondrial DNA replication.Biochemical Society transactions · 2024Review
- Mechanisms and pathologies of human mitochondrial DNA replication and deletion formation.The Biochemical journal · 2024Review
- Genetic/epigenetic effects in NF1 microdeletion syndrome: beyond the haploinsufficiency, looking at the contribution of not deleted genes.Human genetics · 2024Article
- Mitochondrial protein synthesis quality control.Human molecular genetics · 2024Review
- RNA degradation in human mitochondria: the journey is not finished.Human molecular genetics · 2024Review
- Mitochondria transcription and cancer.Cell death discovery · 2024Review
55 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Here we show that c17orf42, hereafter TEFM (transcription elongation factor of mitochondria), makes a critical contribution to mitochondrial transcription. Inactivation of TEFM in cells by RNA interference results in respiratory incompetence owing to decreased levels of H- and L-strand promoter-distal mitochondrial transcripts. Affinity purification of TEFM from human mitochondria yielded a complex comprising mitochondrial transcripts, mitochondrial RNA polymerase (POLRMT), pentatricopeptide repeat domain 3 protein (PTCD3), and a putative DEAD-box RNA helicase, DHX30. After RNase treatment only POLRMT remained associated with TEFM, and in human cultured cells TEFM formed foci coincident with newly synthesized mitochondrial RNA. Based on deletion mutants, TEFM interacts with the catalytic region of POLRMT, and in vitro TEFM enhanced POLRMT processivity on ss- and dsDNA templates. TEFM contains two HhH motifs and a Ribonuclease H fold, similar to the nuclear transcription elongation regulator Spt6. These findings lead us to propose that TEFM is a mitochondrial transcription elongation factor.
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