Evidence map›Paper›PMID 17062618›Full record

ArticleNucleic acids research2006

Alterations to the expression level of mitochondrial transcription factor A, TFAM, modify the mode of mitochondrial DNA replication in cultured human cells.

Jaakko L O Pohjoismäki, Sjoerd Wanrooij, Anne K Hyvärinen, Steffi Goffart, Ian J Holt, Johannes N Spelbrink, Howard T Jacobs

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
3.8field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

89 citing papers in PubMed, 166 citations in OpenAlex.

  1. Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025
    Review
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  19. Dynamic features of human mitochondrial DNA maintenance and transcription.Frontiers in cell and developmental biology · 2022
    Review
  20. Article

29 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Jaakko L O PohjoismäkiInstitute of Medical Technology and Tampere University Hospital, FI-33014, University of Tampere, Finland.
Sjoerd Wanrooij
Anne K Hyvärinen
Steffi Goffart
Ian J Holt
Johannes N Spelbrink
Howard T Jacobs
Tampere University · FITampere University Hospital · FIMRC Human Nutrition Research · GBUniversity of Glasgow · GB

Funding

Medical Research Council MC_U105663140
6 · The paper itself

Abstract

Mitochondrial transcription factor A (TFAM) is an abundant mitochondrial protein of the HMG superfamily, with various putative roles in mitochondrial DNA (mtDNA) metabolism. In this study we have investigated the effects on mtDNA replication of manipulating TFAM expression in cultured human cells. Mammalian mtDNA replication intermediates (RIs) fall into two classes, whose mechanistic relationship is not properly understood. One class is characterized by extensive RNA incorporation on the lagging strand, whereas the other has the structure of products of conventional, strand-coupled replication. TFAM overexpression increased the overall abundance of RIs and shifted them substantially towards those of the conventional, strand-coupled type. The shift was most pronounced in the rDNA region and at various replication pause sites and was accompanied by a drop in the relative amount of replication-termination intermediates, a substantial reduction in mitochondrial transcripts, mtDNA decatenation and progressive copy number depletion. TFAM overexpression could be partially phenocopied by treatment of cells with dideoxycytidine, suggesting that its effects are partially attributable to a decreased rate of fork progression. TFAM knockdown also resulted in mtDNA depletion, but RIs remained mainly of the ribosubstituted type, although termination intermediates were enhanced. We propose that TFAM influences the mode of mtDNA replication via its combined effects on different aspects of mtDNA metabolism.

Indexed as

DNA ReplicationCell LineDNA-Binding ProteinsDNA, MitochondrialGene ExpressionHumansMitochondrial ProteinsRNA InterferenceTranscription FactorsZalcitabineDNA-Binding ProteinsDNA, MitochondrialMitochondrial ProteinsTFAM protein, humanTranscription FactorsZalcitabine

Identifiers

PMID17062618
PMCPMC1635303
OpenAlexW2108429189

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.