Evidence map›Paper›PMID 27625068›Full record

ArticleScientific reports2016

Characterization of human mitochondrial ferritin promoter: identification of transcription factors and evidences of epigenetic control.

Michela Guaraldo, Paolo Santambrogio, Elisabetta Rovelli, Augusta Di Savino, Giuseppe Saglio, Davide Cittaro, Antonella Roetto, Sonia Levi

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. A novel view of ferritin in cancer.Biochimica et biophysica acta. Reviews on cancer · 2023
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Iron Metabolism in Cancer.International journal of molecular sciences · 2018
    Review
  12. Article
  13. Article
  14. Article
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

8 authors.

Michela GuaraldoSan Raffaele Scientific Institute, Division of Neuroscience, 20132 Milano, Italy.
Paolo SantambrogioSan Raffaele Scientific Institute, Division of Neuroscience, 20132 Milano, Italy.
Elisabetta RovelliSan Raffaele Scientific Institute, Division of Neuroscience, 20132 Milano, Italy.
Augusta Di SavinoUniversity of Torino, Department of Clinical and Biological Sciences, AOU San Luigi Gonzaga, 10043 Orbassano, Torino, Italy.
Giuseppe SaglioUniversity of Torino, Department of Clinical and Biological Sciences, AOU San Luigi Gonzaga, 10043 Orbassano, Torino, Italy.
Davide CittaroSan Raffaele Scientific Institute, Center for Translational Genomics and Bioinformatics, 20132 Milano, Italy.
Antonella RoettoUniversity of Torino, Department of Clinical and Biological Sciences, AOU San Luigi Gonzaga, 10043 Orbassano, Torino, Italy.
Sonia LeviSan Raffaele Scientific Institute, Division of Neuroscience, 20132 Milano, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial ferritin (FtMt) is an iron storage protein belonging to the ferritin family but, unlike the cytosolic ferritin, it has an iron-unrelated restricted tissue expression. FtMt appears to be preferentially expressed in cell types characterized by high metabolic activity and oxygen consumption, suggesting a role in protecting mitochondria from iron-dependent oxidative damage. The human gene (FTMT) is intronless and its promoter region has not been described yet. To analyze the regulatory mechanisms controlling FTMT expression, we characterized the 5' flanking region upstream the transcriptional starting site of FTMT by in silico enquiry of sequences conservation, DNA deletion analysis, and ChIP assay. The data revealed a minimal promoter region and identified the presence of SP1, CREB and YY1 as positive regulators, and GATA2, FoxA1 and C/EBPβ as inhibitors of the transcriptional regulation. Furthermore, the FTMT transcription is increased by acetylating and de-methylating agent treatments in K562 and HeLa cells. These treatments up-regulate FtMt expression even in fibroblasts derived from a Friedreich ataxia patient, where it might exert a beneficial effect against mitochondrial oxidative damage. The expression of FTMT appears regulated by a complex mechanism involving epigenetic events and interplay between transcription factors.

Indexed as

Epigenesis, GeneticPromoter Regions, GeneticBase SequenceComputer SimulationFerritinsFibroblastsFriedreich AtaxiaHeLa CellsHumansK562 CellsLuciferasesMitochondrial ProteinsTranscription FactorsFerritinsLuciferasesmitochondrial ferritin, humanMitochondrial ProteinsTranscription Factors

Identifiers

PMID27625068
PMCPMC5022048

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Registered trials

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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.