Evidence map›Paper›PMID 21555518›Full record

ArticleThe Journal of biological chemistry2011

The BTB and CNC homology 1 (BACH1) target genes are involved in the oxidative stress response and in control of the cell cycle.

Hans-Jörg Warnatz, Dominic Schmidt, Thomas Manke, Ilaria Piccini, Marc Sultan, Tatiana Borodina, Daniela Balzereit, Wasco Wruck, Alexey Soldatov, Martin Vingron and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

116 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Modulation of the Receptor Tyrosine Kinase TIE2/International journal of molecular sciences · 2026
    Article
  9. Dissecting the Interplay Between NRF2 and BACH1 at CsMBEs.Antioxidants (Basel, Switzerland) · 2025
    Article
  10. A BACH1 inhibitor ameliorates myocardial infarction and limb ischemia in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  11. Article
  12. Review
  13. Significance of Malic Enzyme 1 in Cancer: A Review.Current issues in molecular biology · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Update on heme biosynthesis, tissue-specific regulation, heme transport, relation to iron metabolism and cellular energy.Liver international : official journal of the International Association for the Study of the Liver · 2024
    Review
  19. Review
  20. Article

56 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

12 authors at 2 institutions in 1 country.

Hans-Jörg WarnatzDepartment of Vertebrate Genomics, Max Planck Institute for Molecular Genetics, 14195 Berlin, Germany.
Dominic Schmidt
Thomas Manke
Ilaria Piccini
Marc Sultan
Tatiana Borodina
Daniela Balzereit
Wasco Wruck
Alexey Soldatov
Martin Vingron
Hans Lehrach
Marie-Laure Yaspo
Max Planck Society · DEMax Planck Institute for Molecular Genetics · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The regulation of gene expression in response to environmental signals and metabolic imbalances is a key step in maintaining cellular homeostasis. BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAF recognition elements, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation sequencing analysis of BACH1 target genes in HEK 293 cells with knockdown of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by chromatin immunoprecipitation sequencing were found highly enriched in genes showing expression changes after BACH1 knockdown, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, and SLC48A1) and redox regulation (GCLC, GCLM, and SLC7A11), we also discovered BACH1 target genes affecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, and MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, and vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis.

Indexed as

Basic-Leucine Zipper Transcription FactorsCell CycleFanconi Anemia Complementation Group ProteinsGene Expression ProfilingGene Expression RegulationHEK293 CellsHumansOligonucleotide Array Sequence AnalysisOxidative StressResponse ElementsBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsFanconi Anemia Complementation Group Proteins

Identifiers

PMID21555518
PMCPMC3123115
OpenAlexW1976272474

What OpenQuestion holds

Textmetadata
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.