Evidence map›Paper›PMID 22500024›Full record

ArticleThe Journal of biological chemistry2012

Nrf1 CNC-bZIP protein promotes cell survival and nucleotide excision repair through maintaining glutathione homeostasis.

Weinong Han, Mei Ming, Rui Zhao, Jingbo Pi, Chunli Wu, Yu-Ying He

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 41 citations in OpenAlex.

  1. Global cis-regulatory landscape of double-stranded DNA viruses.bioRxiv : the preprint server for biology · 2025
    Article
  2. Review
  3. Nrf1 Reduces COX-2 Expression and Maintains Cellular Homeostasis After Cerebral Ischemia/Reperfusion By Targeting IL-6/TNF-α Protein Production.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    Article
  4. Review
  5. Roles of NRF2 in DNA damage repair.Cellular oncology (Dordrecht, Netherlands) · 2023
    Review
  6. Autophagy regulates tumor growth and metastasis.bioRxiv : the preprint server for biology · 2023
    Article
  7. Article
  8. Review
  9. Overexpression ofInternational journal of molecular sciences · 2020
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

6 authors at 3 institutions in 2 countries.

Weinong HanDepartment of Medicine, University of Chicago, Chicago, Illinois 60637, USA.
Mei Ming
Rui Zhao
Jingbo Pi
Chunli Wu
Yu-Ying He
University of Chicago · USThe Hamner Institutes for Health Sciences · USChina Medical University · CN

Funding

VIRAL ONCOLOGY CORE FACILITYP30CA014599 · NCI · UNIVERSITY OF CHICAGO · PI MARK W. LINGEN · 1985 to 2026
$122.1M
TRANSLATIONAL RESEARCH UNIVERSITY OF CHICAGO: CLINICAL TRIALSUL1RR024999 · NCRR · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2007 to 2011
$25.3M
Paradoxical roles of Nrf2 activation in arsenic-induced beta-cell dysfunctionR01ES016005 · NIEHS · THE HAMNER INSTITUTES · PI PI, JINGBO · 2008 to 2012
$2.5M
Mechanisms of UVA-induced skin cancerR01ES016936 · NIEHS · UNIVERSITY OF CHICAGO · PI HE, YU-YING · 2010 to 2014
$2.2M
NCI NIH HHS P30 CA014599NCRR NIH HHS UL1 RR024999NCRR NIH HHS UL1RR024999NIEHS NIH HHS ES016005NIEHS NIH HHS ES016936NIEHS NIH HHS R01 ES016005NIEHS NIH HHS R01 ES016936
6 · The paper itself

Abstract

Skin cancer is the most common cancer in the United States. Its major environmental risk factor is UVB radiation in sunlight. In response to UVB damage, epidermal keratinocytes activate a specific repair pathway, i.e. nucleotide excision repair, to remove UVB-induced DNA lesions. However, the regulation of UVB response is not fully understood. Here we show that the long isoform of the nuclear factor erythroid 2-related factor 1 (Nrf1, also called NFE2L1), a cytoprotective transcription factor critical for the expression of multiple antioxidant response element-dependent genes, plays an important role in the response of keratinocytes to UVB. Nrf1 loss sensitized keratinocytes to UVB-induced apoptosis by up-regulating the expression of the proapoptotic Bcl-2 family member Bik through reducing glutathione levels. Knocking down Bik reduced UVB-induced apoptosis in Nrf1-inhibited cells. In UVB-irradiated surviving cells, however, disruption of Nrf1 impaired nucleotide excision repair through suppressing the transcription of xeroderma pigmentosum C (XPC), a factor essential for initiating the global genome nucleotide excision repair by recognizing the DNA lesion and recruiting downstream factors. Nrf1 enhanced XPC expression by increasing glutathione availability but was independent of the transcription repressor of XPC. Adding XPC or glutathione restored the DNA repair capacity in Nrf1-inhibited cells. Finally, we demonstrate that Nrf1 levels are significantly reduced by UVB radiation in mouse skin and are lower in human skin tumors than in normal skin. These results indicate a novel role of Nrf1 in UVB-induced DNA damage repair and suggest Nrf1 as a tumor suppressor in the skin.

Indexed as

Cell SurvivalDNA RepairHomeostasisGlutathioneHumansNuclear ProteinsNuclear Respiratory Factor 1RNA-Binding ProteinsTranscription FactorsALYREF protein, humanGlutathioneNRF1 protein, humanNuclear ProteinsNuclear Respiratory Factor 1RNA-Binding ProteinsTranscription Factors

Identifiers

PMID22500024
PMCPMC3365774
OpenAlexW2066742532

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.