Evidence map›Paper›PMID 24416372›Full record

ArticlePloS one2014

SPBP is a sulforaphane induced transcriptional coactivator of NRF2 regulating expression of the autophagy receptor p62/SQSTM1.

Sagar Ramesh Darvekar, Julianne Elvenes, Hanne Britt Brenne, Terje Johansen, Eva Sjøttem

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. The sequestosome 1 protein: therapeutic vulnerabilities in ovarian cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  6. Article
  7. Disruption of MeCP2-TCF20 complex underlies distinct neurodevelopmental disorders.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Review
  9. Review
  10. Article
  11. p62/Antioxidants & redox signaling · 2019
    Review
  12. Article
  13. The Potential Role of Nrf2 Signaling in Leishmania Infection Outcomes.Frontiers in cellular and infection microbiology · 2019
    Review
  14. Article
  15. Autophagic Regulation of p62 is Critical for Cancer Therapy.International journal of molecular sciences · 2018
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Sagar Ramesh DarvekarMolecular Cancer Research Group, Department of Medical Biology, University of Tromsø, Tromsø, Norway.
Julianne ElvenesMolecular Cancer Research Group, Department of Medical Biology, University of Tromsø, Tromsø, Norway.
Hanne Britt BrenneMolecular Cancer Research Group, Department of Medical Biology, University of Tromsø, Tromsø, Norway.
Terje JohansenMolecular Cancer Research Group, Department of Medical Biology, University of Tromsø, Tromsø, Norway.
Eva SjøttemMolecular Cancer Research Group, Department of Medical Biology, University of Tromsø, Tromsø, Norway.
UiT The Arctic University of Norway · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Organisms exposed to oxidative stress respond by orchestrating a stress response to prevent further damage. Intracellular levels of antioxidant agents increase, and damaged components are removed by autophagy induction. The KEAP1-NRF2 signaling pathway is the main pathway responsible for cell defense against oxidative stress and for maintaining the cellular redox balance at physiological levels. Sulforaphane, an isothiocyanate derived from cruciferous vegetables, is a potent inducer of KEAP1-NRF2 signaling and antioxidant response element driven gene expression. In this study, we show that sulforaphane enhances the expression of the transcriptional coregulator SPBP. The expression curve peaks 6-8 hours post stimulation, and parallels the sulforaphane-induced expression of NRF2 and the autophagy receptor protein p62/SQSTM1. Reporter gene assays show that SPBP stimulates the expression of p62/SQSTM1 via ARE elements in the promoter region, and siRNA mediated knock down of SPBP significantly decreases the expression of p62/SQSTM1 and the formation of p62/SQSTM1 bodies in HeLa cells. Furthermore, SPBP siRNA reduces the sulforaphane induced expression of NRF2, and the expression of the autophagy marker protein LC3B. Both these proteins contain ARE-like elements in their promoter regions. Over-expressed SPBP and NRF2 acts synergistically on the p62/SQSTM1 promoter and colocalize in nuclear speckles in HeLa cells. Collectively, these results suggest that SPBP is a coactivator of NRF2, and hence may be important for securing enhanced and sustained expression of NRF2 induced genes such as proteins involved in selective autophagy.

Indexed as

Adaptor Proteins, Signal TransducingAnticarcinogenic AgentsAutophagyGene Expression Regulation, NeoplasticHeLa CellsHumansIntracellular Signaling Peptides and ProteinsIsothiocyanatesKelch-Like ECH-Associated Protein 1Microtubule-Associated ProteinsNF-E2-Related Factor 2Promoter Regions, GeneticRNA, Small InterferingSequestosome-1 ProteinSignal TransductionSulfoxidesAdaptor Proteins, Signal TransducingAnticarcinogenic AgentsIntracellular Signaling Peptides and ProteinsIsothiocyanatesKEAP1 protein, humanKelch-Like ECH-Associated Protein 1MAP1LC3B protein, humanMicrotubule-Associated ProteinsNFE2L2 protein, humanNF-E2-Related Factor 2RNA, Small InterferingSequestosome-1 ProteinSQSTM1 protein, humansulforaphaneSulfoxidesTCF20 protein, humanTranscription Factors

Identifiers

PMID24416372
PMCPMC3887019
OpenAlexW1985026615

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.