Evidence map›Paper›PMID 36994473›Full record

ReviewMolecules and cells2023

Molecular Basis of the KEAP1-NRF2 Signaling Pathway.

Takafumi Suzuki, Jun Takahashi, Masayuki Yamamoto

Open access · diamondAbstract readReview
In one paragraph

Review in Molecules and cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed
37.6field-weighted citation impact, top 1% 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

155 citing papers in PubMed, 244 citations in OpenAlex.

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95 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

3 authors at 1 institution in 1 country.

Takafumi SuzukiDepartment of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.ORCID https://orcid.org/0000-0002-3425-8208
Jun TakahashiDepartment of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.ORCID https://orcid.org/0009-0006-9953-0176
Masayuki YamamotoDepartment of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.ORCID https://orcid.org/0000-0002-9073-9436
Tohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcription factor NRF2 (NF-E2-related factor 2) is a master regulator of cellular responses against environmental stresses. NRF2 induces expression of detoxification and antioxidant enzymes and suppresses inductions of pro-inflammatory cytokine genes. KEAP1 (Kelch-like ECH-associated protein 1) is an adaptor subunit of CULLIN 3 (CUL3)-based E3 ubiquitin ligase. KEAP1 regulates the activity of NRF2 and acts as a sensor for oxidative and electrophilic stresses. NRF2 has been found to be activated in many types of cancers with poor prognosis. Therapeutic strategies to control NRF2-overeactivated cancers have been considered not only by targeting cancer cells with NRF2 inhibitors or NRF2 synthetic lethal chemicals, but also by targeting host defense with NRF2 inducers. Understanding precise molecular mechanisms how the KEAP1-NRF2 system senses and regulates the cellular response is critical to overcome intractable NRF2-activated cancers.

Indexed as

NF-E2-Related Factor 2Signal TransductionGene Expression RegulationKelch-Like ECH-Associated Protein 1Oxidative StressUbiquitin-Protein LigasesKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Ubiquitin-Protein Ligasescancer therapydefense systemKEAP1NRF2stress sensing

Identifiers

PMID36994473
PMCPMC10070164
OpenAlexW4361275931

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.