Evidence map›Paper›PMID 30237533›Full record

ArticleScientific reports2018

Anti-inflammatory action of cysteine derivative S-1-propenylcysteine by inducing MyD88 degradation.

Jun-Ichiro Suzuki, Yukihiro Kodera, Satomi Miki, Mitsuyasu Ushijima, Miyuki Takashima, Toshiaki Matsutomo, Naoaki Morihara

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
7.1field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Unravelling the Therapeutic Potential of Cysteine for Cardiovascular Health.International journal of molecular sciences · 2026
    Review
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  8. BML-281 promotes neuronal differentiation by modulating Wnt/CaMolecular and cellular biochemistry · 2024
    Article
  9. Article
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  11. Article
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  13. Article
  14. Experimental and therapeutic medicine · 2020
    Article
  15. Review
  16. Article
  17. Review
  18. Regulation of immune response byExperimental and therapeutic medicine · 2020
    Review
  19. Review
  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

7 authors at 1 institution in 1 country.

Jun-Ichiro SuzukiCentral research laboratory, Wakunaga Pharmaceutical Co., Ltd., Hiroshima, Japan. suzuki_j@wakunaga.co.jp.
Yukihiro KoderaCentral research laboratory, Wakunaga Pharmaceutical Co., Ltd., Hiroshima, Japan.
Satomi MikiCentral research laboratory, Wakunaga Pharmaceutical Co., Ltd., Hiroshima, Japan.
Mitsuyasu UshijimaCentral research laboratory, Wakunaga Pharmaceutical Co., Ltd., Hiroshima, Japan.
Miyuki TakashimaCentral research laboratory, Wakunaga Pharmaceutical Co., Ltd., Hiroshima, Japan.
Toshiaki MatsutomoCentral research laboratory, Wakunaga Pharmaceutical Co., Ltd., Hiroshima, Japan.
Naoaki MoriharaCentral research laboratory, Wakunaga Pharmaceutical Co., Ltd., Hiroshima, Japan.
Wakunaga (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The degradation of target proteins by small molecules utilizing the cellular proteolytic system is featured as a treatment strategy of several diseases. We found that S-1-propenylcysteine (S1PC) among several cysteine derivatives in aged garlic extract inhibited TLR-mediated IL-6 production by inducing the degradation of adaptor protein MyD88. We showed that S1PC directly denatured MyD88 and induced the formation of protein aggregates. Consequently, MyD88 was degraded by aggresome-autophagy pathway. On the other hand, S-allylcysteine, a structural analog of S1PC, failed to induce the degradation of MyD88 because of its inability to denature MyD88 although it also activated autophagy. Our findings suggest that S1PC induces MyD88 degradation through the denaturation of MyD88 and the activation of autophagy. Thus, S1PC may serve as the base to develop a therapeutic means for immune diseases associated with aberrant TLR signaling pathways.

Indexed as

AnimalsAnti-Inflammatory AgentsAutophagyCell LineCysteineHumansLymphocytesMaleMyeloid Differentiation Factor 88RatsRats, Inbred WKYSignal TransductionToll-Like ReceptorsAnti-Inflammatory AgentsCysteineMyeloid Differentiation Factor 88Toll-Like Receptors

Identifiers

PMID30237533
PMCPMC6148218
OpenAlexW2891236012

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.