high mobility group box1 protein is involved in endoplasmic reticulum stress induced by clostridium difficile toxin a

Clicks: 193
ID: 191898
2016
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #478 of 1,324 articles by views in spectrochimica acta - part a: molecular and biomolecular spectroscopy

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 1,324 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Abstract
High Mobility Group Box1 (HMGB1), a damage-associated inflammatory factor, plays an important role in the pathogenesis of numerous chronic inflammatory and autoimmune diseases. In this study, the role of the HMGB1 in TcdA-induced ER stress was identified. Clostridium difficile toxin A is one of the major virulence factors of C. difficile infection (CDI) and has been proved to induce apoptotic cell death through ER stress. Our results showed that HMGB1 might play an important role in the TcdA-induced ER stress and unfolded protein response. HMGB1 activated molecular markers and induced the C/EBP homologous protein upregulation (CHOP). This study may provide the essential information for better understanding of the molecular mechanisms involved in CDI.
Reference Key
liu2016biomedhigh Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Ji Liu;Yi Ma;Chun-Li Sun;Shan Li;Ju-Fang Wang
Journal spectrochimica acta - part a: molecular and biomolecular spectroscopy
Year 2016
DOI
10.1155/2016/4130834
URL
Keywords

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.