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Recent Advances in the Molecular Research of Gastrointestinal Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 2405

Special Issue Editors


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Guest Editor
Nutritional Sciences Division, School of Medicine, King’s College London, London, UK
Interests: intestinal sugar transport; nutrient sensing; vitamin C; polyphenolics; diabetes; obesity
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Nutritional Sciences Division , School of Medicine, King's College London, London, UK
Interests: intestinal lipid transport; intestinal transit; nutrient sensing; dietary fibre; obesity; diabetes

Special Issue Information

Dear Colleagues,

All disease begins in the gut—Hippocrates. Research has shown that a healthy gut is an important driver of overall health, and that alterations in its function can result not only in gut disease but also in metabolic diseases such as obesity, diabetes, and CVD in addition to neurological disorders such as autism and depression. This Special Issue of IJMS, “Recent Advances in the Molecular Research of Gastrointestinal Disease”, is requesting primary data and systematic review research papers to be submitted for peer review. We are interested in papers focussed on identifying changes in gut function at the molecular level that contribute towards disease. We are particularly interested in papers on dietary, drug, surgical, and microbial interventions that can improve gut function and, thus, overall health.

Topics of interest include (but are not limited to):

  • Molecular response to dietary or pharmaceutical interventions in the gut
  • Host–microbiome interactions
  • Regulation of intestinal mucosal function in health and disease
  • Regulation in gut neuromuscular function in health and disease

Dr. Christopher Corpe
Dr. Balazs Bajka
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • gastrointestinal
  • diet
  • microbiome
  • nutrient digestion
  • absorption
  • motility
  • inflammation
  • peptide signaling
  • short chain fatty acids

Published Papers (1 paper)

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Research

18 pages, 5157 KiB  
Article
Kinase Activity of PAR1b, Which Mediates Nuclear Translocation of the BRCA1 Tumor Suppressor, Is Potentiated by Nucleic Acid-Mediated PAR1b Multimerization
by Hiroko Nishikawa, Priscillia Christiany, Takeru Hayashi, Hisashi Iizasa, Hironori Yoshiyama and Masanori Hatakeyama
Int. J. Mol. Sci. 2022, 23(12), 6634; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23126634 - 14 Jun 2022
Cited by 1 | Viewed by 1870
Abstract
PAR1b is a cytoplasmic serine/threonine kinase that controls cell polarity and cell–cell interaction by regulating microtubule stability while mediating cytoplasmic-to-nuclear translocation of BRCA1. PAR1b is also a cellular target of the CagA protein of Helicobacter pylori, which leads to chronic infection causatively associated [...] Read more.
PAR1b is a cytoplasmic serine/threonine kinase that controls cell polarity and cell–cell interaction by regulating microtubule stability while mediating cytoplasmic-to-nuclear translocation of BRCA1. PAR1b is also a cellular target of the CagA protein of Helicobacter pylori, which leads to chronic infection causatively associated with the development of gastric cancer. The CagA-PAR1b interaction inactivates the kinase activity of PAR1b and thereby dampens PAR1b-mediated BRCA1 phosphorylation, which reduces the level of nuclear BRCA1 and thereby leads to BRCAness and BRCAness-associated genome instability underlying gastric carcinogenesis. While PAR1b can multimerize within the cells, little is known about the mechanism and functional role of PAR1b multimerization. We found in the present study that PAR1b was multimerized in vitro by binding with nucleic acids (both single- and double-stranded DNA/RNA) via the spacer region in a manner independent of nucleic-acid sequences, which markedly potentiated the kinase activity of PAR1b. Consistent with these in vitro observations, cytoplasmic introduction of double-stranded DNA or expression of single-stranded RNA increased the PAR1b kinase activity in the cells. These findings indicate that the cytoplasmic DNA/RNA contribute to nuclear accumulation of BRCA1 by constitutively activating/potentiating cytoplasmic PAR1b kinase activity, which is subverted in gastric epithelial cells upon delivery of H. pylori CagA oncoprotein. Full article
(This article belongs to the Special Issue Recent Advances in the Molecular Research of Gastrointestinal Disease)
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