Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.vph.2024.107304 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
NOD-1 activation increases the spontaneous activity and the I(f) current of murine sinoatrial node cells.
Vascul Pharmacol
June 2024
The Cell Physiology MiLab, Department of Biosciences, Università degli Studi di Milano, 20133 Milano, Italy.
A modified BCG with depletion of enzymes associated with peptidoglycan amidation induces enhanced protection against tuberculosis in mice.
Elife
April 2024
DST/NRF Centre of Excellence for Biomedical TB Research, Faculty of Health Sciences, University of the Witwatersrand, National Health Laboratory Service, Johannesburg, South Africa.
Mechanisms by which (Mtb) evades pathogen recognition receptor activation during infection may offer insights for the development of improved tuberculosis (TB) vaccines. Whilst Mtb elicits NOD-2 activation through host recognition of its peptidoglycan-derived muramyl dipeptide (MDP), it masks the endogenous NOD-1 ligand through amidation of glutamate at the second position in peptidoglycan side-chains. As the current BCG vaccine is derived from pathogenic mycobacteria, a similar situation prevails.
View Article and Find Full Text PDFThe contribution of pattern recognition receptor signalling in the development of age related macular degeneration: the role of toll-like-receptors and the NLRP3-inflammasome.
J Neuroinflammation
March 2024
Department of Anatomy and Physiology, The University of Melbourne, Grattan St, Parkville, Victoria, 3010, Australia.
Article Synopsis
- Age-related macular degeneration (AMD) is a major cause of vision loss, primarily caused by the death of photoreceptors and retinal pigment epithelium (RPE).
- The role of innate immune response, specifically through pattern recognition receptors (PRRs) like Toll-like receptors (TLRs) and NLRP3-inflammasome, is being studied in relation to AMD progression.
- Research shows that inhibiting TLRs and NLRP3 can help reduce RPE cell death and inflammation in animal models, suggesting potential new treatments for advanced AMD.
Discovery of a novel RIPK2 inhibitor for the treatment of inflammatory bowel disease.
Biochem Pharmacol
August 2023
State Key Laboratory of Common Mechanism Research for Major Diseases, and Key Laboratory of Synthetic Biology Regulatory Elements, Suzhou Institute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Suzhou 215123, Jiangsu, China. Electronic address:
Nucleotide-binding oligomerization domain-containing protein 1 and 2 (NOD 1/2) are important cytosolic pattern recognition receptors that initiate host immune response. The dysregulation of NOD signaling is highly associated with inflammatory bowel disease (IBD) that needs novel treatment options. Receptor-interacting protein kinase 2 (RIPK2) is a critical mediator of NOD signaling and considered a promising therapeutic target for IBD treatment.
View Article and Find Full Text PDFMechanisms by which (Mtb) evades pathogen recognition receptor activation during infection may offer insights for the development of improved tuberculosis (TB) vaccines. Whilst Mtb elicits NOD-2 activation through host recognition of its peptidoglycan-derived muramyl dipeptide (MDP), it masks the endogenous NOD-1 ligand through amidation of glutamate at the second position in peptidoglycan sidechains. As the current BCG vaccine is derived from pathogenic mycobacteria, a similar situation prevails.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!