Results 51 to 60 of about 20,611 (234)

Engineering Microbial Particles for Next‐Generation Biomedical Platforms

open access: yesAdvanced Science, EarlyView.
Microbe‐derived particles (MDPs), which include extracellular vesicles, outer membrane vesicles, inclusion bodies, polysaccharide particles, and virus‐like particles, represent a rapidly expanding category of bioinspired nanomaterials. With their natural origin, intrinsic biocompatibility, and highly programmable functionality, MDPs serve as a ...
Yuting Li   +7 more
wiley   +1 more source

Structure of human NOD2.

open access: yes, 2023
These structural representations were generated from UniProt entry Q9HC29 (“NOD2_HUMAN”) folded with AlphaFold. Approximately 180° of rotation separates the images from the top and bottom rows.
Jean-Yves Dubé (12300110)   +1 more
core   +1 more source

Influence of muramyl peptides on the production of chemokines, growth factors, pro-inflammatory and anti-inflammatory cytokines

open access: yesRUDN Journal of Medicine
Relevance.The recent increase in inflammatory, allergic and infectious diseases needs to update new ways of raising non-specific resistance of the organism.
Svetlana V. Guryanova
doaj   +1 more source

Activation of nucleotide oligomerization domain 2 (NOD2) by human cytomegalovirus initiates innate immune responses and restricts virus replication. [PDF]

open access: yesPLoS ONE, 2014
Nucleotide-binding oligomerization domain 2 (NOD2) is an important innate immune sensor of bacterial pathogens. Its induction results in activation of the classic NF-κB pathway and alternative pathways including type I IFN and autophagy.
Arun Kapoor   +2 more
doaj   +1 more source

Prmt6 Deficiency or Inhibition Restores Microglial Homeostasis and Promotes Scar‐Limited Repair in Adult Spinal Cord Injury

open access: yesAdvanced Science, EarlyView.
After spinal cord injury, adult microglia remain persistently activated with chronic PRMT6 (protein arginine methyltransferase 6) upregulation. Prmt6 deficiency or inhibition reestablishes microglial homeostasis and promotes a scar‐limited repairment, enhancing axonal regrowth.
Weilin Peng   +9 more
wiley   +1 more source

Image_5_Blau syndrome NOD2 mutations result in loss of NOD2 cross-regulatory function.jpeg

open access: yes, 2022
The studies described here provide an analysis of the pathogenesis of Blau syndrome and thereby the function of NOD2 as seen through the lens of its dysfunction resulting from Blau-associated NOD2 mutations in its nucleotide-binding domain (NBD). As such,
Kim Montgomery-Recht (13798072)   +8 more
core   +1 more source

NOD2 function in Crohn's disease [PDF]

open access: yesJournal of Translational Medicine, 2011
not submitted for publication Published: 23 November 2011 doi:10.1186/1479-5876-9-S2-I10 Cite this article as: Simmons: NOD2 function in Crohn’s disease. Journal of Translational Medicine 2011 9(Suppl 2):I10. Submit your next manuscript to BioMed Central and take full advantage of: • Convenient online submission • Thorough peer review • No space ...
openaire   +2 more sources

From Inflammatory Bowel Disease to Cancer: Gut Microbiota–Immune Microenvironment Crosstalk and Natural Product‐Based Therapeutic Opportunities

open access: yesCancer Nexus, EarlyView.
ABSTRACT Inflammatory bowel disease (IBD), primarily Crohn's disease and ulcerative colitis, is a chronic relapsing inflammatory disorder of the gastrointestinal tract and an important risk factor for IBD‐associated cancer. Increasing evidence suggests that gut microbiota dysbiosis, epithelial barrier dysfunction, and immune microenvironment remodeling
Xue Zhang   +4 more
wiley   +1 more source

CEACAM6 gene variants in inflammatory bowel disease. [PDF]

open access: yes, 2011
The carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) acts as a receptor for adherent-invasive E. coli (AIEC) and its ileal expression is increased in patients with Crohn's disease (CD). Given its contribution to the pathogenesis of CD,
Seiderer, J.   +67 more
core   +1 more source

Image_3_Blau syndrome NOD2 mutations result in loss of NOD2 cross-regulatory function.jpeg

open access: yes, 2022
The studies described here provide an analysis of the pathogenesis of Blau syndrome and thereby the function of NOD2 as seen through the lens of its dysfunction resulting from Blau-associated NOD2 mutations in its nucleotide-binding domain (NBD). As such,
Kim Montgomery-Recht (13798072)   +8 more
core   +1 more source

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