Results 41 to 50 of about 20,611 (234)
Image_4_Blau syndrome NOD2 mutations result in loss of NOD2 cross-regulatory function.jpeg
, 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
The pathogen recognition sensor, NOD2, is variably expressed in patients with pulmonary tuberculosis
BMC Infectious Diseases, 2007 Background NOD2, an intracellular pathogen recognition sensor, modulates innate defences to muropeptides derived from various bacterial species, including Mycobacterium tuberculosis (MTB). Experimentally, NOD2 attenuates two key putative mycobactericidal
Johnson Margaret A +8 more
doaj +1 more source
Characterization and Genetic Analyses of New Genes Coding for NOD2 Interacting Proteins. [PDF]
PLoS ONE, 2016 NOD2 contributes to the innate immune response and to the homeostasis of the intestinal mucosa. In response to its bacterial ligand, NOD2 interacts with RICK and activates the NF-κB and MAPK pathways, inducing gene transcription and synthesis of proteins
Raphaële Thiébaut +11 more
doaj +1 more source
, 2023 We provide evidence here from loss-of-function studies in mice and gain-of-function studies in human cells (1, 2) which demonstrate control of CDKN1A-interacting zinc finger protein 1, CIZ1, by the NLR (nucleotide-binding oligomerization domain-like receptor) family protein NOD2.
openaire +1 more source
FRMBP2 directs NOD2 to the membrane [PDF]
Proceedings of the National Academy of Sciences, 2012 The immune system acts as a shield against harmful microbes and requires exquisite control of the activation and resolution of multiple signaling pathways. Tight regulation of these processes is required not only to produce an effective response, but also to maintain immune homeostasis and prevent autoinflammatory disease.
Amrita, Kabi, Christine, McDonald
openaire +2 more sources
T cell intrinsic NOD2 is dispensable for CD8 T cell immunity. [PDF]
PLoS ONE, 2013 NOD2 is an intracellular pattern recognition receptor that provides innate sensing of bacterial muramyl dipeptide by host cells, such as dendritic cells, macrophages and epithelial cells. While NOD2's role as an innate pathogen sensor is well established,
Gloria H Y Lin +4 more
doaj +1 more source
Ubiquitination and phosphorylation in the regulation of NOD2 signaling and NOD2-mediated disease
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2012 The immune system is exquisitely balanced. It has the ability to effectively respond to and control infections while at the same time preventing inappropriate responses to self and environmental antigens. When this response goes awry, either through a failure to activate the immune response, or failure to terminate it, inflammatory pathology results ...
Tigno-Aranjuez, Justine T. +1 more
openaire +2 more sources
Cells, 2021 The innate immune system plays a critical role in the early detection of pathogens, primarily by relying on pattern-recognition receptor (PRR) signaling molecules.
Shamila D. Alipoor, Mehdi Mirsaeidi
doaj +1 more source
Advanced Science, EarlyView.ABSTRACT The E3 ubiquitin ligase tripartite motif 27 (TRIM27) is a negative regulator of NF‐κB activation and the innate immune response, and TRIM27 deficiency significantly impairs dextran sulfate sodium (DSS)‐induced colitis. The function of TRIM27 in intestinal epithelial cells (IECs), the mechanism by which TRIM27 inhibits the NF‐κB pathway and its
Weimin Xu +10 more
wiley +1 more source
Image_1_Blau syndrome NOD2 mutations result in loss of NOD2 cross-regulatory function.jpeg
, 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