Results 31 to 40 of about 106,008 (282)

IKKα negatively regulates ASC-dependent inflammasome activation. [PDF]

open access: yes, 2014
The inflammasomes are multiprotein complexes that activate caspase-1 in response to infections and stress, resulting in the secretion of pro-inflammatory cytokines.
Alnemri, Emad S   +19 more
core   +1 more source

Knocking In the NLRP3 Inflammasome [PDF]

open access: yesImmunity, 2009
Mutations in the human NLRP3 gene cause interleukin-1beta-related autoinflammatory syndromes. In this issue of Immunity, Brydges et al. (2009) and Meng et al. (2009) report the characterization of Nlrp3 gene-targeted mice harboring mutations mimicking those causing disease in humans.
openaire   +2 more sources

RORγ regulates the NLRP3 inflammasome [PDF]

open access: yesJournal of Biological Chemistry, 2019
RAR-related orphan receptor γ (RORγ) is a nuclear receptor that plays an essential role in the development of T helper 17 (Th17) cells of the adaptive immune system. The NLRP3 inflammasome is a component of the innate immune system that processes interleukin (IL)-1β into a mature cytokine.
Billon, Cyrielle   +3 more
openaire   +3 more sources

NLRP3 Inflammasome—A Key Player in Antiviral Responses

open access: yesFrontiers in Immunology, 2020
The NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome is an oligomeric complex comprised of the NOD-like receptor NLRP3, the adaptor ASC, and caspase-1.
Chunyuan Zhao   +4 more
doaj   +1 more source

C3a/C3aR synergies with TGF-β to promote epithelial-mesenchymal transition of renal tubular epithelial cells via the activation of the NLRP3 inflammasome

open access: yesJournal of Translational Medicine, 2023
Background Complement component 3a and its receptor (C3a/C3aR) and the nucleotide-binding oligomerization domain-like receptor protein-3 (NLRP3) inflammasome contribute to epithelial-mesenchymal transition (EMT).
Danyu You   +7 more
doaj   +1 more source

Tivantinib alleviates inflammatory diseases by directly targeting NLRP3

open access: yesiScience, 2023
Summary: NLRP3 inflammasome-mediated immune responses are involved in the pathogenesis of multiple inflammatory diseases, but few clinical drugs are identified that directly target the NLRP3 inflammasome to treat these diseases to date.
Yi Huang   +6 more
doaj   +1 more source

Peroxynitrite activates the NLRP3 inflammasome cascade in SOD1(G93A) mouse model of amyotrophic lateral sclerosis [PDF]

open access: yes, 2017
Neuroinflammation, characterized by the appearance of reactive microglial and astroglial cells, is one of the several pathogenic mechanisms of amyotrophic lateral sclerosis (ALS), a fast-progressing and fatal neurodegenerative disease.
Adamo, Sergio   +10 more
core   +1 more source

Novel Role for Tranilast in Regulating NLRP3 Ubiquitination, Vascular Inflammation, and Atherosclerosis

open access: yesJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 2020
Background Aberrant activation of the NLRP3 (nucleotide‐binding oligomerization domain, leucine‐rich repeat–containing receptor family pyrin domain‐containing 3) inflammasome is thought to play a causative role in atherosclerosis.
Suwen Chen   +11 more
doaj   +1 more source

The AIM2 inflammasome is critical for innate immunity to Francisella tularensis. [PDF]

open access: yes, 2010
Francisella tularensis, the causative agent of tularemia, infects host macrophages, which triggers production of the proinflammatory cytokines interleukin 1beta (IL-1beta) and IL-18. We elucidate here how host macrophages recognize F.
Alnemri, Emad S   +12 more
core   +3 more sources

Nlrp6 promotes recovery after peripheral nerve injury independently of inflammasomes [PDF]

open access: yes, 2015
Background: NOD-like receptors (Nlrs) are key regulators of immune responses during infection and autoimmunity. A subset of Nlrs assembles inflammasomes, molecular platforms that are activated in response to endogenous danger and microbial ligands and ...
De Winter, Vicky   +6 more
core   +2 more sources

Home - About - Disclaimer - Privacy