Diphtheria toxin activates ribotoxic stress and NLRP1 inflammasome-driven pyroptosis. [PDF]
The ZAKα-driven ribotoxic stress response (RSR) is activated by ribosome stalling and/or collisions. Recent work demonstrates that RSR also plays a role in innate immunity by activating the human NLRP1 inflammasome. Here, we report that ZAKα and NLRP1 sense bacterial exotoxins that target ribosome elongation factors.
Robinson KS +13 more
europepmc +4 more sources
The CARD8 T60 variant associates with NLRP1 and negatively regulates its activation
The NLRP1 inflammasome functions as canonical cytosolic sensor in response to intracellular infections and is implicated in auto-inflammatory diseases. But the regulation and signal transduction mechanisms of NLRP1 are incompletely understood.
Zhihao Xu +17 more
doaj +1 more source
The NLRP1 Inflammasome Induces Pyroptosis in Human Corneal Epithelial Cells. [PDF]
Inflammasomes are multiprotein complexes that detect danger-associated signals and trigger an immunostimulatory form of cell death called pyroptosis. NLRP1 is an innate immune receptor that assembles into an inflammasome, but the primary cell types in which NLRP1 is functional have not yet been fully established.
Griswold AR, Huang HC, Bachovchin DA.
europepmc +3 more sources
Ubiquitination as a key regulatory mechanism for O3-induced cutaneous redox inflammasome activation
NLRP1 is one of the major inflammasomes modulating the cutaneous inflammatory responses and therefore linked to a variety of cutaneous conditions. Although NLRP1 has been the first inflammasome to be discovered, only in the past years a significant ...
Francesca Ferrara +8 more
doaj +1 more source
NLRP1 inflammasome promotes senescence and senescence-associated secretory phenotype. [PDF]
Abstract Background Senescence is a cellular aging-related process triggered by different stresses and characterized by the secretion of various inflammatory factors referred to as senescence-associated secretory phenotype (SASP), some of which are produced by the NLRP3 inflammasome.
Muela-Zarzuela I +12 more
europepmc +3 more sources
Functional and Evolutionary Analyses Identify Proteolysis as a General Mechanism for NLRP1 Inflammasome Activation. [PDF]
Inflammasomes are cytosolic multi-protein complexes that initiate immune responses to infection by recruiting and activating the Caspase-1 protease.
Joseph Chavarría-Smith +4 more
doaj +1 more source
The NLRP1 and CARD8 inflammasomes detect reductive stress
The danger signals that activate the related nucleotide-binding domain leucine-rich repeat pyrin domain-containing 1 (NLRP1) and caspase activation and recruitment domain-containing 8 (CARD8) inflammasomes have not been fully established. We recently reported that the oxidized form of TRX1 binds to NLRP1 and represses inflammasome activation.
Qinghui Wang +8 more
openaire +2 more sources
Oxidized thioredoxin-1 restrains the NLRP1 inflammasome [PDF]
AbstractAt least six human proteins detect danger-associated signals, assemble into complexes called inflammasomes, and trigger pyroptotic cell death. NLRP1 was the first protein discovered to form an inflammasome, but the danger signals and molecular mechanisms that control its activation have not yet been fully established.
Daniel P. Ball +6 more
openaire +1 more source
NLRP1- A CINDERELLA STORY: a perspective of recent advances in NLRP1 and the questions they raise
NLRP1, while the first inflammasome described, has only recently begun to gain significant attention in disease pathology, inflammation research, and potentially, as a therapeutic target. Recently identified human variants provide key insights into NLRP1
Kristian Barry +2 more
doaj +1 more source
Nlrp6 promotes recovery after peripheral nerve injury independently of inflammasomes [PDF]
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

