Inflammasome and immune disorders

This paper identifies proteolytic cleavage as the mechanism regulating fungal gasdermin activity, showing that HET-Q1 is cleaved by HET-Q2 to induce cell death and that gasdermin genes are clustered with protease genes.

This study shows SARS-CoV-2 activates microglial NLRP3 inflammasome via spike-ACE2 interaction, potentially linking viral infection to neurological symptoms like Parkinson's.

This study shows that NLRP3 inhibition after reperfusion reduces brain injury in ischemia by protecting the blood-brain barrier and reducing inflammation.

The paper identifies a SNP in the 3' UTR of the Pycard gene in mice that affects mRNA stability and inflammasome activity through CRISPR/Cas9 editing.

This paper shows that ASC controls AA amyloidosis by interacting with SAA and that anti-ASC antibodies reduce amyloid loads in mice.

The paper shows that PPARA upregulates Gm15441, which suppresses TXNIP and reduces NLRP3 inflammasome activation during metabolic stress.

The paper identifies a mutation in Cdc42 that causes a severe autoinflammatory syndrome by trapping the protein in the Golgi and disrupting its membrane interaction.

The paper shows that defective microglial pyroptosis in mice leads to ADHD-like behaviors, suggesting a link between microglial cell death and neurodevelopmental disorders.

This study identifies a novel mutation in A20 causing haploinsufficiency and shows it impairs the protein-protein interactome, leading to enhanced NLRP3 inflammasome activation through caspase-8.

This study shows that stavudine reduces NLRP3 inflammasome activation and enhances Aβ autophagy in an in vitro AD model.

The paper reports the crystal structure of GSDMD's C-terminal domain to analyze activation determinants and interactions with the N-terminal domain.