K. Mukai

A non-toxic equinatoxin-II reveals the dynamics of sphingomyelin in the cytosolic leaflet of the plasma membrane

The paper uses a non-toxic SM probe to show dynamic SM and cholesterol domains in the cytosolic leaflet of plasma membranes.

TLR7/8 stress response drives histiocytosis in SLC29A3 disorders

This study identifies TLR7/8 as drivers of histiocytosis in SLC29A3 disorders by responding to lysosomal nucleoside stress and enhancing monocyte proliferation and phagocyte maturation.

Lysosomal vesiculophagy terminates STING signalling

This study identifies lysosomal vesiculophagy as a mechanism for STING degradation, preventing sustained type I interferon response.

Aberrant localization of CDC42 C-terminal variants to the Golgi apparatus drives pyrin inflammasome-dependent autoinflammation

This study identifies that CDC42 C-terminal variants cause aberrant Golgi localization, leading to pyrin inflammasome activation and autoinflammation.

Kinase activity of TBK1 is required for its binding to STING, but not for its recruitment to the Golgi

The paper investigates TBK1's role in STING signaling, showing kinase activity is not needed for TBK1 recruitment to the Golgi but is required for stable complex formation.

Implications of cholesterol and sphingomyelin in STING phosphorylation by TBK1

The paper shows that cholesterol and sphingomyelin are required for TBK1-mediated phosphorylation of STING at the TGN, mirroring in vivo conditions.

A defect in COPI-mediated transport of STING causes immune dysregulation in COPA syndrome

This study shows that defective COPI transport of STING due to COPA mutations leads to immune dysregulation and type I interferon signaling in COPA syndrome.

Homeostatic regulation of STING by Golgi-to-ER membrane traffic

This study identifies STING as a cargo of Golgi-to-ER transport and shows that impaired retrograde transport due to COPA syndrome mutations leads to STING activation and autoinflammation.