Wang Liu

TL;DR: It is demonstrated that the liposome-leakage and pore-forming activities of the gasdermin-N domain are required for pyroptosis and provide insights into the roles of theGasdermin family in necrosis, immunity and diseases.

TL;DR: It is shown that GSDME, which was originally identified as DFNA5 (deafness, autosomal dominant 5), can switch caspase-3-mediated apoptosis induced by TNF or chemotherapy drugs to pyroptosis, suggesting that casp enzyme activation can trigger necrosis by cleaving G SDME and offer new insights into cancer chemotherapy.

TL;DR: It is shown that granzyme A cleaves and activates gasdermin B (GSDMB), a central player in the highly inflammatory cell death process known as pyroptosis, suggesting that this pathway may be a target for future cancer immunotherapies.

TL;DR: It is found that Pyrin is phosphorylated on two serine sites which keep Pyrin inactive through binding by 14-3-3 proteins, and reveals that site-specific (de)phosphorylation and microtubule dynamics critically control Pyrin inflammasome activation, illustrating a fine and complex mechanism in cytosolic immunity.

TL;DR: In this article, a post-translational modification, termed ADP-riboxanation, which is mediated by the Shigella effector OspC3 and inactivates the cytosolic lipopolysaccharide (LPS) sensing pathway of caspase-4 and caspases-11, was found to protect mice from S. flexneri infection.