The research group of Prof. Han Jiahuai published their research paper Ppm1b negatively regulates necroptosis　through dephosphorylating Rip3 on the latest Nature Cell Biology—a subordinate journal of Nature. This research found that Ppm1b negatively regulates necroptosis through dephosphorylating Rip3, revealing the importance of accurate regulation of phosphorylaed Rip3 to the survival of cells and organism physically and pathologically.

Necroptosis plays an important part in various physical and pathological processes such as development, host defenses, inflammation and tumour. Being the key molecule causing necroptosis, Rip3 has been widely studied in recent years; however, how Rip3 phosphorylation is regulated is still largely unknown.

 The research group of Prof. Han Jiahuai identified Ppm1b by analyzing the immunoprecipitate complex of Rip3 using mass spectrometric technique, proving that Rip3 phosphorylation was accurately regulated by cells for the first time. The research found that without stimulus, Ppm1b would suppress the self-activation of Rip3 by interacting with it and then help cells to live; with programmed necroptosis factor stimulating, Ppm1b would inhibit programmed cell necroptosis through dephosphorylating Rip3. Furthermore, the group showed that in the experiment of tumour necrosis factor-α (TNF)-induced systemic inflammatory syndrome in mice, Ppm1b could reduce the caecum damage of mice and therefore increase their surviving rate through dephosphorylating Rip3. Thus, accurate regulation of Rip3 phosphorylation was essential to the survival of cells both physically and pathologically. The research was crucial to treat systemic inflammatory syndrome induced by excessive production of TNF for it offered a brand-new perspective.

PhD student Chen Wanze is the first author and Prof. Han Jiahuai is the corresponding author of the paper.