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Metabolic and oxidative stress regulation of gasdermin D-mediated cell death

Microbe invasion or damage associated endogenous molecules lead to fast immune response that can also result in cell death called pyroptosis. Several host proteases are able to cleave protein gasdermin D. The central event in pyroptosis is when gasdermin D N-terminal domain forms pores in the plasma membrane.

Researchers showed that the key metabolic signaling pathway mTORC1 and oxidative stress promote gasdermin D pore formation. This study demonstrates that gasdermin D pore formation and pyroptosis can be regulated at the final step with implications in control of inflammation.

The study was published in the prestigious journal Cell. Slovenian part of the research was supported by Slovenian Research Agency. The study started during Fulbright visit in the lab of J.C. Kagan (Boston Children's Hospital & Harvard Medical School) in 2019.

Authors: Charles L. Evavold, Iva Hafner-Bratkovič, Pascal Devant, Jasmin M. D’Andrea, Elsy M. Ngwa, Elvira Boršić, John G. Doench, Martin W. LaFleur, Arlene H. Sharpe, Jay R. Thiagarajah in Jonathan C. Kagan.


For further information please contact: iva.hafner[at]


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