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Times Cited: 145
Times Cited: 145
Times Cited
Times Co-cited
Similarity
Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death.
Jianjin Shi, Yue Zhao, Kun Wang, Xuyan Shi, Yue Wang, Huanwei Huang, Yinghua Zhuang, Tao Cai, Fengchao Wang, Feng Shao. Nature 2015
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Chemotherapy drugs induce pyroptosis through caspase-3 cleavage of a gasdermin.
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The gasdermins, a protein family executing cell death and inflammation.
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Inflammatory caspases are innate immune receptors for intracellular LPS.
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Pathogen blockade of TAK1 triggers caspase-8-dependent cleavage of gasdermin D and cell death.
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Gasdermin E suppresses tumour growth by activating anti-tumour immunity.
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GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death.
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Granzyme A from cytotoxic lymphocytes cleaves GSDMB to trigger pyroptosis in target cells.
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Non-canonical inflammasome activation targets caspase-11.
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Caspase-8 induces cleavage of gasdermin D to elicit pyroptosis during Yersinia infection.
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FDA-approved disulfiram inhibits pyroptosis by blocking gasdermin D pore formation.
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Gasdermin pores permeabilize mitochondria to augment caspase-3 activation during apoptosis and inflammasome activation.
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GsdmD p30 elicited by caspase-11 during pyroptosis forms pores in membranes.
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Noncanonical inflammasome signaling elicits gasdermin D-dependent neutrophil extracellular traps.
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PD-L1-mediated gasdermin C expression switches apoptosis to pyroptosis in cancer cells and facilitates tumour necrosis.
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Caspase-1 initiates apoptosis in the absence of gasdermin D.
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Cryo-EM structure of the gasdermin A3 membrane pore.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.