Kohsuke Tsuchiya, Shinsuke Nakajima, Shoko Hosojima, Dinh Thi Nguyen, Tsuyoshi Hattori, Thuong Manh Le, Osamu Hori, Mamunur Rashid Mahib, Yoshifumi Yamaguchi, Masayuki Miura, Takeshi Kinoshita, Hiroko Kushiyama, Mayumi Sakurai, Toshihiko Shiroishi, Takashi Suda. Nat Commun 2019
Times Cited: 154
Times Cited: 154
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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Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling.
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Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores.
Xing Liu, Zhibin Zhang, Jianbin Ruan, Youdong Pan, Venkat Giri Magupalli, Hao Wu, Judy Lieberman. Nature 2016
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Chemotherapy drugs induce pyroptosis through caspase-3 cleavage of a gasdermin.
Yupeng Wang, Wenqing Gao, Xuyan Shi, Jingjin Ding, Wang Liu, Huabin He, Kun Wang, Feng Shao. Nature 2017
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Pore-forming activity and structural autoinhibition of the gasdermin family.
Jingjin Ding, Kun Wang, Wang Liu, Yang She, Qi Sun, Jianjin Shi, Hanzi Sun, Da-Cheng Wang, Feng Shao. Nature 2016
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Gasdermin D is an executor of pyroptosis and required for interleukin-1β secretion.
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Pathogen blockade of TAK1 triggers caspase-8-dependent cleavage of gasdermin D and cell death.
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Caspase-8 induces cleavage of gasdermin D to elicit pyroptosis during Yersinia infection.
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Cleavage of DFNA5 by caspase-3 during apoptosis mediates progression to secondary necrotic/pyroptotic cell death.
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Inflammatory caspases are innate immune receptors for intracellular LPS.
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Non-canonical inflammasome activation targets caspase-11.
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Gasdermin pores permeabilize mitochondria to augment caspase-3 activation during apoptosis and inflammasome activation.
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Granzyme A from cytotoxic lymphocytes cleaves GSDMB to trigger pyroptosis in target cells.
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The gasdermins, a protein family executing cell death and inflammation.
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GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death.
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ESCRT-dependent membrane repair negatively regulates pyroptosis downstream of GSDMD activation.
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Extrinsic and intrinsic apoptosis activate pannexin-1 to drive NLRP3 inflammasome assembly.
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N-GSDMD trafficking to neutrophil organelles facilitates IL-1β release independently of plasma membrane pores and pyroptosis.
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Caspase-8 is the molecular switch for apoptosis, necroptosis and pyroptosis.
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Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis.
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AIM2 and NLRP3 inflammasomes activate both apoptotic and pyroptotic death pathways via ASC.
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Noncanonical inflammasome activation by intracellular LPS independent of TLR4.
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Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation.
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Activity of caspase-8 determines plasticity between cell death pathways.
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GsdmD p30 elicited by caspase-11 during pyroptosis forms pores in membranes.
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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.