Caspase-2: the orphan caspase

Bouchier‐Hayes, Lisa; Green, Douglas R.

doi:10.1038/cdd.2011.157

Cited by 98 publications

(83 citation statements)

References 69 publications

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“…1 Recent evidence suggests that caspase-2 may have a role in the suppression of tumorigenesis. Loss of caspase-2 in a mouse model of lymphoma, induced by transgenic c-Myc on the m-enhancer (Em-Myc), greatly accelerated tumor growth.…”

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confidence: 99%

Genetic deletion of caspase-2 accelerates MMTV/c-neu-driven mammary carcinogenesis in mice

et al. 2013

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confidence: 99%

Genetic deletion of caspase-2 accelerates MMTV/c-neu-driven mammary carcinogenesis in mice

et al. 2013

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“…Identification of the definitive molecular mechanism for IpaDmediated apoptosis in macrophages will require further study. Caspase-2 and caspase-8 have been identified as processors of Bid, a protein that activates intrinsic apoptosis (58,59). Our findings with these caspases merit assessment of this pathway in future studies.…”

Section: Discussionmentioning

confidence: 99%

Macrophage Apoptosis Triggered by IpaD from Shigella flexneri

Arizmendi

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2016

Infect Immun

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Shigellosis, a potentially severe bacillary dysentery, is an infectious gastrointestinal disease caused by Shigella spp. Shigella invades the human colonic epithelium and avoids clearance by promoting apoptosis of resident immune cells in the gut. This process is dependent on the Shigella type III secretion system (T3SS), which injects effector proteins into target cells to alter their normal cellular functions. Invasion plasmid antigen D (IpaD) is a structural component that forms a complex at the tip of the T3SS apparatus needle. Recently, IpaD has also been shown to indirectly induce apoptosis in B lymphocytes. In this study, we explored the cytotoxicity profile during macrophage infection by Shigella and discovered that the pathogen induces macrophage cell death independent of caspase-1. Our results demonstrate that IpaD triggers apoptosis in macrophages through activation of host caspases accompanied by mitochondrial disruption. Additionally, we found that the IpaD N-terminal domain is necessary for macrophage killing and SipD, a structural homologue from Salmonella, was found to promote similar cytotoxicity. Together, these findings indicate that IpaD is a contributing factor to macrophage cell death during Shigella infection.

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“…Caspase 2 (CASP2) is a protease that is activated in response to stress (DNA damage) and it appears to participate more in the regulation of the cell cycle than in apoptosis [32]. Moreover, CASP2 acts as a tumor suppressor by inducing cell cycle arrest.…”

Section: Discussionmentioning

confidence: 99%