Sam68 is cleaved by caspases under apoptotic cell death induced by ionizing radiation

Cho, Seong‐Jun; Choi, Moo Hyun; Nam, Sang Yong; Kim, Ji Young; Kim, Cha Soon; Pyo, Suhkneung; Yang, Kwang Hee

doi:10.1093/jrr/rru113

Cited by 2 publications

(2 citation statements)

References 31 publications

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“…Sam68 was confirmed to be recruited to the TNF receptor and promote the recruitment and ubiquitylation of RIP ( Ramakrishnan and Baltimore, 2011 ). Moreover, Sam68 is a part of the TNF-induced cytoplasmic caspase-8-FADD complex, and its cleavage by activated caspase, especially caspase-8, triggers the apoptosis pathway ( Cho et al, 2015 ). However, the mechanism by which MD2 acts on Sam68 and whether other molecules can interact with MD2 remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Neuronal MD2 induces long-term mental impairments in septic mice by facilitating necroptosis and apoptosis

Fan

et al. 2022

Front. Pharmacol.

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Sepsis-associated encephalopathy (SAE) is a complication of sepsis with high morbidity rates. Long-lasting mental health issues in patients with SAE result in a substantial decrease in quality of life. However, its underlying mechanism is unclear, and effective treatments are not available. In the current study, we explored the role of apoptosis and necroptosis related to mental dysfunction in sepsis. In a mouse model of sepsis constructed by cecal ligation and puncture (CLP), altered behavior was detected by the open field, elevated-plus maze and forced swimming tests on the fourteenth day. Moreover, apoptosis- and necroptosis-associated proteins and morphological changes were examined in the hippocampus of septic mice. Long-lasting depression-like behaviors were detected in the CLP mice, as well as significant increases in neuronal apoptosis and necroptosis. Importantly, we found that apoptosis and necroptosis were related according to Ramsay’s rule in the brains of the septic mice. Inhibiting myeloid differentiation factor 2 (MD2), the crosstalk mediator of apoptosis and necroptosis, in neurons effectively reduced neuronal loss and alleviated depression-like behaviors in the septic mice. These results suggest that neuronal death in the hippocampus contributes to the mental impairments in SAE and that inhibiting neuronal MD2 is a new strategy for treating mental health issues in sepsis by inhibiting necroptosis and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Neuronal MD2 induces long-term mental impairments in septic mice by facilitating necroptosis and apoptosis

Fan

et al. 2022

Front. Pharmacol.

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show abstract

“…Sam68 was con rmed to be recruited to the TNF receptor and promote the recruitment and ubiquitylation of RIP [31]. Moreover, Sam68 is a part of the TNF-induced cytoplasmic caspase-8-FADD complex, and its cleavage by activated caspase, especially caspase-8, triggers the apoptosis pathway [32]. However, the mechanism by which MD2 acts on Sam68 and whether other molecules can interact with MD2 remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Neuronal MD2 Induces Long-term Mental Impairments in Septic Mice by Facilitating Necroptosis and Apoptosis

Fan¹,

et al. 2021

Preprint

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Sepsis-associated encephalopathy (SAE) is a complication of sepsis that has high morbidity rates. Long-lasting depression is a major mental health disorder in patients with SAE that results in a substantial decrease in quality of life and economic burden. However, the underlying mechanism of SAE is unclear, and effective treatments are not available. In the current study, we explored the role of apoptosis and necroptosis related to depression in sepsis. In a mouse model of cecal ligation and puncture (CLP), we detected mental impairments by the open field test, elevated-plus maze and forced swimming test on the fourteenth day. Moreover, apoptosis- and necroptosis-associated proteins and morphological changes were examined in the hippocampus of the septic mice. These mice showed depression-like behaviors at 14 days after CLP, with substantial increases in neuronal apoptosis and necroptosis. Importantly, we found that apoptosis and necroptosis were related according to Ramsay’s rule in the brains of the septic mice. Inhibiting the function of MD2, the crosstalk mediator of apoptosis and necroptosis, in neurons effectively reduced neuronal loss and alleviated depression-like behaviors in the septic mice. These results suggest that neuronal death in the hippocampus contributes to the mental impairments in SAE and that inhibiting neuronal MD2 is a new strategy for treatment of mental health issues in sepsis by inhibiting necroptosis and apoptosis.

show abstract

Sam68 is cleaved by caspases under apoptotic cell death induced by ionizing radiation

Cited by 2 publications

References 31 publications

Neuronal MD2 induces long-term mental impairments in septic mice by facilitating necroptosis and apoptosis

Neuronal MD2 induces long-term mental impairments in septic mice by facilitating necroptosis and apoptosis

Neuronal MD2 Induces Long-term Mental Impairments in Septic Mice by Facilitating Necroptosis and Apoptosis

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