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The 'death switch' in sepsis also promotes survival
Date:2/2/2011

and a graduate student at the Alpert Medical School and Rhode Island Hospital, says, "In our animal models, we discovered that survival decreased when we suppressed RIP1. Our findings imply that RIP1's capacity to contribute to the onset of programmed cell death is not its central role in the septic animal and it appears to be necessary for survival of septic injury."

RIP1 is a multifunctional adaptor protein that has three domains: kinase, intermediate and death. The findings from this study indicate that the kinase domain of this protein is more involved in cell function than was previously thought. McNeal explains that this finding is important because knowledge of how the kinase domain is regulated may uncover new therapeutic targets that can be used to mitigate the effects of cellular/organ damage caused by trauma, shock, sepsis or other related conditions.

McNeal says, "The function of RIP1 is much more nuanced than we originally thought. We believe it plays a key role in cell function during sepsis, and if the pro-survival trigger can be identified, it could have major implications on how sepsis is treated in the future."


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Contact: Nancy Cawley Jean
njean@lifespan.org
Lifespan
Source:Eurekalert

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