Abstract
ASC is an adaptor of the inflammasome: a multiprotein complex necessary for the activation of proinflammatory cytokines. Formation of the inflammasome complex depends primarily on the self-association capabilities of ASC via its two Death Domains (PYD and CARD). ASCb, an isoform of ASC, produces a lower inflammatory response compared to ASC. The two isoforms differ only in the length of the linker connecting the two Death Domains. We hypothesize that this difference influences ASC and ASCb self-association capabilities, thus playing a role in inflammasome regulation at the molecular level.
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