Cell death via apoptosis is a key cellular function triggered by the cell death receptor family and their ligands. This regulated process then transmits downstream signals through adaptor molecules ending with the caspase cysteine proteases. Caspase 11 has a heterotetrameric structure consisting of two anti-parallel heterodimers. Upon activation, it is cleaved by an autocatalytic mechanism to give rise to individual subunits. This post-translational regulation enables rapid activation. Expression levels of caspase 11 are highest in lung and spleen. This protein plays a role in apoptosis, cell migration, and the inflammatory response.
Immunocytochemistry/Immunofluorescence: Caspase 11 Antibody
Data published in Nature from Kayagaki's group at Genentech relied upon the caspase 11 antibody to highlight a unique pro-inflammatory role for caspase 11 in the cellular response to bacterial infections (1). Their results challenge previous thinking and demonstrate that caspase 11, rather than caspase 1 as previously thought, is required for non-canonical inflammasome-triggered cell death. Studies with the caspase 11 antibody in traumatic brain injury models show that therapeutic hypothermia protects an injured central nervous system (CNS) by minimizing the detrimental effects of the inflammasome innate immune response and signaling of triggers such as caspases 1 and 11 (2). Interleukins IL1-beta and IL-18 are activated by caspase-1 in a microglial cathepsin B-dependent fashion; Sun et al employed the caspase 11 antibody to further investigate the role of cathepsin B in peripheral inflammation-induced chronic pain and hypersensitvity (3). Further inflammation studies with caspase 11 antibody in myeloid cells demonstrated that the TREM-1 receptor plays a key role in macrophage survival (4). Jin’s group at the Scripps Research Institute performed characterization studies with caspase 11 antibody to better understand the role of microRNAs (miRNAs) in lymphomagenesis, and found that the miR-17~92 coordinates multiple oncogenic pathways (PI3Kinase, NFkB) and holds promise as a powerful therapeutic for those particular cancers that involve miRNA dysregulation (5).
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