Active caspase-1 is a regulator of unconventional protein secretion.

By Martin Keller, Andreas Rüegg, S. Werner, H. Beer. Cell, 2008

898 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c2304ed854c6808c9994659232956541d964de50

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Citations in the corpus

Origin and physiological roles of inflammation (2008, background): “A recent study has shown that this non-canonical secretion is mediated by activated caspase 1, implying that the secretion is regulated by inflammasome”
Inflammasomes and their roles in health and disease. (2012, background): “Similarly, caspase-1 was required for secretion of FGF2 by macrophages, UVA-irradiated fibroblasts, and UVB-irradiated keratinocytes (Keller et al. 2008).”
Programmed cell death in the plant immune system (2011, background): “Caspase-1 also regulates the release of these and other pro-inflammatory cytokines into the extracellular millieu.(35) These secreted molecules are instrumental for Figure 2 Cell death modalities in response to infection.”
The IL-33/ST2 pathway: therapeutic target and novel biomarker (2008, background): “The heterochromatin-binding of IL-33 resembles the biology of IL-1α more closely than other members of the IL-1 family and, as has recently been suggested for pro-IL-1α, it is possible that caspase-1 acts as a secretory targeting factor for pro-IL-33 (Ref”
Inflammasomes in health and disease (2012, background): “Similarly, caspase-1 is responsible for the processing and secretion of IL-18, as well as the secretion of other proteins such as IL-1α and fibroblast growth factor-2 through an unconventional protein secretion pathwa”
The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases (2011, background): “Activation of caspase-1 leads to the processing of IL-1β and IL-18 as well as to the unconventional secretion of a subset of leaderless proteins which might facilitate tissue repair (7).”
Skin immune sentinels in health and disease (2009, background): “It has recently been established that ultraviolet (UV) irradiation activates the inflammasome in human keratinocyte”
The sterile inflammatory response (2010, background): “This step may not require the inflammasome, although reduced IL-1α production has been reported from caspase I-deficient cells (74) and physical interactions between pro- IL-1α and caspase-1 have been reported (86)”
The FGF family: biology, pathophysiology and therapy (2009, neutral): “Other possible physiological roles for FGF2 include inflammation, in which stress-induced activation of caspase 1 leads to release of FGF2 (Ref”
CD36 coordinates NLRP3 inflammasome activation by facilitating the intracellular nucleation from soluble to particulate ligands in sterile inflammation (2013, background): “In the AD brain and diabetic pancreas, amyloid plaques arise from the aggregation of pre-fibrillar amyloidogenic peptides such as the Aβ(1-42) peptide17, 18, 19 or IAPP20, 21, 22, which oligomerize and give rise to higher order structures, including fibrils.”
The interleukin‐1 receptor/Toll‐like receptor superfamily: 10 years of progress (2008, background): “Caspase-1 has also been shown to be a regulator of unconventional protein secretion, regulating the secretion of multiple pro-inflammatory proteins (80).”
Pyroptosis: host cell death and inflammation (2009, background): “Active caspase 1 has been shown to bind to and facilitate secretion of IL-1α by an unknown mechanis”
Differential requirement for Caspase-1 autoproteolysis in pathogen-induced cell death and cytokine processing (2010, background): “Detection of Caspase-1 processing is routinely carried out on culture supernatants, since active Caspase-1 is released via a secretion pathway that has yet to be characterized (Keller et al., 2008).”
The Inflammasome: A Caspase-1 Activation Platform Regulating Immune Responses and Disease Pathogenesis (2009, background): “In addition, caspase-1 cleaves other cellular protein substrates, including pro-caspase-7, and mediates unconventional protein secretion as well as membrane repair and cell survival in response to bacterial pore-forming toxins by mechanisms that remain mostly undefine”
The inflammasome: an integrated view (2011, background): “Altogether, these data suggest that protection from the lethal effect of LPS is achieved by either completely blocking IL-1 signaling, as in IL-1R-deficient mice, or by the concomitant reduction of active IL-1 and of the amplifier HMGB1.”
Autophagy‐based unconventional secretory pathway for extracellular delivery of IL‐1β (2011, background): “…agonist based on the reports that HMGB1, along with additional unconventional substrates, depends on inflammasome for secretion although the protein itself is not subjected to proteolytic processing by caspase 1 (Keller et al, 2008; Willingham et al, 2009; Lamkanfi et al, 2010; Lamkanfi, 2011).”