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Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity

Overview of attention for article published in The Journal of Experimental Medicine, February 2018
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About this Attention Score

  • In the top 5% of all research outputs scored by Altmetric
  • Among the highest-scoring outputs from this source (#18 of 8,117)
  • High Attention Score compared to outputs of the same age (98th percentile)
  • High Attention Score compared to outputs of the same age and source (93rd percentile)

Mentioned by

news
17 news outlets
twitter
91 tweeters
facebook
9 Facebook pages

Readers on

mendeley
44 Mendeley
Title
Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity
Published in
The Journal of Experimental Medicine, February 2018
DOI 10.1084/jem.20172222
Pubmed ID
Authors

Dave Boucher, Mercedes Monteleone, Rebecca C. Coll, Kaiwen W. Chen, Connie M. Ross, Jessica L. Teo, Guillermo A. Gomez, Caroline L. Holley, Damien Bierschenk, Katryn J. Stacey, Alpha S. Yap, Jelena S. Bezbradica, Kate Schroder

Abstract

Host-protective caspase-1 activity must be tightly regulated to prevent pathology, but mechanisms controlling the duration of cellular caspase-1 activity are unknown. Caspase-1 is activated on inflammasomes, signaling platforms that facilitate caspase-1 dimerization and autoprocessing. Previous studies with recombinant protein identified a caspase-1 tetramer composed of two p20 and two p10 subunits (p20/p10) as an active species. In this study, we report that in the cell, the dominant species of active caspase-1 dimers elicited by inflammasomes are in fact full-length p46 and a transient species, p33/p10. Further p33/p10 autoprocessing occurs with kinetics specified by inflammasome size and cell type, and this releases p20/p10 from the inflammasome, whereupon the tetramer becomes unstable in cells and protease activity is terminated. The inflammasome-caspase-1 complex thus functions as a holoenzyme that directs the location of caspase-1 activity but also incorporates an intrinsic self-limiting mechanism that ensures timely caspase-1 deactivation. This intrinsic mechanism of inflammasome signal shutdown offers a molecular basis for the transient nature, and coordinated timing, of inflammasome-dependent inflammatory responses.

Twitter Demographics

The data shown below were collected from the profiles of 91 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 44 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 44 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 12 27%
Researcher 9 20%
Student > Master 6 14%
Unspecified 4 9%
Student > Bachelor 3 7%
Other 10 23%
Readers by discipline Count As %
Immunology and Microbiology 15 34%
Agricultural and Biological Sciences 12 27%
Unspecified 5 11%
Biochemistry, Genetics and Molecular Biology 5 11%
Medicine and Dentistry 4 9%
Other 3 7%

Attention Score in Context

This research output has an Altmetric Attention Score of 184. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 18 May 2018.
All research outputs
#51,711
of 10,791,774 outputs
Outputs from The Journal of Experimental Medicine
#18
of 8,117 outputs
Outputs of similar age
#3,144
of 270,558 outputs
Outputs of similar age from The Journal of Experimental Medicine
#4
of 62 outputs
Altmetric has tracked 10,791,774 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 99th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 8,117 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.4. This one has done particularly well, scoring higher than 99% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 270,558 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 98% of its contemporaries.
We're also able to compare this research output to 62 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 93% of its contemporaries.