Evidence map›Paper›PMID 20020448›Full record

ArticleJournal of cellular physiology2010

Kinetic properties of ASC protein aggregation in epithelial cells.

Jun Cheng, Andrea L Waite, Eric R Tkaczyk, Kevin Ke, Neil Richards, Alan J Hunt, Deborah L Gumucio

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.9field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. NLRC4 inflammasomopathies.Current opinion in allergy and clinical immunology · 2017
    Review
  9. Dynamics of in vivo ASC speck formation.The Journal of cell biology · 2017
    Article
  10. Assembly and regulation of ASC specks.Cellular and molecular life sciences : CMLS · 2017
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Structural mechanisms in NLR inflammasome signaling.Current opinion in structural biology · 2014
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Jun ChengDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan 48109-2099, USA.
Andrea L Waite
Eric R Tkaczyk
Kevin Ke
Neil Richards
Alan J Hunt
Deborah L Gumucio
University of Michigan–Ann Arbor · US

Funding

Cellular Biotechnology Training Program (CBTP) - Years 31-35T32GM145304 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Guizhi Zhu · 2022 to 2026
$2.6M
Ultra-Precise Laser Surgery to study Cell BiomechanicsR01GM072006 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MAYER, MICHAEL, YAMASHITA, YUKIKO · 2004 to 2013
$2.4M
Molecular Etiology of Familial Mediterranean FeverR01AI053262 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUMUCIO, DEBORAH L. · 2003 to 2007
$1.6M
NIAID NIH HHS R01 AI053262NIAID NIH HHS R01-AI53262NIGMS NIH HHS R01 GM072006NIGMS NIH HHS R01-GM072006NIGMS NIH HHS T32 GM145304
6 · The paper itself

Abstract

Apoptosis-associated speck-like protein with CARD domain (ASC), an adaptor protein composed of caspase recruitment and pyrin domains, can efficiently self-associate to form a large spherical structure, called a speck. Although ASC aggregation is generally involved with both inflammatory processes and apoptosis, the detailed dynamics of speck formation have not been characterized. In this report, speck formation in HeLa cells transfected with ASC is examined by time-lapse live-imaging by confocal laser scanning microscopy. The results show that ASC aggregation is a very rapid and tightly regulated process. Prior to speck formation, soluble ASC aggregation is a low probability event, and the affinity of ASC subunits for one another is very low. Following a speck nucleation event, the affinity for further addition of ASC subunits increases dramatically, and aggregation is a highly energetically favorable reaction (Gibbs free energy approximately -40 kJ/mol). This leads to a rapid depletion of soluble ASC, making it highly unlikely that a second speck will form inside the same cell and assuring that speck formation is "all or none," with a well-defined end point. Comparison with kinetic models of the aggregation process indicates diffusion, instead of active transport, is the dominant process for speck growth. Though speck formation and aggresome formation share some properties, we show that the two processes are distinct.

Indexed as

Biological Transport, ActiveCARD Signaling Adaptor ProteinsCell NucleusComputer SimulationCytoskeletal ProteinsCytosolDiffusionEpithelial CellsHeLa CellsHumansKineticsMicroscopy, ConfocalMicroscopy, VideoModels, BiologicalProtein MultimerizationProtein TransportCARD Signaling Adaptor ProteinsCytoskeletal ProteinsPYCARD protein, humanRecombinant Fusion Proteins

Identifiers

PMID20020448
PMCPMC10067259
OpenAlexW1988654439

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.