Evidence map›Paper›PMID 9566966›Full record

ArticleThe Journal of cell biology1998

Calpain regulates actin remodeling during cell spreading.

D A Potter, J S Tirnauer, R Janssen, D E Croall, C N Hughes, K A Fiacco, J W Mier, M Maki, I M Herman

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

78 citing papers in PubMed, 269 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Synaptic tau: A pathological or physiological phenomenon?Acta neuropathologica communications · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Mechanisms protecting host cells against bacterial pore-forming toxins.Cellular and molecular life sciences : CMLS · 2019
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

18 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

D A PotterDivision of Hematology and Oncology, Tupper Research Institute, Department of Medicine, New England Medical Center, Boston, Massachusetts, USA. dpottervmhc@opal.tufts.edu
J S Tirnauer
R Janssen
D E Croall
C N Hughes
K A Fiacco
J W Mier
M Maki
I M Herman
Tufts University · USUniversity of Maine · USNagoya University · JP

Funding

RETINAL MICROVASCULAR CELLS, MATRIX, &OCULAR DISORDERSR01EY009033 · NEI · TUFTS UNIVERSITY BOSTON · PI HERMAN, IRA M · 1993 to 2002
$817k
REGULATION OF ISOACTIN DYNAMICS IN LIVING CELLSR01GM055110 · NIGMS · TUFTS UNIVERSITY BOSTON · PI HERMAN, IRA M · 1997 to 2000
$288k
FUNCTIONAL ANALYSIS OF TRANSCRIPTION FACTORS IN HIV-1K08CA001562 · NCI · TUFTS MEDICAL CENTER · PI POTTER, DAVID ALEXANDER · 1991 to 1996
–
NCI NIH HHS K08 CA001562NCI NIH HHS K08-CA 1562NEI NIH HHS EY 09033NIGMS NIH HHS GM 55110
6 · The paper itself

Abstract

Previous studies suggest that the Ca2+-dependent proteases, calpains, participate in remodeling of the actin cytoskeleton during wound healing and are active during cell migration. To directly test the role that calpains play in cell spreading, several NIH-3T3- derived clonal cell lines were isolated that overexpress the biological inhibitor of calpains, calpastatin. These cells stably overexpress calpastatin two- to eightfold relative to controls and differ from both parental and control cell lines in morphology, spreading, cytoskeletal structure, and biochemical characteristics. Morphologic characteristics of the mutant cells include failure to extend lamellipodia, as well as abnormal filopodia, extensions, and retractions. Whereas wild-type cells extend lamellae within 30 min after plating, all of the calpastatin-overexpressing cell lines fail to spread and assemble actin-rich processes. The cells genetically altered to overexpress calpastatin display decreased calpain activity as measured in situ or in vitro. The ERM protein ezrin, but not radixin or moesin, is markedly increased due to calpain inhibition. To confirm that inhibition of calpain activity is related to the defect in spreading, pharmacological inhibitors of calpain were also analyzed. The cell permeant inhibitors calpeptin and MDL 28, 170 cause immediate inhibition of spreading. Failure of the intimately related processes of filopodia formation and lamellar extension indicate that calpain is intimately involved in actin remodeling and cell spreading.

Indexed as

3T3 CellsActinsAnimalsCalcium-Binding ProteinsCalpainCell MovementCysteine Proteinase InhibitorsCytoskeletal ProteinsDown-RegulationEzrinHumansMicePhosphoproteinsSubstrate SpecificityUp-RegulationActinsCalcium-Binding ProteinsCalpaincalpastatinCysteine Proteinase InhibitorsCytoskeletal ProteinsEzrinPhosphoproteins

Identifiers

PMID9566966
PMCPMC2132736
OpenAlexW2043305034

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.