Evidence map›Paper›PMID 17414215›Full record

ReviewCurrent opinion in hematology2007

Calpain-mediated regulation of platelet signaling pathways.

Shafi M Kuchay, Athar H Chishti

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in hematology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

27 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy.International journal of molecular sciences · 2022
    Review
  6. Article
  7. The C2 domain of calpain 5 contributes to enzyme activation and membrane localization.Biochimica et biophysica acta. Molecular cell research · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

2 authors at 1 institution in 1 country.

Shafi M KuchayDepartment of Pharmacology, University of Illinois College of Medicine, Chicago, IL 60612, USA.
Athar H Chishti
University of Illinois Urbana-Champaign · US

Funding

FUNCTIONAL STUDIES OF RED BLOOD CELL DEMATINR01HL051445 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHISHTI, ATHAR H. · 1994 to 2010
$1.9M
Functional Studies of Erythrocyte DematinR56HL051445 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHISHTI, ATHAR H. · 2008 to 2008
$393k
NHLBI NIH HHS HL51445NHLBI NIH HHS R01 HL051445NHLBI NIH HHS R56 HL051445
6 · The paper itself

Abstract

purpose of reviewThere is considerable interest in understanding the function and mechanism of calpains in platelet aggregation, spreading, and granular secretion pathways. Recent insights from the calpain-1 knockout platelets suggest a pivotal role of these cysteine proteases in the regulation of outside-in signaling, aggregation, and clot retraction. RECENT

findingsThe calpain-1 knockout mouse provided direct evidence for the role of calpain-1 in platelet aggregation and clot retraction. Reduced tyrosine phosphorylation of platelet proteins correlated with reduced platelet aggregation and clot retraction. Future investigations of the mechanism of platelet defects in calpain-1 null mice may unveil the physiological functions of this important and elusive protease in mammalian cells. SUMMARY: This review focuses on the role of calpains in platelets with a particular emphasis on recent findings in calpain-1 null platelets. Previous studies used synthetic inhibitors to study the role of calpains in platelet function yielding useful information about the identification of calpain substrates. The development of calpain-1 null mice demonstrated that calpain-1 plays an important function in the regulation of platelet aggregation and clot retraction. Since the combined deletion of calpain-1 and calpain-2 genes results in embryonic lethality, the calpain-1 null mouse remains the only experimental model available to study the physiological role of calpains in mammalian cells.

Indexed as

Signal TransductionAnimalsBlood PlateletsCalpainMiceCalpainCapn1 protein, mouse

Identifiers

PMID17414215
PMCPMC3959858
OpenAlexW2107158501

What OpenQuestion holds

Textmetadata
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.