Evidence map›Paper›PMID 20346680›Full record

ReviewTrends in biochemical sciences2010

The molecular regulation of programmed necrotic cell injury.

David Moquin, Francis Ka-Ming Chan

Open access · greenAbstract readReview
In one paragraph

Review in Trends in biochemical sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
8.1field-weighted citation impact, top 2% 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, 153 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Protein kinase D: A therapeutic target in experimental alcoholic pancreatitis.Biochimica et biophysica acta. Molecular basis of disease · 2022
    Article
  5. Review
  6. Review
  7. Mitochondria signaling pathways in allergic asthma.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2022
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Necroptosis, the Other Main Caspase-Independent Cell Death.Advances in experimental medicine and biology · 2021
    Article
  16. Mitochondrial Mechanisms of Necroptosis in Liver Diseases.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Review
  19. Review
  20. Guidelines for evaluating myocardial cell death.American journal of physiology. Heart and circulatory physiology · 2019
    Review

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

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.

David MoquinDepartment of Pathology, Immunology and Virology Program, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA.
Francis Ka-Ming Chan
University of Massachusetts Chan Medical School · US

Funding

PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
TRAINING IN IMMUNOLOGY (COMPETITIVE RENEWAL OF AI07439)T32AI007349 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI STERN, LAWRENCE J. · 1989 to 2024
$4.5M
Programmed necrosis in Immune ResponsesR01AI083497 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CHAN, FRANCIS KAMING · 2010 to 2013
$1.6M
Regulation of necrotic cell death by protein kinase A and cylindromatosisR21AI088502 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CHAN, FRANCIS KAMING · 2010 to 2011
$450k
NIAID NIH HHS R01 AI083497NIAID NIH HHS R21 AI088502NIAID NIH HHS T32 AI007349NIAID NIH HHS T32 AI07349NIDDK NIH HHS DK32520
6 · The paper itself

Abstract

Proper regulation of cell death is essential for metazoan development and functions. Unlike apoptosis, necrosis is a more inflammatory form of cell death that might contribute to antiviral immunity. Indeed, necrotic cell injury is distinguished from apoptosis by extensive organelle and cell swelling and plasma membrane rupture. Recent evidence indicates that an elaborate biochemical network emanating from receptors in the TNF superfamily can induce apoptosis as well as necrotic cell death. The induction of necrosis by TNF-like cytokines requires biochemical components that are distinct from those involved in apoptosis. Specifically, serine/threonine protein kinases in the receptor interacting protein (RIP) family are required for "programmed" necrotic cell injury. In this review, we discuss the molecular crosstalk between apoptosis and programmed necrosis, with a special emphasis on how caspases, protein ubiquitylation and phosphorylation regulate the induction of necrotic cell injury.

Indexed as

NecrosisAnimalsApoptosisCaspasesHumansPhosphorylationReceptor-Interacting Protein Serine-Threonine KinasesUbiquitinationCaspasesReceptor-Interacting Protein Serine-Threonine Kinases

Identifiers

PMID20346680
PMCPMC2904865
OpenAlexW2066518793

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.