Evidence map›Paper›PMID 20536557›Full record

ReviewImmunological reviews2010

Granzyme A activates another way to die.

Judy Lieberman

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

137 citing papers in PubMed, 234 citations in OpenAlex.

  1. Effects of gender on gene expression in the blood of ischemic stroke patients.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012
    Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Development of Granzyme A Turn-ON Fluorescent Activity-Based Probes.Chembiochem : a European journal of chemical biology · 2025
    Article
  11. FOXP3+ T Cells-An Emerging Evidence in Periodontitis Therapeutics.Clinical and experimental dental research · 2025
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Cytotoxic T Cells: Kill, Memorize, and Mask to Maintain Immune Homeostasis.International journal of molecular sciences · 2025
    Review
  18. Article
  19. NK-derived exosomes in anti-tumor strategies.Medical oncology (Northwood, London, England) · 2025
    Review
  20. Review

77 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

1 author at 1 institution in 1 country.

Judy LiebermanImmune Disease Institute and Program in Cellular and Molecular Medicine, Children's Hospital Boston, Harvard Medical School, Boston, MA, USA. lieberman@idi.harvard.edu
Boston Children's Hospital · US

Funding

Granzyme a Pathway of CTL-Mediated Cell DeathR01AI045587 · NIAID · IMMUNE DISEASE INSTITUTE, INC. · PI LIEBERMAN, JUDY · 1999 to 2008
$4.4M
Mechanism of perforin activityR01AI063430 · NIAID · IMMUNE DISEASE INSTITUTE, INC. · PI LIEBERMAN, JUDY · 2006 to 2010
$3.1M
Granzyme A Pathway of CTL-Mediated Cell DeathR56AI045587 · NIAID · IMMUNE DISEASE INSTITUTE, INC. · PI LIEBERMAN, JUDY · 2010 to 2010
$525k
NIAID NIH HHS AI045587NIAID NIH HHS AI063430NIAID NIH HHS R01 AI045587NIAID NIH HHS R01 AI063430NIAID NIH HHS R56 AI045587
6 · The paper itself

Abstract

Granzyme A (GzmA) is the most abundant serine protease in killer cell cytotoxic granules. GzmA activates a novel programed cell death pathway that begins in the mitochondrion, where cleavage of NDUFS3 in electron transport complex I disrupts mitochondrial metabolism and generates reactive oxygen species (ROS). ROS drives the endoplasmic reticulum-associated SET complex into the nucleus, where it activates single-stranded DNA damage. GzmA also targets other important nuclear proteins for degradation, including histones, the lamins that maintain the nuclear envelope, and several key DNA damage repair proteins (Ku70, PARP-1). Cells that are resistant to the caspases or GzmB by overexpressing bcl-2 family anti-apoptotic proteins or caspase or GzmB protease inhibitors are sensitive to GzmA. By activating multiple cell death pathways, killer cells provide better protection against a variety of intracellular pathogens and tumors. GzmA also has proinflammatory activity; it activates pro-interleukin-1beta and may also have other proinflammatory effects that remain to be elucidated.

Indexed as

Cytotoxicity, ImmunologicAnimalsCell DeathGranzymesHumansInflammation MediatorsProtein ConformationSecretory VesiclesSerine Proteinase InhibitorsSignal TransductionStructure-Activity RelationshipT-Lymphocytes, CytotoxicGranzymesInflammation MediatorsSerine Proteinase Inhibitors

Identifiers

PMID20536557
PMCPMC2905780
OpenAlexW2136245934

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.