Evidence map›Paper›PMID 16857739›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Nitric oxide inhibits exocytosis of cytolytic granules from lymphokine-activated killer cells.

Marcella Ferlito, Kaikobad Irani, Nauder Faraday, Charles J Lowenstein

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  8. VAMP-1, VAMP-2, and syntaxin-4 regulate ANP release from cardiac myocytes.Journal of molecular and cellular cardiology · 2010
    Article
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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

4 authors at 2 institutions in 1 country.

Marcella FerlitoDepartment of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Kaikobad Irani
Nauder Faraday
Charles J Lowenstein
Johns Hopkins University · USUniversity of Pittsburgh Medical Center · US

Funding

Stat3 in Post-Ischemic Myocardial InflammationP01HL065608 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BECKER, LEWIS C · 2000 to 2011
$22.0M
Genotypic Determinants of Aspirin Response in High Risk FamiliesU01HL072518 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BECKER, LEWIS C · 2002 to 2008
$12.8M
Role of the Granzyme B Pathway in AGAP01HL056091 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BALDWIN, WILLIAM M · 1997 to 2007
$10.9M
Redox-and acetylation-dependent control of vascular toneR01HL070929 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI IRANI, KAIKOBAD J. · 2002 to 2011
$3.3M
Regulation of Vascular InflammationR01HL074061 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI LOWENSTEIN, CHARLES J · 2004 to 2007
$1.3M
REGULATION OF NOS2 IN ISCHEMIC MYOCARDIUMR01HL063706 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI LOWENSTEIN, CHARLES J · 2000 to 2003
$1.3M
Redox-and acetylation-dependent control of vascular toneR56HL070929 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI IRANI, KAIKOBAD J. · 2007 to 2007
$371k
NHLBI NIH HHS HL70929NHLBI NIH HHS HL72518NHLBI NIH HHS P01 HL056091NHLBI NIH HHS P01 HL065608NHLBI NIH HHS P01 HL56091NHLBI NIH HHS P01 HL65608NHLBI NIH HHS R01 HL063706NHLBI NIH HHS R01 HL070929NHLBI NIH HHS R01 HL074061NHLBI NIH HHS R01 HL63706NHLBI NIH HHS R56 HL070929NHLBI NIH HHS U01 HL072518
6 · The paper itself

Abstract

NO inhibits cytotoxic T lymphocyte killing of target cells, although the precise mechanism is unknown. We hypothesized that NO decreases exocytosis of cytotoxic granules from activated lymphocytes. We now show that NO inhibits lymphokine-activated killer cell killing of K562 target cells. Exogenous and endogenous NO decreases the release of granzyme B, granzyme A, and perforin: all contents of cytotoxic granules. NO inhibits the signal transduction cascade initiated by cross-linking of the T cell receptor that leads to granule exocytosis. In particular, we found that NO decreases the expression of Ras, a critical signaling component within the exocytic pathway. Ectopic expression of Ras prevents NO inhibition of exocytosis. Our data suggest that Ras mediates NO inhibition of lymphocyte cytotoxicity and emphasize that alterations in the cellular redox state may regulate the exocytic signaling pathway.

Indexed as

Lymphocyte SubsetsAnimalsCD3 ComplexCytoplasmic GranulesExocytosisHumansK562 CellsKiller Cells, Lymphokine-ActivatedNitric OxideNitric Oxide DonorsNitroso CompoundsOxidation-Reductionras ProteinsSignal Transduction2,2'-(hydroxynitrosohydrazono)bis-ethanamineCD3 ComplexNitric OxideNitric Oxide DonorsNitroso Compoundsras Proteins

Identifiers

PMID16857739
PMCPMC1544231
OpenAlexW1982949024

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.