Evidence map›Paper›PMID 10447711›Full record

ArticleImmunology1999

Role of mitogen-activated protein kinases in activation-induced apoptosis of T cells.

L Zhu, X Yu, Y Akatsuka, J A Cooper, C Anasetti

Open access · greenAbstract read
In one paragraph

Article in Immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 54 citations in OpenAlex.

  1. ERK1/2 activation in anti-inflammatory effects and underlying signaling mechanisms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. The role of Raf-1 kinase in diabetic retinopathy.Expert opinion on therapeutic targets · 2011
    Review
  9. Article
  10. Article
  11. Article
  12. Effects of heavy metals on mitogen-activated protein kinase pathways.Environmental health and preventive medicine · 2002
    Article
  13. 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

5 authors at 3 institutions in 2 countries.

L ZhuHuman Immunogenetics Program, Division of Clinical Research, Fred Hutc hinson Cancer Research Center, Seattle, WA 98104, USA.
X Yu
Y Akatsuka
J A Cooper
C Anasetti
Immungenetics (Germany) · DEFred Hutch Cancer Center · USUniversity of Washington · US

Funding

VIRUS-MEDIATED MYELOSUPPRESSIONP01CA018029 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Geoffrey Roger HILL · 1985 to 2026
$128.4M
STUDIES ON MARROW GRAFT RESISTANCEP01CA018221 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI STORB, RAINER F. · 1985 to 2001
$2.7M
Antigen Specific T Cell Tolerance by Anti CD3 AntibodieR21AI040680 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI ANASETTI, CLAUDIO · 2001 to 2001
$365k
ANTIGEN SPECIFIC T CELL TOLERANCE BY ANTI CD3 ANTIBODIESR01AI040680 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI ANASETTI, CLAUDIO · 1998 to 2000
$300k
NCI NIH HHS CA18029NCI NIH HHS CA18221NCI NIH HHS P01 CA018029NIAID NIH HHS AI40680
6 · The paper itself

Abstract

A member of the mitogen-activated protein (MAP) kinase family, Jun N-terminal kinase (JNK), has been implicated in regulating apoptosis in various cell types. We have investigated the requirement for another type of MAP kinase, extracellular signal-regulated protein kinase (ERK) in activation-induced cell death (AICD) of T cells. AICD is the process by which recently activated T cells undergo apoptosis when restimulated through the T-cell antigen receptor. Here we show that both JNK and ERK are activated rapidly upon T-cell receptor (TCR) ligation prior to the onset of AICD. A chemical inhibitor of ERK activation, PD 098059, inhibits ERK activation and apoptosis, while JNK activation is not inhibited. This suggests that JNK activation is not sufficient for apoptosis. TCR cross-linking induces expression of the apoptosis-inducing factor, Fas ligand (FasL), and its expression correlates with ERK activation. In addition, apoptosis induced by direct ligation of the Fas receptor by anti-Fas antibody is not associated with ERK activation and is not inhibited by PD 098059. These data suggest that ERK activation is an early event during T-cell apoptosis induced by antigen-receptor ligation, and is not involved in apoptosis per se but in the expression of FasL. MAP kinase family members may be similarly involved in inducing apoptosis signals in other cell types.

Indexed as

AnimalsApoptosisCD3 ComplexEnzyme InhibitorsFas Ligand Proteinfas ReceptorFlavonoidsHumansJNK Mitogen-Activated Protein KinasesLymphocyte ActivationMAP Kinase Kinase 1Membrane GlycoproteinsMiceMice, Inbred BALB CMice, TransgenicMitogen-Activated Protein Kinase 12-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneCD3 ComplexEnzyme InhibitorsFASLG protein, humanFas Ligand ProteinFasl protein, mousefas ReceptorFlavonoidsJNK Mitogen-Activated Protein KinasesMAP2K1 protein, humanMap2k1 protein, mouseMAP Kinase Kinase 1Membrane GlycoproteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesProtein Serine-Threonine Kinases

Identifiers

PMID10447711
PMCPMC2326808
OpenAlexW2069104445

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.