Evidence map›Paper›PMID 8887541›Full record

ArticleThe EMBO journal1996

Ras signaling in tumor necrosis factor-induced apoptosis.

J C Trent, D J McConkey, S M Loughlin, M T Harbison, A Fernandez, H N Ananthaswamy

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.6field-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

18 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. TNF ligands and receptors--a matter of life and death.British journal of pharmacology · 2002
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. TNF-induced signaling in apoptosis.Journal of clinical immunology · 1999
    Review
  14. Article
  15. Article
  16. Ceramide inhibits inwardly rectifying K+ currents via a Ras- and Raf-1-dependent pathway in cultured oligodendrocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    Article
  17. Histopathological evaluation of apoptosis in cancer.The American journal of pathology · 1998
    Review
  18. 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

6 authors at 1 institution in 1 country.

J C TrentDepartment of Immunology, The University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.
D J McConkey
S M Loughlin
M T Harbison
A Fernandez
H N Ananthaswamy
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
MECHANISMS OF INDUCTION OF SKIN CANCERS BY UV LIGHTR01CA046523 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI ANANTHASWAMY, HONNAVARA N. · 1988 to 2004
$813k
NCI NIH HHS CA16672NCI NIH HHS CA46523NCI NIH HHS R01-CA-46523
6 · The paper itself

Abstract

Tumor necrosis factor (TNF) exerts cytotoxicity on many types of tumor cells but not on normal cells. The molecular events leading to cell death triggered by TNF are still poorly understood. Our previous studies have shown that enforced expression of an activated H-ras oncogene converted non-tumorigenic, TNF-resistant C3H 10T1/2 fibroblasts into tumorigenic cells that also became very sensitive to TNF-induced apoptosis. This finding suggested that Ras activation may play a role in TNF-induced apoptosis. In this study we investigated whether Ras activation is an obligatory step in TNF-induced apoptosis. Introduction of two different molecular antagonists of Ras, the rap1A tumor suppressor gene or the dominant-negative rasN17 gene, into H-ras-transformed 10TEJ cells inhibited TNF-induced apoptosis. Similar results were obtained with L929 cells, a fibroblast cell line sensitive to TNF-induced apoptosis, which does not have a ras mutation. While Ras is constitutively activated in TNF-sensitive 10TEJ cells, TNF treatment increased Ras-bound GTP in TNF-sensitive L929 cells but not in TNF-resistant 10T1/2 cells. Moreover, RasN17 expression blocked TNF-induced Ras-GTP formation in L929 cells. These results demonstrate that Ras activation is required for TNF-induced apoptosis in mouse fibroblasts.

Indexed as

Signal TransductionAnimalsApoptosisCell LineDNA Restriction EnzymesMiceMice, Inbred C3Hras ProteinsTumor Necrosis Factor-alphaDNA Restriction Enzymesras ProteinsTumor Necrosis Factor-alpha

Identifiers

PMID8887541
PMCPMC452179
OpenAlexW152667517

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.