Evidence map›Paper›PMID 25611386›Full record

ArticleCell death & disease2015

The BH3-only protein Bad is dispensable for TNF-mediated cell death.

E Ottina, M Sochalska, R Sgonc, A Villunger

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Necroptosis: A new way of dying?Cancer biology & therapy · 2016
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

E OttinaDivision of Developmental Immunology, Biocenter, Medical University Innsbruck, Innsbruck, Austria.
M SochalskaDivision of Developmental Immunology, Biocenter, Medical University Innsbruck, Innsbruck, Austria.
R SgoncDivision of Experimental Pathophysiology and Immunology, Biocenter, Medical University Innsbruck, Innsbruck, Austria.
A VillungerDivision of Developmental Immunology, Biocenter, Medical University Innsbruck, Innsbruck, Austria.
Innsbruck Medical University · AT

Funding

Austrian Science Fund FWF W 1101
6 · The paper itself

Abstract

Tumor necrosis factor (TNF) is a key signaling molecule orchestrating immune and inflammatory responses and possesses the capacity to trigger apoptotic as well as necroptotic cell death. Apoptotic cell death elicited by TNF has been demonstrated to engage pro-apoptotic Bcl-2 family proteins, most prominently the BH3-only protein Bid, a key substrate of caspase-8, the key effector protease downstream of TNF receptor I. Most recently, the BH3 domain-containing protein Bad (Bcl-2-antagonist of cell death) has been shown to be rate limiting for TNF-mediated cell death, suggesting possible synergy with Bid, but genetic analyses presented here demonstrate that it is dispensable for this process.

Indexed as

Animalsbcl-Associated Death ProteinCell DeathEmbryo, MammalianFibroblastsHepatitisHeterocyclic Compounds, 3-RingHumansI-kappa B KinaseMice, Inbred C57BLPyridinesThymocytesTumor Necrosis Factor-alphabcl-Associated Death ProteinHeterocyclic Compounds, 3-RingI-kappa B KinasePS1145PyridinesTumor Necrosis Factor-alpha

Identifiers

PMID25611386
PMCPMC4669773
OpenAlexW2039341019

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.