Evidence map›Paper›PMID 27383048›Full record

ReviewCell death & disease2016

Post-translational modifications as key regulators of TNF-induced necroptosis.

X Liu, F Shi, Y Li, X Yu, S Peng, W Li, X Luo, Y Cao

Abstract readReview
In one paragraph

Review in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
–field-weighted citation impact
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

38 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Orexins in apoptosis: a dual regulatory role.Frontiers in cellular neuroscience · 2024
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors.

X LiuCancer Research Institute, Xiangya School of Medicine, Central South University, Hunan, China.
F ShiCancer Research Institute, Xiangya School of Medicine, Central South University, Hunan, China.
Y LiCancer Research Institute, Xiangya School of Medicine, Central South University, Hunan, China.
X YuCancer Research Institute, Xiangya School of Medicine, Central South University, Hunan, China.
S PengCancer Research Institute, Xiangya School of Medicine, Central South University, Hunan, China.
W LiCancer Research Institute, Xiangya School of Medicine, Central South University, Hunan, China.
X LuoCancer Research Institute, Xiangya School of Medicine, Central South University, Hunan, China.
Y CaoCancer Research Institute, Xiangya School of Medicine, Central South University, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Necroptosis is a novel form of programmed cell death that is independent of caspase activity. Different stimuli can trigger necroptosis. At present, the most informative studies about necroptosis derive from the tumor necrosis factor (TNF)-triggered system. The initiation of TNF-induced necroptosis requires the kinase activity of receptor-interacting protein 1 and 3 (RIP1 and RIP3). Evidence now reveals that the ability of RIP1 and RIP3 to modulate this key cellular event is tightly controlled by post-translational modifications, including ubiquitination, phosphorylation, caspase 8-mediated cleavage and GlcNAcylation. These regulatory events coordinately determine whether a cell will survive or die by apoptosis or necroptosis. In this review, we highlight recent advances in the study of post-translational modifications during TNF-induced necroptosis and discuss how these modifications regulate the complex and delicate control of programmed necrosis.

Indexed as

AnimalsApoptosisCaspase 8HumansNecrosisProtein Processing, Post-TranslationalTumor Necrosis Factor-alphaUbiquitinationCaspase 8Tumor Necrosis Factor-alpha

Identifiers

PMID27383048
PMCPMC4973344

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.