Evidence map›Paper›PMID 10822366›Full record

ArticleOncogene2000

Caspase-dependent cleavage of the retinoblastoma protein is an early step in neuronal apoptosis.

A L Boutillier, E Trinh, J P Loeffler

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Cell Cycle Proteins as Key Regulators of Postmitotic Cell Death.The Yale journal of biology and medicine · 2019
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Tumor promotion by caspase-resistant retinoblastoma protein.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  12. Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

A L BoutillierUMR 7519 CNRS-21, Strasbourg, France.
E Trinh
J P Loeffler
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rb-deficient embryos (Rb-/-) show abnormal degeneration of neurons and die at mid-gestation, suggesting that RB may protect against apoptosis. Having previously shown that cyclin D1 accumulates during K+-induced apoptosis of granule neurons, we chose to investigate the role of RB under these conditions. We show that RB is cleaved in its C-terminus during the onset of neuronal apoptosis. Caspase 3-like activity increases following K+ deprivation and the time course correlates with RB cleavage and apoptosis. Although the use of a specific caspase 3-like inhibitor (z-DEBD.fmk) delays RB cleavage and reduces DNA fragmentation, data implicate other caspases in these processes. However, K+ deprivation induces a gradual production of the active p20 subunit of caspase 3 (CPP32) that coincides with RB disappearance at the cellular level. Nuclear detection of a transfected HA-tagged caspase cleavage-resistant RB mutant (DEAG/D to DEAA/D) revealed a significant decrease in apoptosis of neurons expressing the RB mutant (less than 5%) relative to the wild type form of RB (40%) during K+ deprivation. Taken together, these data show that caspase-dependent cleavage of RB is an early permissive step of the apoptosis-inducing signaling pathway in neurons. They indicate a major role of RB in neuronal protection.

Indexed as

ApoptosisAmino Acid Chloromethyl KetonesAnimalsCaspase 3Caspase InhibitorsCaspasesCations, MonovalentCerebellumDNA FragmentationMiceNeuronsOligopeptidesPotassiumRecombinant ProteinsRetinoblastoma ProteinAmino Acid Chloromethyl Ketonesbenzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketonebenzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketoneCasp3 protein, mouseCaspase 3Caspase InhibitorsCaspasesCations, MonovalentOligopeptidesPotassiumRecombinant ProteinsRetinoblastoma Protein

Identifiers

PMID10822366
OpenAlexW2077847217

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.