Evidence map›Paper›PMID 17229557›Full record

ReviewBiochimica et biophysica acta2007

Cell cycle molecules define a pathway required for neuron death in development and disease.

Lloyd A Greene, David X Liu, Carol M Troy, Subhas C Biswas

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Cyclin-dependent kinases: Masters of the eukaryotic universe.Wiley interdisciplinary reviews. RNA · 2023
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Cell Cycle Proteins as Key Regulators of Postmitotic Cell Death.The Yale journal of biology and medicine · 2019
    Review
  15. Primary neurons can enter M-phase.Scientific reports · 2019
    Article
  16. Review
  17. Article
  18. Article
  19. LncRNAs in genetic basis of glaucoma.BMJ open ophthalmology · 2018
    Review
  20. Reduced Expression of Foxp1 as a Contributing Factor in Huntington's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article

9 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Lloyd A GreeneDepartment of Pathology and Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, 630 W. 168th Street, New York, NY 10032, USA. Lag3@columbia.edu
David X Liu
Carol M Troy
Subhas C Biswas
Columbia University · US

Funding

TRANSLATIONAL APPROACHES TO NEUROPROTECTION OF AXONS IN PDrP50NS038370 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BURKE, ROBERT E · 1999 to 2014
$24.0M
NEUROTROPHIC FACTOR DEPRIVATION AND NEURONAL CELL DEATHR01NS033689 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GREENE, LLOYD A · 1995 to 2017
$8.9M
Downstream Regulators of Beta-Amyloid Induced Neuronal DeathR01NS043089 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TROY, CAROL M · 2001 to 2010
$2.2M
NINDS NIH HHS P50 NS038370NINDS NIH HHS R01 NS033689NINDS NIH HHS R01 NS043089
6 · The paper itself

Abstract

We review here evidence defining a molecular pathway that includes cell cycle-related molecules and that appears to play a required role in neuron death during normal development as well as in disease and trauma. The pathway starts with inappropriate activation of cyclin dependent kinase 4 (Cdk4) in neurons which leads to hyper-phosphorylation of the pRb family member p130. This in turn results in dissociation of p130 and its associated chromatin modifiers Suv39H1 and HDAC1 from the transcription factor E2F4. Dissociation of this complex results in de-repression of genes with E2F binding sites including those encoding the transcription factors B- and C-Myb. Once elevated in neurons, B- and C-Myb proteins bind to the promoter for the pro-apoptotic BH3-only protein Bim and promote its induction. Bim then interacts with the core cellular apoptotic machinery, leading to caspase activation and apoptotic death. This pathway is supported by a variety of observations and experimental findings that implicate it as a required element for neuron loss in development and in many nervous system traumas and disorders. The components of this pathway appear to represent potential therapeutic targets for prevention of disease-associated neuron death.

Indexed as

PathologyAnimalsApoptosisCell CycleCell DeathCell SurvivalDeathHumansModels, BiologicalNeuronsWounds and Injuries

Identifiers

PMID17229557
PMCPMC1885990
OpenAlexW2131141529

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.