Evidence map›Paper›PMID 16093393›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

PolyADP-ribosylation is involved in neurotrophic activity.

Leonid Visochek, Ruth A Steingart, Ina Vulih-Shultzman, Rodica Klein, Esther Priel, Illana Gozes, Malka Cohen-Armon

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Role of NADCellular and molecular neurobiology · 2023
    Review
  5. PARP1 and OGG1 in Medicated Patients With Depression and the Response to ECT.The international journal of neuropsychopharmacology · 2023
    Article
  6. Review
  7. Review
  8. The role of poly(ADP-ribose) polymerases in manganese exposed Caenorhabditis elegans.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2020
    Article
  9. Review
  10. Neuronal Cell Death.Physiological reviews · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Comprehensive Catalog of Currently Documented Histone Modifications.Cold Spring Harbor perspectives in biology · 2015
    Review
  16. Article
  17. Association of poly(ADP-ribose) polymerase-1 polymorphism with Tourette syndrome.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2013
    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

7 authors at 2 institutions in 1 country.

Leonid VisochekThe Neufeld Cardiac Research Institute, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv 69978, Israel.
Ruth A Steingart
Ina Vulih-Shultzman
Rodica Klein
Esther Priel
Illana Gozes
Malka Cohen-Armon
Tel Aviv University · ILBen-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PolyADP-ribosylation is a transient posttranslational modification of proteins, mainly catalyzed by poly(ADP-ribose)polymerase-1 (PARP-1). This highly conserved nuclear protein is activated rapidly in response to DNA nick formation and promotes a fast DNA repair. Here, we examine a possible association between polyADP-ribosylation and the activity of neurotrophins and neuroprotective peptides taking part in life-or-death decisions in mammalian neurons. The presented results indicate an alternative mode of PARP-1 activation in the absence of DNA damage by neurotrophin-induced signaling mechanisms. PARP-1 was activated in rat cerebral cortical neurons briefly exposed to NGF-related nerve growth factors and to the neuroprotective peptides NAP (the peptide NAPVSIPQ, derived from the activity-dependent neuroprotective protein ADNP) and ADNF-9 (the peptide SALLRSIPA, derived from the activity-dependent neurotrophic factor ADNF) In addition, polyADP-ribosylation was involved in the neurotrophic activity of NGF-induced and NAP-induced neurite outgrowth in differentiating pheochromocytoma 12 cells as well as in the neuroprotective activity of NAP in neurons treated with the Alzheimer's disease neurotoxin beta-amyloid. A fast loosening of the highly condensed chromatin structure by polyADP-ribosylation of histone H1, which renders DNA accessible to transcription and repair, may underlie the role of polyADP-ribosylation in neurotrophic activity.

Indexed as

Amyloid beta-PeptidesAnimalsCells, CulturedCerebral CortexEnzyme ActivationHistonesNerve Growth FactorsNeuritesNeuronsNeuroprotective AgentsOligopeptidesPC12 CellsPoly Adenosine Diphosphate RibosePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesRatsactivity-dependent neurotrophic factorAmyloid beta-PeptidesdavunetideHistonesNerve Growth FactorsNeuroprotective AgentsOligopeptidesParp1 protein, ratPoly Adenosine Diphosphate RibosePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerases

Identifiers

PMID16093393
PMCPMC6725295
OpenAlexW2029253143

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.