Evidence map›Paper›PMID 11016956›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Misregulation of gene expression in primary fibroblasts lacking poly(ADP-ribose) polymerase.

C M Simbulan-Rosenthal, D H Ly, D S Rosenthal, G Konopka, R Luo, Z Q Wang, P G Schultz, M E Smulson

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 126 citations in OpenAlex.

  1. Article
  2. PARP-1-Associated Pathological Processes: Inhibition by Natural Polyphenols.International journal of molecular sciences · 2021
    Review
  3. Review
  4. PARP1 in Carcinomas and PARP1 Inhibitors as Antineoplastic Drugs.International journal of molecular sciences · 2017
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. PARP inhibition: PARP1 and beyond.Nature reviews. Cancer · 2010
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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 at 3 institutions in 2 countries.

C M Simbulan-RosenthalDepartment of Biochemistry and Molecular Biology, Georgetown University School of Medicine, 3900 Reservoir Road NW, Washington, DC 20007, USA.
D H Ly
D S Rosenthal
G Konopka
R Luo
Z Q Wang
P G Schultz
M E Smulson
Centre International de Recherche sur le Cancer · FRGeorgetown University · USScripps Research Institute · US

Funding

THYMIDINE KINASE AND BRAIN TUMOR RADIATION RESISTANCEP01CA074175 · NCI · GEORGETOWN UNIVERSITY · PI DRITSCHILO, ANATOLY · 1997 to 2006
$13.2M
CARCINOGENS AND CHROMATIN STRUCTURE AND FUNCTIONR01CA025344 · NCI · GEORGETOWN UNIVERSITY · PI SMULSON, MARK E · 1985 to 2002
$727k
NCI NIH HHS 1P01 CA74175NCI NIH HHS CA25344NCI NIH HHS P01 CA074175
6 · The paper itself

Abstract

Poly(ADP-ribose) polymerase (PARP) is implicated in the maintenance of genomic integrity, given that inhibition or depletion of this enzyme increases genomic instability in cells exposed to genotoxic agents. We previously showed that immortalized fibroblasts derived from PARP(-/-) mice exhibit an unstable tetraploid population, and partial chromosomal gains and losses in PARP(-/-) mice and immortalized fibroblasts are accompanied by changes in the expression of p53, Rb, and c-Jun, as well as other proteins. A tetraploid population has also now been detected in primary fibroblasts derived from PARP(-/-) mice. Oligonucleotide microarray analysis was applied to characterize more comprehensively the differences in gene expression between asynchronously dividing primary fibroblasts derived from PARP(-/-) mice and their wild-type littermates. Of the 11,000 genes monitored, 91 differentially expressed genes were identified. The loss of PARP results in down-regulation of the expression of several genes involved in regulation of cell cycle progression or mitosis, DNA replication, or chromosomal processing or assembly. PARP deficiency also up-regulates genes that encode extracellular matrix or cytoskeletal proteins that are implicated in cancer initiation or progression or in normal or premature aging. These results provide insight into the mechanism by which PARP deficiency impairs mitotic function, thereby resulting in the genomic alterations and chromosomal abnormalities as well as in altered expression of genes that may contribute to genomic instability, cancer, and aging.

Indexed as

AnimalsCellular SenescenceDNA RepairDNA ReplicationFemaleFibroblastsGene Expression RegulationMiceMice, Inbred C57BLMice, KnockoutNeoplasms, ExperimentalPoly(ADP-ribose) PolymerasesPoly(ADP-ribose) Polymerases

Identifiers

PMID11016956
PMCPMC17190
OpenAlexW2022781542

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.