Evidence map›Paper›PMID 18463164›Full record

ArticleMolecular biology of the cell2008

Rad54B targeting to DNA double-strand break repair sites requires complex formation with S100A11.

Ulrike Murzik, Peter Hemmerich, Stefanie Weidtkamp-Peters, Tobias Ulbricht, Wendy Bussen, Julia Hentschel, Ferdinand von Eggeling, Christian Melle

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Article
  8. The Calcium Binding Protein S100A11 and Its Roles in Diseases.Frontiers in cell and developmental biology · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Functions of S100 proteins.Current molecular medicine · 2013
    Review
  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 at 3 institutions in 2 countries.

Ulrike MurzikCore Unit Chip Application (CUCA), Institute of Human Genetics and Anthropology, Medical Faculty, Friedrich-Schiller-University, 07740 Jena, Germany.
Peter Hemmerich
Stefanie Weidtkamp-Peters
Tobias Ulbricht
Wendy Bussen
Julia Hentschel
Ferdinand von Eggeling
Christian Melle
Friedrich Schiller University Jena · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

S100A11 is involved in a variety of intracellular activities such as growth regulation and differentiation. To gain more insight into the physiological role of endogenously expressed S100A11, we used a proteomic approach to detect and identify interacting proteins in vivo. Hereby, we were able to detect a specific interaction between S100A11 and Rad54B, which could be confirmed under in vivo conditions. Rad54B, a DNA-dependent ATPase, is described to be involved in recombinational repair of DNA damage, including DNA double-strand breaks (DSBs). Treatment with bleomycin, which induces DSBs, revealed an increase in the degree of colocalization between S100A11 and Rad54B. Furthermore, S100A11/Rad54B foci are spatially associated with sites of DNA DSB repair. Furthermore, while the expression of p21(WAF1/CIP1) was increased in parallel with DNA damage, its protein level was drastically down-regulated in damaged cells after S100A11 knockdown. Down-regulation of S100A11 by RNA interference also abolished Rad54B targeting to DSBs. Additionally, S100A11 down-regulated HaCaT cells showed a restricted proliferation capacity and an increase of the apoptotic cell fraction. These observations suggest that S100A11 targets Rad54B to sites of DNA DSB repair sites and identify a novel function for S100A11 in p21-based regulation of cell cycle.

Indexed as

DNA Breaks, Double-StrandedDNA RepairGene Expression RegulationApoptosisCell CycleCell ProliferationCyclin-Dependent Kinase Inhibitor p21DNA DamageDNA HelicasesHumansKeratinocytesMicroscopy, ConfocalNuclear ProteinsProteomicsRecombination, GeneticS100 ProteinsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNA HelicasesNuclear ProteinsRAD54B protein, humanS100A11 protein, humanS100 Proteins

Identifiers

PMID18463164
PMCPMC2441681
OpenAlexW2154754979

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.