Evidence map›Paper›PMID 29880855›Full record

ArticleNature communications2018

Modular ssDNA binding and inhibition of telomerase activity by designer PPR proteins.

Henrik Spåhr, Tiongsun Chia, James P Lingford, Stefan J Siira, Scott B Cohen, Aleksandra Filipovska, Oliver Rackham

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Structures of pentatricopeptide repeat proteins.Acta crystallographica. Section F, Structural biology communications · 2026
    Review
  2. Review
  3. Decoding mJournal of translational medicine · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Plant organellar RNA maturation.The Plant cell · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Manipulating and elucidating mitochondrial gene expression with engineered proteins.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Review
  18. Review
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 3 institutions in 2 countries.

Henrik SpåhrDepartment of Mitochondrial Biology, Max Planck Institute for Biology of Ageing, D-50931, Cologne, Germany.
Tiongsun ChiaHarry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, 6009, Australia.ORCID http://orcid.org/0000-0002-7328-6615
James P LingfordHarry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, 6009, Australia.ORCID http://orcid.org/0000-0003-1980-3949
Stefan J SiiraHarry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, 6009, Australia.
Scott B CohenChildren's Medical Research Institute, University of Sydney, 214 Hawkesbury Road, Westmead, NSW, 2145, Australia.
Aleksandra FilipovskaHarry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, 6009, Australia.
Oliver RackhamHarry Perkins Institute of Medical Research and Centre for Medical Research, The University of Western Australia, Nedlands, WA, 6009, Australia. oliver.rackham@uwa.edu.au.ORCID http://orcid.org/0000-0002-5301-9624
The University of Western Australia · AUMax Planck Institute for Biology of Ageing · DEThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA is typically found as a double helix, however it must be separated into single strands during all phases of DNA metabolism; including transcription, replication, recombination and repair. Although recent breakthroughs have enabled the design of modular RNA- and double-stranded DNA-binding proteins, there are currently no tools available to manipulate single-stranded DNA (ssDNA). Here we show that artificial pentatricopeptide repeat (PPR) proteins can be programmed for sequence-specific ssDNA binding. Interactions occur using the same code and specificity as for RNA binding. We solve the structures of DNA-bound and apo proteins revealing the basis for ssDNA binding and how hydrogen bond rearrangements enable the PPR structure to envelope its ssDNA target. Finally, we show that engineered PPRs can be designed to bind telomeric ssDNA and can block telomerase activity. The modular mode of ssDNA binding by PPR proteins provides tools to target ssDNA and to understand its importance in cells.

Indexed as

Amino Acid MotifsBinding SitesCrystallography, X-RayDNA-Binding ProteinsDNA ReplicationDNA, Single-StrandedEnzyme AssaysHEK293 CellsHumansModels, MolecularProtein BindingProtein EngineeringRecombinant ProteinsTelomeraseTelomereDNA-Binding ProteinsDNA, Single-StrandedRecombinant ProteinsTelomerase

Identifiers

PMID29880855
PMCPMC5992170
OpenAlexW2805446998

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.