Evidence map›Paper›PMID 16473937›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Z-DNA-forming sequences generate large-scale deletions in mammalian cells.

Guliang Wang, Laura A Christensen, Karen M Vasquez

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed, 1 pooled it
3.7field-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

125 citing papers in PubMed, 1 synthesis or guideline pooled it, 191 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. MACRO-MOLECULAR CROWDING FAVORS WRITHE IN UNWOUND DNA.bioRxiv : the preprint server for biology · 2026
    Article
  8. Aging alters DNA structure-induced genetic instability in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Article
  10. Review
  11. Formation and biological implications of Z-DNA.Trends in genetics : TIG · 2026
    Review
  12. Review
  13. Characterization of Z-DNA dynamics across the tree of life.bioRxiv : the preprint server for biology · 2025
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

65 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

3 authors at 1 institution in 1 country.

Guliang WangDepartment of Carcinogenesis, University of Texas M. D. Anderson Cancer Center, Science Park-Research Division, 1808 Park Road 1-C, Smithville, TX 78957, USA.
Laura A Christensen
Karen M Vasquez
The University of Texas MD Anderson Cancer Center · US

Funding

Pilot Project ProgramP30ES007784 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI STROM, SARA S. · 1996 to 2011
$16.4M
REPAIR OF GENOME DESTABILIZING DNA STRUCTURESR01CA093729 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Karen M Vasquez · 2002 to 2026
$8.2M
NCI NIH HHS CA93729NCI NIH HHS R01 CA093729NIEHS NIH HHS ES07784NIEHS NIH HHS P30 ES007784
6 · The paper itself

Abstract

Spontaneous chromosomal breakages frequently occur at genomic hot spots in the absence of DNA damage and can result in translocation-related human disease. Chromosomal breakpoints are often mapped near purine-pyrimidine Z-DNA-forming sequences in human tumors. However, it is not known whether Z-DNA plays a role in the generation of these chromosomal breakages. Here, we show that Z-DNA-forming sequences induce high levels of genetic instability in both bacterial and mammalian cells. In mammalian cells, the Z-DNA-forming sequences induce double-strand breaks nearby, resulting in large-scale deletions in 95% of the mutants. These Z-DNA-induced double-strand breaks in mammalian cells are not confined to a specific sequence but rather are dispersed over a 400-bp region, consistent with chromosomal breakpoints in human diseases. This observation is in contrast to the mutations generated in Escherichia coli that are predominantly small deletions within the repeats. We found that the frequency of small deletions is increased by replication in mammalian cell extracts. Surprisingly, the large-scale deletions generated in mammalian cells are, at least in part, replication-independent and are likely initiated by repair processing cleavages surrounding the Z-DNA-forming sequence. These results reveal that mammalian cells process Z-DNA-forming sequences in a strikingly different fashion from that used by bacteria. Our data suggest that Z-DNA-forming sequences may be causative factors for gene translocations found in leukemias and lymphomas and that certain cellular conditions such as active transcription may increase the risk of Z-DNA-related genetic instability.

Indexed as

DNA DamageGenomic InstabilitySequence DeletionAnimalsCell ExtractsChlorocebus aethiopsCOS CellsDNADNA ReplicationDNA, Z-FormEscherichia coliHeLa CellsHumansMutationPlasmidsTranscription, GeneticCell ExtractsDNADNA, Z-Form

Identifiers

PMID16473937
PMCPMC1413824
OpenAlexW2075593502

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.