Evidence map›Paper›PMID 17954560›Full record

ArticleMolecular and cellular biology2008

Mechanism of R-loop formation at immunoglobulin class switch sequences.

Deepankar Roy, Kefei Yu, Michael R Lieber

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

100 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. R-loops: a key driver of inflammatory responses in cancer.Experimental & molecular medicine · 2025
    Review
  6. Article
  7. Gene regulation inCurrent research in parasitology & vector-borne diseases · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

40 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.

Deepankar RoyUSC Norris Comprehensive Cancer Ctr., Rm. 5428, 1441 Eastlake Ave., MC9176, Los Angeles, CA 90089-9176, USA.
Kefei Yu
Michael R Lieber

Funding

Mechanism of R-loop Formation in CSR and SHMR01GM056984 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LIEBER, MICHAEL R · 1998 to 2015
$2.7M
NIGMS NIH HHS R01 GM056984
6 · The paper itself

Abstract

R-loops have been described in vivo at the immunoglobulin class switch sequences and at prokaryotic and mitochondrial origins of replication. However, the biochemical mechanism and determinants of R-loop formation are unclear. We find that R-loop formation is nearly eliminated when RNase T(1) is added during transcription but not when it is added afterward. Hence, rather than forming simply as an extension of the RNA-DNA hybrid of normal transcription, the RNA must exit the RNA polymerase and compete with the nontemplate DNA strand for an R-loop to form. R-loops persist even when transcription is done in Li(+) or Cs(+), which do not support G-quartet formation. Hence, R-loop formation does not rely on G-quartet formation. R-loop formation efficiency decreases as the number of switch repeats is decreased, although a very low level of R-loop formation occurs at even one 49-bp switch repeat. R-loop formation decreases sharply as G clustering is reduced, even when G density is kept constant. The critical level for R-loop formation is approximately the same point to which evolution drove the G clustering and G density on the nontemplate strand of mammalian switch regions. This provides an independent basis for concluding that the primary function of G clustering, in the context of high G density, is R-loop formation.

Indexed as

AnimalsBase SequenceImmunoglobulinsImmunoglobulin Switch RegionMiceRibonuclease T1ImmunoglobulinsRibonuclease T1

Identifiers

PMID17954560
PMCPMC2223306

What OpenQuestion holds

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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.