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Replication stress induces specific enrichment of RECQ1 at common fragile sites FRA3B and FRA16D

Overview of attention for article published in Molecular Cancer, April 2013
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Title
Replication stress induces specific enrichment of RECQ1 at common fragile sites FRA3B and FRA16D
Published in
Molecular Cancer, April 2013
DOI 10.1186/1476-4598-12-29
Pubmed ID
Authors

Xing Lu, Swetha Parvathaneni, Toshifumi Hara, Ashish Lal, Sudha Sharma

Abstract

Stalled replication forks at common fragile sites are a major cause of genomic instability. RecQ helicases, a highly conserved family of DNA-unwinding enzymes, are believed to ease 'roadblocks' that pose challenge to replication fork progression. Among the five known RecQ homologs in humans, functions of RECQ1, the most abundant of all, are poorly understood. We previously determined that RECQ1 helicase preferentially binds and unwinds substrates that mimic DNA replication/repair intermediates, and interacts with proteins involved in DNA replication restart mechanisms.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 44 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 44 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 12 27%
Researcher 8 18%
Professor > Associate Professor 5 11%
Student > Bachelor 3 7%
Student > Master 3 7%
Other 6 14%
Unknown 7 16%
Readers by discipline Count As %
Agricultural and Biological Sciences 19 43%
Biochemistry, Genetics and Molecular Biology 11 25%
Medicine and Dentistry 4 9%
Pharmacology, Toxicology and Pharmaceutical Science 1 2%
Chemistry 1 2%
Other 0 0%
Unknown 8 18%