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Role of the telomeric DNA‐binding protein TRF2 in the stability of human chromosome ends
Author(s) -
Ancelin Katia,
Brun Christine,
Gilson Eric
Publication year - 1998
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/(sici)1521-1878(199811)20:11<879::aid-bies2>3.0.co;2-i
Subject(s) - telomere , biology , dna , chromosome , telomere binding protein , genetics , chromosome segregation , cell division , microbiology and biotechnology , chromosome instability , dna binding protein , cell , gene , transcription factor
A major issue in telomere research is to understand how the integrity of chromosome ends is preserved. A recent study shows that expression of a dominant‐negative form of the human telomeric protein TRF2 increases the number of chromosome fusions in immortalized cells and decreases the quantity of G‐rich telomeric DNA 3' overhang, the G tail. (1) Consequently, TRF2 appears to control the structure of the very end of the chromosomal DNA molecule and to prevent recombination between two telomeres. Remarkably, the same study reveals a potential role of TRF2 in cell division control. BioEssays 20:879–883, 1998. © 1998 John Wiley & Sons, Inc.