Structure-specific endonucleases

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Structure-specific endonucleases: guardians of fragile site stability

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Structure-specific endonucleases : guardians of fragile site stability. / Minocherhomji, Sheroy; Hickson, Ian D.

In: Trends in Cell Biology, Vol. 24, No. 5, 05.2014, p. 321-327.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Minocherhomji, S & Hickson, ID 2014, 'Structure-specific endonucleases: guardians of fragile site stability', Trends in Cell Biology, vol. 24, no. 5, pp. 321-327. https://doi.org/10.1016/j.tcb.2013.11.007

APA

Minocherhomji, S., & Hickson, I. D. (2014). Structure-specific endonucleases: guardians of fragile site stability. Trends in Cell Biology, 24(5), 321-327. https://doi.org/10.1016/j.tcb.2013.11.007

Vancouver

Minocherhomji S, Hickson ID. Structure-specific endonucleases: guardians of fragile site stability. Trends in Cell Biology. 2014 May;24(5):321-327. https://doi.org/10.1016/j.tcb.2013.11.007

Author

Minocherhomji, Sheroy ; Hickson, Ian D. / Structure-specific endonucleases : guardians of fragile site stability. In: Trends in Cell Biology. 2014 ; Vol. 24, No. 5. pp. 321-327.

Bibtex

@article{896a3e5048004c73a38e094ca9d05e21,

title = "Structure-specific endonucleases: guardians of fragile site stability",

abstract = "Fragile sites are conserved loci predisposed to form breaks in metaphase chromosomes. The inherent instability of these loci is associated with chromosomal rearrangements in cancers and is a feature of cells from patients with chromosomal instability syndromes. One class of fragile sites, the common fragile sites (CFSs), have previously been shown to recruit several DNA repair proteins after the completion of bulk DNA synthesis in the cell, probably indicative of their inability to complete timely DNA replication. CFS loci are also prone to trigger mitotic non-disjunction of sister chromatids, leading to the formation of ultra-fine anaphase bridges (UFBs) and micronuclei. We discuss recent developments in the CFS field; in particular, the role of DNA structure-specific endonucleases in promoting cleavage at CFSs.",

author = "Sheroy Minocherhomji and Hickson, {Ian D}",

year = "2014",

month = may,

doi = "10.1016/j.tcb.2013.11.007",

language = "English",

volume = "24",

pages = "321--327",

journal = "Trends in Cell Biology",

issn = "0962-8924",

publisher = "Elsevier Ltd. * Trends Journals",

number = "5",

}

RIS

TY - JOUR

T1 - Structure-specific endonucleases

T2 - guardians of fragile site stability

AU - Minocherhomji, Sheroy

AU - Hickson, Ian D

PY - 2014/5

Y1 - 2014/5

N2 - Fragile sites are conserved loci predisposed to form breaks in metaphase chromosomes. The inherent instability of these loci is associated with chromosomal rearrangements in cancers and is a feature of cells from patients with chromosomal instability syndromes. One class of fragile sites, the common fragile sites (CFSs), have previously been shown to recruit several DNA repair proteins after the completion of bulk DNA synthesis in the cell, probably indicative of their inability to complete timely DNA replication. CFS loci are also prone to trigger mitotic non-disjunction of sister chromatids, leading to the formation of ultra-fine anaphase bridges (UFBs) and micronuclei. We discuss recent developments in the CFS field; in particular, the role of DNA structure-specific endonucleases in promoting cleavage at CFSs.

AB - Fragile sites are conserved loci predisposed to form breaks in metaphase chromosomes. The inherent instability of these loci is associated with chromosomal rearrangements in cancers and is a feature of cells from patients with chromosomal instability syndromes. One class of fragile sites, the common fragile sites (CFSs), have previously been shown to recruit several DNA repair proteins after the completion of bulk DNA synthesis in the cell, probably indicative of their inability to complete timely DNA replication. CFS loci are also prone to trigger mitotic non-disjunction of sister chromatids, leading to the formation of ultra-fine anaphase bridges (UFBs) and micronuclei. We discuss recent developments in the CFS field; in particular, the role of DNA structure-specific endonucleases in promoting cleavage at CFSs.

U2 - 10.1016/j.tcb.2013.11.007

DO - 10.1016/j.tcb.2013.11.007

M3 - Journal article

C2 - 24361091

VL - 24

SP - 321

EP - 327

JO - Trends in Cell Biology

JF - Trends in Cell Biology

SN - 0962-8924

IS - 5

ER -

ID: 108671883