SHORT COMMUNICATIONAphidicolin-Induced FRA3B Breakpoints Cluster in Two Distinct Regions
References (22)
- et al.
Intragenic matrix attachment and DNA–protein interactions in the human X-linked HPRT gene
Biochem. Biophys. Acta
(1995) - et al.
Chromosomal loop anchorage of the kappa immunoglobulin gene occurs next to the enhancer in a region containing topoisomerase II sites
Cell
(1986) - et al.
Cohabitation of scaffold binding regions with upstream enhancer elements of three developmentally regulated genes ofD
Melanogaster. Cell
(1986) - et al.
Precise localization of aphidicolin-induced breakpoints on the short arm of human chromosome 3
Genomics
(1995) - et al.
A 350 kb cosmid contig in 3p14.2 that crosses the t(3;8) hereditary renal cell carcinoma translocation breakpoint and 17 aphidicolin-induced FRA3B breakpoints
Genomics
(1996) - et al.
Involvement of band 3p14 in t(3;8) hereditary renal carcinoma
Cancer Genet. Cytogenet.
(1984) - et al.
Determination of the specificity of aphidicolin-induced breakage of the human 3p14.2 fragile site
Genomics
(1993) - et al.
Multicolor FISH mapping of YAC clones in 3p14 and identification of a YAC spanning both FRA3B and the t(3;8) associated with renal cell carcinoma
Genomics
(1994) - et al.
Positional cloning of the hereditary renal carcinoma 3;8 translocation breakpoint
Proc. Natl. Acad. Sci. USA
(1993) - et al.
Hereditary renal cell carcinoma associated with a chromosomal translocation
N. Engl. J. Med.
(1979)
Cited by (49)
A Comprehensive Analysis of the Dynamic Response to Aphidicolin-Mediated Replication Stress Uncovers Targets for ATM and ATMIN
2016, Cell ReportsCitation Excerpt :Such regions are particularly difficult to replicate and are susceptible to replication-stress-induced DSBs (Durkin and Glover, 2007). As such, these regions are hotspots for genomic aberrations (Wang et al., 1997). To counteract DNA damage during DNA replication, cells have evolved a network of DNA damage surveillance pathways that maintain genome integrity.
DNA replication stress: Causes, resolution and disease
2014, Experimental Cell ResearchCitation Excerpt :The three most frequently expressed CFSs are FRA3B, FRA16D, and FRA6E [16–18]. Several studies in cell culture models have shown that under conditions that induce replication stress, fragile sites are hotspots for sister chromatid exchange, translocations and deletions [19]. The frequent alterations within these regions in multiple cancers have led to the identification of a number of extremely large genes contained within CFSs.
Collisions between Replication and Transcription Complexes Cause Common Fragile Site Instability at the Longest Human Genes
2011, Molecular CellCitation Excerpt :Thus, it is tempting to speculate that CFS formation may be provoked by collisions of transcribing RNA Pol IIs with replication forks in human cells. Importantly, the centers of breakage in FHIT, WWOX and IMMP2L have been narrowed down to regions including S phase transcribed areas (Helmrich et al., 2007; Krummel et al., 2000; Wang et al., 1997) (Figure 1A). To test whether transcription is involved in CFS instability, we compared CFS break formation and expression levels of the underlying long genes.
Failure of Origin Activation in Response to Fork Stalling Leads to Chromosomal Instability at Fragile Sites
2011, Molecular CellCitation Excerpt :Preferential instability at fragile sites is also found in vitro. These sites are hot spots for sister chromatid exchange, translocations, and deletions in tissue cultured cells grown under replication stress conditions (Glover and Stein, 1987; Glover and Stein, 1988; Wang et al., 1997). CFSs are regions within the normal human chromosomal structure and are thus considered to be present in all individuals (Durkin and Glover, 2007).
Mechanisms of genomic instabilities underlying two common fragile-site-associated Loci, PARK2 and DMD, in germ cell and cancer cell lines
2010, American Journal of Human GeneticsCitation Excerpt :The breakpoint-clustering region in PARK2 in patients with AR-JP coincided with the center of FRA6E, and the breakpoint-clustering region in DMD in patients with DMD/BMD was fully embedded in FRAXC (Figure 2), strongly suggesting that the clustering of the breakpoints is closely related to the mechanisms underlying fragility within the CFSs. Although the mechanisms underlying CFS breakage are still unclear, several factors that may contribute to instability at CFSs have been suggested, including late-replicating regions,13,14,30,31 high-flexibility peaks,32,33 regions rich in nuclear-matrix-attachment regions,32,34,35 and regions located at the interface of G and R bands.36 On the basis of these reports, breakpoint-clustering regions in PARK2 and DMD were analyzed for investigation of the association of these regions with sequence motifs, replication timing, flexibility peaks, nuclear-matrix-attachment regions, and R/G bands.
Low-copy repeats on chromosome 22q11.2 show replication timing switches, DNA flexibility peaks and stress inducible asynchrony, sharing instability features with fragile sites
2010, Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
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