The molecular basis of fragile sites in human chromosomes
References (40)
- et al.
Nature of distamycin A-inducible fragile sites
Cancer Genet Cytogenet
(1988) - et al.
Dynamic mutations: a new class of mutations causing human disease
Cell
(1992) - et al.
Cryptic and polar variation of the fragile X repeat could result in predisposing normal alleles
Cell
(1994) - et al.
Length of uninterrupted CGG repeats determines instability in the FMR1 gene
Nature Genet
(1994) Heritable fragile sites on human chromosomes. I. Factors affecting expression in lymphocyte culture
Am J Hum Genet
(1979)- et al.
Simple tandem DNA repeats and human genetic disease
Proc Natl Acad Sci USA
(1995) - et al.
The fragile site (16)(q22) I. Induction by AT-specific DNA-ligands and population frequency
Hum Genet
(1986) Heritable fragile sites on human chromosomes. IX. Population cytogenetics and segregation analysis of the BrdU requiring fragile site at 10q25
Am J Hum Genet
(1982)- et al.
A new folate sensitive fragile site at 1p21.3
J Med Genet
(1991) - et al.
The fragile X site in somatic cell hybrids: an approach for molecular cloning of fragile sites
Science
(1987)
Chromosome breakage and recombination at fragile sites
Am J Hum Genet
Physical linkage of the fragile site FRA11B and a Jacobsen syndrome chromosome deletion breakpoint in 11q23.3
Hum Mol Genet
Clinical and molecular characterization of patients with distal 11q deletions
Am J Hum Genet
Unusual behaviour of a human autosome having two rare folate sensitive fragile sites
Ann Genet
The detection of fragile sites on human chromosomes
DNA polymerase inhibition by application induces gaps and breaks at common fragile sites in human chromosomes
Hum Genet
New classes of fragile sites induced by 5-azacytidine and BrdU
Hum Genet
Simple repeat DNA is not replicated simply
Nature Genet
Instability of a 550-base pair DNA segment and abnormal methylation in fragile X syndrome
Science
Multicolor FISH mapping of YAC clones in 3p14 and identification of a YAC spanning both FRA3B and the t(3;8) associated with hereditary renal cell carcinoma
Genomics
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2016, Molecular CellInfluence of physiologic folate deficiency on human papillomavirus type 16 (HPV16)-harboring human keratinocytes in vitro and in vivo
2012, Journal of Biological ChemistryCitation Excerpt :Several studies have documented that the locus of integration of HPV16 DNA within the human genome is frequently found within common fragile sites (54–56). Although the majority of rare fragile sites in genomic DNA are induced by folate deficiency (57–60), among the common fragile sites, the one at 3p14.2 (FRA3B) (the most sensitive site on normal human chromosomes, which also contains a spontaneous HPV16 integration site (54)) as well as several other common fragile sites can also develop gaps and breaks when DNA replication is perturbed by “folate stress” (involving depletion of cellular deoxynucleotide pools by either folate deficiency or methotrexate) (54, 60–62). Because there is direct evidence for the coincidence of viral integration sites and fragile sites (54), it is possible that HPV16-low folate-organotypic rafts contained integration of HPV16 DNA into these folate-sensitive or “folate-stressed” fragile sites in genomic DNA.