isopropyl-thiogalactoside and Polycystic-Kidney--Autosomal-Dominant

isopropyl-thiogalactoside has been researched along with Polycystic-Kidney--Autosomal-Dominant* in 1 studies

Other Studies

1 other study(ies) available for isopropyl-thiogalactoside and Polycystic-Kidney--Autosomal-Dominant

Article	Year
Breakpoints of gross deletions coincide with non-B DNA conformations. Proceedings of the National Academy of Sciences of the United States of America, 2004, Sep-28, Volume: 101, Issue:39 Genomic rearrangements are a frequent source of instability, but the mechanisms involved are poorly understood. A 2.5-kbp poly(purine.pyrimidine) sequence from the human PKD1 gene, known to form non-B DNA structures, induced long deletions and other instabilities in plasmids that were mediated by mismatch repair and, in some cases, transcription. The breakpoints occurred at predicted non-B DNA structures. Distance measurements also indicated a significant proximity of alternating purine-pyrimidine and oligo(purine.pyrimidine) tracts to breakpoint junctions in 222 gross deletions and translocations, respectively, involved in human diseases. In 11 deletions analyzed, breakpoints were explicable by non-B DNA structure formation. We conclude that alternative DNA conformations trigger genomic rearrangements through recombination-repair activities. Topics: Base Composition; Base Sequence; Chromosome Breakage; Colony Count, Microbial; DNA; DNA Repair; Escherichia coli; Gene Deletion; Gene Rearrangement; Humans; Isopropyl Thiogalactoside; Molecular Sequence Data; Nucleic Acid Conformation; Plasmids; Polycystic Kidney, Autosomal Dominant; Restriction Mapping; Transcription, Genetic; Transformation, Bacterial; Translocation, Genetic	2004

Article

Year

Breakpoints of gross deletions coincide with non-B DNA conformations.

Proceedings of the National Academy of Sciences of the United States of America, 2004, Sep-28, Volume: 101, Issue:39

Genomic rearrangements are a frequent source of instability, but the mechanisms involved are poorly understood. A 2.5-kbp poly(purine.pyrimidine) sequence from the human PKD1 gene, known to form non-B DNA structures, induced long deletions and other instabilities in plasmids that were mediated by mismatch repair and, in some cases, transcription. The breakpoints occurred at predicted non-B DNA structures. Distance measurements also indicated a significant proximity of alternating purine-pyrimidine and oligo(purine.pyrimidine) tracts to breakpoint junctions in 222 gross deletions and translocations, respectively, involved in human diseases. In 11 deletions analyzed, breakpoints were explicable by non-B DNA structure formation. We conclude that alternative DNA conformations trigger genomic rearrangements through recombination-repair activities.

Topics: Base Composition; Base Sequence; Chromosome Breakage; Colony Count, Microbial; DNA; DNA Repair; Escherichia coli; Gene Deletion; Gene Rearrangement; Humans; Isopropyl Thiogalactoside; Molecular Sequence Data; Nucleic Acid Conformation; Plasmids; Polycystic Kidney, Autosomal Dominant; Restriction Mapping; Transcription, Genetic; Transformation, Bacterial; Translocation, Genetic

2004