Verification of somatic CAG repeat expansion by pre-PCR fractionation

[1]  L. Ingram,et al.  Pms2 is a genetic enhancer of trinucleotide CAG.CTG repeat somatic mosaicism: implications for the mechanism of triplet repeat expansion. , 2004, Human molecular genetics.

[2]  Elizabeth Evans,et al.  Dramatic tissue-specific mutation length increases are an early molecular event in Huntington disease pathogenesis. , 2003, Human molecular genetics.

[3]  Alessandro Filla,et al.  DNA damage induced by polyglutamine-expanded proteins. , 2003, Human molecular genetics.

[4]  C. McMurray,et al.  Nuclease-Deficient FEN-1 Blocks Rad51/BRCA1-Mediated Repair and Causes Trinucleotide Repeat Instability , 2003, Molecular and Cellular Biology.

[5]  M. MacDonald,et al.  Mismatch repair gene Msh2 modifies the timing of early disease in Hdh(Q111) striatum. , 2003, Human molecular genetics.

[6]  O. Andreassen,et al.  Increased oxidative damage to DNA in a transgenic mouse model of Huntington's disease , 2001, Journal of neurochemistry.

[7]  I. Kanazawa,et al.  Age‐dependent and tissue‐specific CAG repeat instability occurs in mouse knock‐in for a mutant Huntington's disease gene , 2001, Journal of neuroscience research.

[8]  W. Strauss Preparation of genomic DNA from mammalian tissue. , 2001, Current protocols in neuroscience.

[9]  R. Albin,et al.  Neurological abnormalities in a knock-in mouse model of Huntington's disease. , 2001, Human molecular genetics.

[10]  P. Shelbourne,et al.  Dramatic mutation instability in HD mouse striatum: does polyglutamine load contribute to cell-specific vulnerability in Huntington's disease? , 2000, Human molecular genetics.

[11]  C. McMurray,et al.  DNA secondary structure: a common and causative factor for expansion in human disease. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[12]  T. Petes,et al.  Triplet repeats form secondary structures that escape DNA repair in yeast. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[13]  M. Dragunow,et al.  Trinucleotide (CAG) repeat length is positively correlated with the degree of DNA fragmentation in Huntington's disease striatum , 1998, Neuroscience.

[14]  W. Strauss Preparation of Genomic DNA from Mammalian Tissue , 1998, Current protocols in molecular biology.

[15]  C. Caskey,et al.  Hypermutable myotonic dystrophy CTG repeats in transgenic mice , 1997, Nature Genetics.

[16]  C. Junien,et al.  Moderate intergenerational and somatic instability of a 55-CTG repeat in transgenic mice , 1997, Nature Genetics.

[17]  R. Mott,et al.  Instability of highly expanded CAG repeats in mice transgenic for the Huntington's disease mutation , 1997, Nature Genetics.

[18]  P. Detloff,et al.  In vitro synthesis and cloning of long CAG repeats. , 1996, BioTechniques.

[19]  D. Steindler,et al.  DNA End Labeling (TUNEL) in Huntington's Disease and Other Neuropathological Conditions , 1995, Experimental Neurology.

[20]  M. Dragunow,et al.  In situ evidence for DNA fragmentation in Huntington's disease striatum and Alzheimer's disease temporal lobes , 1995, Neuroreport.

[21]  C. Portera-Cailliau,et al.  Evidence for apoptotic cell death in Huntington disease and excitotoxic animal models , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[22]  G. Mutter,et al.  PCR bias in amplification of androgen receptor alleles, a trinucleotide repeat marker used in clonality studies. , 1995, Nucleic acids research.

[23]  R. Roos,et al.  Somatic expansion of the (CAG)n repeat in Huntington disease brains , 1995, Human Genetics.

[24]  M. MacDonald,et al.  Huntington's disease. , 1995, Neuromolecular medicine.

[25]  M. Hayden,et al.  Somatic and gonadal mosaicism of the Huntington disease gene CAG repeat in brain and sperm , 1994, Nature Genetics.

[26]  M. MacDonald,et al.  Gametic but not somatic instability of CAG repeat length in Huntington's disease. , 1993, Journal of medical genetics.

[27]  Manish S. Shah,et al.  A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes , 1993, Cell.

[28]  Victoria Wilson,et al.  Repeat unit sequence variation in minisatellites: A novel source of DNA polymorphism for studying variation and mutation by single molecule analysis , 1990, Cell.

[29]  P. Stączek,et al.  Molecular mechanisms of TRS instability. , 2002, Advances in experimental medicine and biology.

[30]  Jacqueline K. White,et al.  Length-dependent gametic CAG repeat instability in the Huntington's disease knock-in mouse. , 1999, Human molecular genetics.

[31]  A. Jeffreys,et al.  Somatic mutation processes at a human minisatellite. , 1997, Human molecular genetics.

[32]  T. Ashizawa,et al.  Somatic mosaicism, germline expansions, germline reversions and intergenerational reductions in myotonic dystrophy males: small pool PCR analyses. , 1995, Human molecular genetics.