The Experts below are selected from a list of 300 Experts worldwide ranked by ideXlab platform
Takeshi Ikeuchi - One of the best experts on this subject based on the ideXlab platform.
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A CAG trinucleotide repeat expansion and familial schizophrenia.
Psychiatry research, 2000Co-Authors: Koichi Ohara, Takeshi Ikeuchi, Yasuo Suzuki, Mikihisa Ohtani, Kenshiro Ohara, Shoji TsujiAbstract:Studies which showed anticipation in families with schizophrenia suggested that a trinucleotide repeat expansion mechanism may be involved in the pathogenesis of familial schizophrenia. Furthermore, some studies involving the repeat expansion detection (RED) method showed the median length of CAG repeats to be longer in probands with schizophrenia than that in control subjects. We screened for a possible expanded CAG repeat by means of the direct identification of repeat expansion and Cloning Technique in 23 subjects (affected, 14; unaffected, 9) from six families with schizophrenia which showed anticipation. The polymorphism of a long and unstable CAG/CTG trinucleotide repeat, Dir1, was studied by PCR. No unusual expanded CAG/CTG trinucleotide repeat was detected in the subjects with familial schizophrenia. There was no significant difference between the affected and unaffected subjects in the allele frequency of Dir1. Our results suggest that a CAG expansion is not the mechanism underlying familial schizophrenia.
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a novel long and unstable cag ctg trinucleotide repeat on chromosome 17q
Genomics, 1998Co-Authors: Takeshi Ikeuchi, Kazuhiro Sanpei, Gerard D Schellenberg, Hidenao Sasaki, Hiroki Takano, Geraldine Cancel, Thomas D. Bird, Alexis Brice, Kunio Tashiro, Margaret A PericakvanceAbstract:Abstract Using the direct identification of repeat expansion and Cloning Technique, we cloned a novel long CAG/CTG trinucleotide repeat on chromosome 17. Using radiation hybrid panels, the CAG/CTG repeat was mapped to chromosome 17q. The CAG/CTG repeat is highly polymorphic, with a heterozygosity of 85%, and exhibits a bimodal distribution (allele S, 10–26 repeat units, and allele L, 50–92 repeat units). The CAG/CTG repeat of allele L exhibited intergenerational instabilities, which are more prominent in maternal transmission than in paternal transmission. Analyses of Northern blot and RT-PCR indicate that the repeat is transcribed. Although the size of the CAG/CTG repeat of allele L is within the range of the expanded CAG repeat of disease-causing genes, we did not detect any association of allele L with various neurodegenerative diseases, including frontotemporal dementia and parkinsonism, mapped to 17q21–q23.
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A Novel Long and Unstable CAG/CTG Trinucleotide Repeat on Chromosome 17q ☆
Genomics, 1998Co-Authors: Takeshi Ikeuchi, Kazuhiro Sanpei, Gerard D Schellenberg, Hidenao Sasaki, Hiroki Takano, Geraldine Cancel, Thomas D. Bird, Alexis Brice, Kunio Tashiro, Margaret A. Pericak-vanceAbstract:Abstract Using the direct identification of repeat expansion and Cloning Technique, we cloned a novel long CAG/CTG trinucleotide repeat on chromosome 17. Using radiation hybrid panels, the CAG/CTG repeat was mapped to chromosome 17q. The CAG/CTG repeat is highly polymorphic, with a heterozygosity of 85%, and exhibits a bimodal distribution (allele S, 10–26 repeat units, and allele L, 50–92 repeat units). The CAG/CTG repeat of allele L exhibited intergenerational instabilities, which are more prominent in maternal transmission than in paternal transmission. Analyses of Northern blot and RT-PCR indicate that the repeat is transcribed. Although the size of the CAG/CTG repeat of allele L is within the range of the expanded CAG repeat of disease-causing genes, we did not detect any association of allele L with various neurodegenerative diseases, including frontotemporal dementia and parkinsonism, mapped to 17q21–q23.
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identification of the spinocerebellar ataxia type 2 gene using a direct identification of repeat expansion and Cloning Technique direct
Nature Genetics, 1996Co-Authors: Kazuhiro Sanpei, Hidenao Sasaki, Hiroki Takano, Kunio Tashiro, Shuichi Igarashi, Toshiya Sato, Mutsuo Oyake, Akemi Wakisaka, Y Ishida, Takeshi IkeuchiAbstract:Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant, neurodegenerative disorder that affects the cerebellum and other areas of the central nervous system. We have devised a novel strategy, the direct identification of repeat expansion and Cloning Technique (DIRECT), which allows selective detection of expanded GAG repeats and Cloning of the genes involved. By applying DIRECT, we identified an expanded CAG repeat of the gene for SCA2. CAG repeats of normal alleles range in size from 15 to 24 repeat units, while those of SCA2 chromosomes are expanded to 35 to 59 repeat units. The SCA2 cDNA is predicted to code for 1,313 amino acids — with the CAG repeats coding for a polyglutamine tract. DIRECT is a robust strategy for identification of pathologically expanded trinucleotide repeats and will dramatically accelerate the search for causative genes of neuropsychiatric diseases caused by trinucleotide repeat expansions.
Teruhiko Wakayama - One of the best experts on this subject based on the ideXlab platform.
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successful mouse Cloning of an outbred strain by trichostatin a treatment after somatic nuclear transfer
Journal of Reproduction and Development, 2007Co-Authors: Satoshi Kishigami, Sayaka Wakayama, Kenzo Tokunaga, Nguyen Van Thuan, Takafusa Hikichi, Eiji Mizutani, Hiroshi Ohta, Rinako Suetsugu, Tetsutaro Sata, Teruhiko WakayamaAbstract:Although the somatic Cloning Technique has been used for numerous applications and basic research of reprogramming in various species, extremely low success rates have plagued this Technique for a decade. Further in mice, the "clonable" strains have been limited to mainly hybrid F1 strains such as B6D2F1. Recently, we established a new efficient Cloning Technique using trichostatin A (TSA) which leads to a 2-5 fold increase in success rates for mouse Cloning of B6D2F1 cumulus cells. To further test the validity of this TSA Cloning Technique, we tried to clone the adult ICR mouse, an outbred strain, which has never been directly cloned before. Only when TSA was used did we obtain both male and female cloned mice from cumulus and fibroblast cells of adult ICR mice with 4-5% success rates, which is comparable to 5-7% of B6D2F1. Thus, the TSA treatment is the first Cloning Technique to allow us to successfully clone outbred mice, demonstrating that this Technique not only improves the success rates of Cloning from hybrid strains, but also enables mouse Cloning from normally "unclonable" strains.
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54 SUCCESS OF MOUSE Cloning FROM AN OUTBRED STRAIN BY TRICHOSTATIN A TREATMENT AFTER SOMATIC NUCLEAR TRANSFER
Reproduction Fertility and Development, 2007Co-Authors: Satoshi Kishigami, Sayaka Wakayama, Takafusa Hikichi, Eiji Mizutani, Hiroshi Ohta, Rinako Suetsugu, Hong-thuy Bui, N. Van Thuan, Teruhiko WakayamaAbstract:Although the somatic Cloning Technique has been used for numerous applications and basic research of reprogramming in various species, the extremely low success rates have plagued this Technique for a decade. Further, in mice, the clonable strains have been limited mainly to the hybrid F1 strains such as B6D2F1. Recently, we have reported a new efficient Cloning Technique using trichostatin A (TSA) where reconstructed oocytes are activated by 5 mM strontium with 5 nM TSA for 6 h, followed by 3 h of culture in KSOM medium containing the same concentration of TSA. After the TSA treatment, cloned embryos were cultured in KSOM medium without TSA. This TSA treatment leads to a 2–5-fold increase in success rates for mouse Cloning of B6D2F1 cumulus cells. In this study, to further test the validity of this TSA Cloning Technique, we tried to clone the adult ICR mouse, an outbred strain, which has never been directly cloned before. Only when TSA was used did we obtain both male and female cloned mice from cumulus and fibroblast cells of adult ICR mice with 4–5% success rates, which is comparable to 6–7% of B6D2F1. Thus, the TSA Cloning Technique now allows us to successfully clone outbred mice, demonstrating that this Technique not only improves the success rates of Cloning from the hybrid strains but also enables mouse Cloning from normally unclonable strains. Further, our results provide insight into the mechanism underlying why only limited strains can be cloned using the current standard Cloning Technique.
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significant improvement of mouse Cloning Technique by treatment with trichostatin a after somatic nuclear transfer
Biochemical and Biophysical Research Communications, 2006Co-Authors: Satoshi Kishigami, Sayaka Wakayama, Nguyen Van Thuan, Takafusa Hikichi, Eiji Mizutani, Hiroshi Ohta, Teruhiko WakayamaAbstract:The low success rate of animal Cloning by somatic cell nuclear transfer (SCNT) is believed to be associated with epigenetic errors including abnormal DNA hypermethylation. Recently, we elucidated by using round spermatids that, after nuclear transfer, treatment of zygotes with trichostatin A (TSA), an inhibitor of histone deacetylase, can remarkably reduce abnormal DNA hypermethylation depending on the origins of transferred nuclei and their genomic regions [S. Kishigami, N. Van Thuan, T. Hikichi, H. Ohta, S. Wakayama. E. Mizutani, T. Wakayama, Epigenetic abnormalities of the mouse paternal zygotic genome associated with microinsemination of round spermatids, Dev. Biol. (2005) in press]. Here, we found that 5–50 nM TSA-treatment for 10 h following oocyte activation resulted in more efficient in vitro development of somatic cloned embryos to the blastocyst stage from 2- to 5-fold depending on the donor cells including tail tip cells, spleen cells, neural stem cells, and cumulus cells. This TSA-treatment also led to more than 5-fold increase in success rate of mouse Cloning from cumulus cells without obvious abnormality but failed to improve ES Cloning success. Further, we succeeded in establishment of nuclear transfer-embryonic stem (NT-ES) cells from TSA-treated cloned blastocyst at a rate three times higher than those from untreated cloned blastocysts. Thus, our data indicate that TSA-treatment after SCNT in mice can dramatically improve the practical application of current Cloning Techniques.
Kazuhiro Sanpei - One of the best experts on this subject based on the ideXlab platform.
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a novel long and unstable cag ctg trinucleotide repeat on chromosome 17q
Genomics, 1998Co-Authors: Takeshi Ikeuchi, Kazuhiro Sanpei, Gerard D Schellenberg, Hidenao Sasaki, Hiroki Takano, Geraldine Cancel, Thomas D. Bird, Alexis Brice, Kunio Tashiro, Margaret A PericakvanceAbstract:Abstract Using the direct identification of repeat expansion and Cloning Technique, we cloned a novel long CAG/CTG trinucleotide repeat on chromosome 17. Using radiation hybrid panels, the CAG/CTG repeat was mapped to chromosome 17q. The CAG/CTG repeat is highly polymorphic, with a heterozygosity of 85%, and exhibits a bimodal distribution (allele S, 10–26 repeat units, and allele L, 50–92 repeat units). The CAG/CTG repeat of allele L exhibited intergenerational instabilities, which are more prominent in maternal transmission than in paternal transmission. Analyses of Northern blot and RT-PCR indicate that the repeat is transcribed. Although the size of the CAG/CTG repeat of allele L is within the range of the expanded CAG repeat of disease-causing genes, we did not detect any association of allele L with various neurodegenerative diseases, including frontotemporal dementia and parkinsonism, mapped to 17q21–q23.
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A Novel Long and Unstable CAG/CTG Trinucleotide Repeat on Chromosome 17q ☆
Genomics, 1998Co-Authors: Takeshi Ikeuchi, Kazuhiro Sanpei, Gerard D Schellenberg, Hidenao Sasaki, Hiroki Takano, Geraldine Cancel, Thomas D. Bird, Alexis Brice, Kunio Tashiro, Margaret A. Pericak-vanceAbstract:Abstract Using the direct identification of repeat expansion and Cloning Technique, we cloned a novel long CAG/CTG trinucleotide repeat on chromosome 17. Using radiation hybrid panels, the CAG/CTG repeat was mapped to chromosome 17q. The CAG/CTG repeat is highly polymorphic, with a heterozygosity of 85%, and exhibits a bimodal distribution (allele S, 10–26 repeat units, and allele L, 50–92 repeat units). The CAG/CTG repeat of allele L exhibited intergenerational instabilities, which are more prominent in maternal transmission than in paternal transmission. Analyses of Northern blot and RT-PCR indicate that the repeat is transcribed. Although the size of the CAG/CTG repeat of allele L is within the range of the expanded CAG repeat of disease-causing genes, we did not detect any association of allele L with various neurodegenerative diseases, including frontotemporal dementia and parkinsonism, mapped to 17q21–q23.
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identification of the spinocerebellar ataxia type 2 gene using a direct identification of repeat expansion and Cloning Technique direct
Nature Genetics, 1996Co-Authors: Kazuhiro Sanpei, Hidenao Sasaki, Hiroki Takano, Kunio Tashiro, Shuichi Igarashi, Toshiya Sato, Mutsuo Oyake, Akemi Wakisaka, Y Ishida, Takeshi IkeuchiAbstract:Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant, neurodegenerative disorder that affects the cerebellum and other areas of the central nervous system. We have devised a novel strategy, the direct identification of repeat expansion and Cloning Technique (DIRECT), which allows selective detection of expanded GAG repeats and Cloning of the genes involved. By applying DIRECT, we identified an expanded CAG repeat of the gene for SCA2. CAG repeats of normal alleles range in size from 15 to 24 repeat units, while those of SCA2 chromosomes are expanded to 35 to 59 repeat units. The SCA2 cDNA is predicted to code for 1,313 amino acids — with the CAG repeats coding for a polyglutamine tract. DIRECT is a robust strategy for identification of pathologically expanded trinucleotide repeats and will dramatically accelerate the search for causative genes of neuropsychiatric diseases caused by trinucleotide repeat expansions.
Hiroki Takano - One of the best experts on this subject based on the ideXlab platform.
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a novel long and unstable cag ctg trinucleotide repeat on chromosome 17q
Genomics, 1998Co-Authors: Takeshi Ikeuchi, Kazuhiro Sanpei, Gerard D Schellenberg, Hidenao Sasaki, Hiroki Takano, Geraldine Cancel, Thomas D. Bird, Alexis Brice, Kunio Tashiro, Margaret A PericakvanceAbstract:Abstract Using the direct identification of repeat expansion and Cloning Technique, we cloned a novel long CAG/CTG trinucleotide repeat on chromosome 17. Using radiation hybrid panels, the CAG/CTG repeat was mapped to chromosome 17q. The CAG/CTG repeat is highly polymorphic, with a heterozygosity of 85%, and exhibits a bimodal distribution (allele S, 10–26 repeat units, and allele L, 50–92 repeat units). The CAG/CTG repeat of allele L exhibited intergenerational instabilities, which are more prominent in maternal transmission than in paternal transmission. Analyses of Northern blot and RT-PCR indicate that the repeat is transcribed. Although the size of the CAG/CTG repeat of allele L is within the range of the expanded CAG repeat of disease-causing genes, we did not detect any association of allele L with various neurodegenerative diseases, including frontotemporal dementia and parkinsonism, mapped to 17q21–q23.
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A Novel Long and Unstable CAG/CTG Trinucleotide Repeat on Chromosome 17q ☆
Genomics, 1998Co-Authors: Takeshi Ikeuchi, Kazuhiro Sanpei, Gerard D Schellenberg, Hidenao Sasaki, Hiroki Takano, Geraldine Cancel, Thomas D. Bird, Alexis Brice, Kunio Tashiro, Margaret A. Pericak-vanceAbstract:Abstract Using the direct identification of repeat expansion and Cloning Technique, we cloned a novel long CAG/CTG trinucleotide repeat on chromosome 17. Using radiation hybrid panels, the CAG/CTG repeat was mapped to chromosome 17q. The CAG/CTG repeat is highly polymorphic, with a heterozygosity of 85%, and exhibits a bimodal distribution (allele S, 10–26 repeat units, and allele L, 50–92 repeat units). The CAG/CTG repeat of allele L exhibited intergenerational instabilities, which are more prominent in maternal transmission than in paternal transmission. Analyses of Northern blot and RT-PCR indicate that the repeat is transcribed. Although the size of the CAG/CTG repeat of allele L is within the range of the expanded CAG repeat of disease-causing genes, we did not detect any association of allele L with various neurodegenerative diseases, including frontotemporal dementia and parkinsonism, mapped to 17q21–q23.
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identification of the spinocerebellar ataxia type 2 gene using a direct identification of repeat expansion and Cloning Technique direct
Nature Genetics, 1996Co-Authors: Kazuhiro Sanpei, Hidenao Sasaki, Hiroki Takano, Kunio Tashiro, Shuichi Igarashi, Toshiya Sato, Mutsuo Oyake, Akemi Wakisaka, Y Ishida, Takeshi IkeuchiAbstract:Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant, neurodegenerative disorder that affects the cerebellum and other areas of the central nervous system. We have devised a novel strategy, the direct identification of repeat expansion and Cloning Technique (DIRECT), which allows selective detection of expanded GAG repeats and Cloning of the genes involved. By applying DIRECT, we identified an expanded CAG repeat of the gene for SCA2. CAG repeats of normal alleles range in size from 15 to 24 repeat units, while those of SCA2 chromosomes are expanded to 35 to 59 repeat units. The SCA2 cDNA is predicted to code for 1,313 amino acids — with the CAG repeats coding for a polyglutamine tract. DIRECT is a robust strategy for identification of pathologically expanded trinucleotide repeats and will dramatically accelerate the search for causative genes of neuropsychiatric diseases caused by trinucleotide repeat expansions.
Hidenao Sasaki - One of the best experts on this subject based on the ideXlab platform.
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a novel long and unstable cag ctg trinucleotide repeat on chromosome 17q
Genomics, 1998Co-Authors: Takeshi Ikeuchi, Kazuhiro Sanpei, Gerard D Schellenberg, Hidenao Sasaki, Hiroki Takano, Geraldine Cancel, Thomas D. Bird, Alexis Brice, Kunio Tashiro, Margaret A PericakvanceAbstract:Abstract Using the direct identification of repeat expansion and Cloning Technique, we cloned a novel long CAG/CTG trinucleotide repeat on chromosome 17. Using radiation hybrid panels, the CAG/CTG repeat was mapped to chromosome 17q. The CAG/CTG repeat is highly polymorphic, with a heterozygosity of 85%, and exhibits a bimodal distribution (allele S, 10–26 repeat units, and allele L, 50–92 repeat units). The CAG/CTG repeat of allele L exhibited intergenerational instabilities, which are more prominent in maternal transmission than in paternal transmission. Analyses of Northern blot and RT-PCR indicate that the repeat is transcribed. Although the size of the CAG/CTG repeat of allele L is within the range of the expanded CAG repeat of disease-causing genes, we did not detect any association of allele L with various neurodegenerative diseases, including frontotemporal dementia and parkinsonism, mapped to 17q21–q23.
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A Novel Long and Unstable CAG/CTG Trinucleotide Repeat on Chromosome 17q ☆
Genomics, 1998Co-Authors: Takeshi Ikeuchi, Kazuhiro Sanpei, Gerard D Schellenberg, Hidenao Sasaki, Hiroki Takano, Geraldine Cancel, Thomas D. Bird, Alexis Brice, Kunio Tashiro, Margaret A. Pericak-vanceAbstract:Abstract Using the direct identification of repeat expansion and Cloning Technique, we cloned a novel long CAG/CTG trinucleotide repeat on chromosome 17. Using radiation hybrid panels, the CAG/CTG repeat was mapped to chromosome 17q. The CAG/CTG repeat is highly polymorphic, with a heterozygosity of 85%, and exhibits a bimodal distribution (allele S, 10–26 repeat units, and allele L, 50–92 repeat units). The CAG/CTG repeat of allele L exhibited intergenerational instabilities, which are more prominent in maternal transmission than in paternal transmission. Analyses of Northern blot and RT-PCR indicate that the repeat is transcribed. Although the size of the CAG/CTG repeat of allele L is within the range of the expanded CAG repeat of disease-causing genes, we did not detect any association of allele L with various neurodegenerative diseases, including frontotemporal dementia and parkinsonism, mapped to 17q21–q23.
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identification of the spinocerebellar ataxia type 2 gene using a direct identification of repeat expansion and Cloning Technique direct
Nature Genetics, 1996Co-Authors: Kazuhiro Sanpei, Hidenao Sasaki, Hiroki Takano, Kunio Tashiro, Shuichi Igarashi, Toshiya Sato, Mutsuo Oyake, Akemi Wakisaka, Y Ishida, Takeshi IkeuchiAbstract:Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant, neurodegenerative disorder that affects the cerebellum and other areas of the central nervous system. We have devised a novel strategy, the direct identification of repeat expansion and Cloning Technique (DIRECT), which allows selective detection of expanded GAG repeats and Cloning of the genes involved. By applying DIRECT, we identified an expanded CAG repeat of the gene for SCA2. CAG repeats of normal alleles range in size from 15 to 24 repeat units, while those of SCA2 chromosomes are expanded to 35 to 59 repeat units. The SCA2 cDNA is predicted to code for 1,313 amino acids — with the CAG repeats coding for a polyglutamine tract. DIRECT is a robust strategy for identification of pathologically expanded trinucleotide repeats and will dramatically accelerate the search for causative genes of neuropsychiatric diseases caused by trinucleotide repeat expansions.