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Yusuke Nakamura - One of the best experts on this subject based on the ideXlab platform.
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A complete Not I restriction map covering the entire long arm of human Chromosome 11
Genes to cells : devoted to molecular & cellular mechanisms, 1997Co-Authors: Fumie Hosoda, Takashi Tokino, Yusuke Nakamura, Yasuhito Arai, Eiko Kitamura, Johji Inazawa, Michiyo Fukushima, Carol Jones, Naoki Kakazu, Tatsuo AbeAbstract:Background: Human Chromosome 11 is one of the autosomes on which many disease genes have been mapped. Many different types of map, including a radiation hybrid map, a genetic map, and an STS-content YAC map, have been constructed for the Chromosome. However, a physical map providing accurate physical distances has not yet been established. A Chromosome-wide Not I restriction map was constructed to understand the overall feature of the genome organization and to facilitate the positional cloning of disease genes. Results: A complete Not I restriction map of the entire long arm of human Chromosome 11 was constructed using linking-clone mapping. This physical map covers 77.6 Mb, from a pericentromeric Not I site to the terminus, and provides the most accurate ordering and distance estimation to date. We also mapped 138 sequence markers in the q13 region that have been poorly mapped previously. Conclusions: The restriction map of the entire long arm of human Chromosome 11 is the longest restriction map of the human genome. This mapping has disclosed unique features regarding the organization of the Chromosome, indicating that restriction sites of Not I, a CpG-recognition enzyme, are primarily distributed in R (or T) bands and that genetic distance is considerably longer in R (or T) bands than in G bands. The mapping, as well as the dense concentration of mapped markers within the q13 region, should help with positional cloning of the genes associated with various diseases.
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fifty sequenced tagged sites on human Chromosome 11
Genomics, 1993Co-Authors: Tokiko Miwa, Yusuke Nakamura, Kazunori Sudo, Takashi ImaiAbstract:Fifty novel sequenced-tagged sites (STSs) were identified from cosmid clones mapped to human Chromosome 11. DNA sequences were determined for one or both cloning ends of 69 cosmid markers that had each been localized to 1 of 24 subchromosomal regions by means of hybridization to somatic cell hybrid panels. Proper primer sequences and appropriate conditions for a polymerase chain reaction (PCR) were determined for each marker. Twenty-one of the cosmids were not suitable for generating STSs, mainly because both of their ends contained repetitive elements such as Alu and L1 sequences; however, some were inappropriate because the sizes of their PCR products from human DNA, used as template, were same as those from yeast DNA. Finally, 50 STSs were established from 48 clones: 20 were derived from markers localized on the short arm and 30 from the long arm. These STSs can serve as new reagents for investigating human DNA in somatic cell hybrids and for isolating yeast artificial Chromosomes to anchor large DNA contigs and fine-scale physical maps of Chromosome 11.
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a high resolution cytogenetic map of 168 cosmid dna markers for human Chromosome 11
Genomics, 1992Co-Authors: Tadaaki Hori, Takashi Tokino, Ei Ichi Takahashi, Akira Tanigami, Yusuke NakamuraAbstract:We have constructed a high-resolution cytogenetic map with 168 DNA markers, including 90 RFLP markers for human Chromosome 11. The cosmid clones were mapped by fluorescence in situ suppression hybridization, in which discrete fluorescent signals can be detected directly on prometaphase R-banded Chromosomes. Although these cosmid clones were distributed throughout the Chromosome, they had some tendency to localize in the regions of R-positive band, such as 11p15, 11p11.2, 11q13, 11q23, and 11q25. Since these regions of Chromosome 11 are considered to contain genes responsible for certain genetic diseases, cancer breakpoints involved in Chromosome rearrangements, and tumor-suppressor genes, this high-resolution cytogenetic map will contribute to the molecular characterization of such genes. This map will also provide many landmarks essential for construction of the complete physical map with contigs of cosmid and YAC clones.
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mapping of 262 dna markers into 24 intervals on human Chromosome 11
American Journal of Human Genetics, 1992Co-Authors: Akira Tanigami, Takashi Tokino, Masaki Mori, Thomas M Glaser, J W Park, Carol Jones, Shuya Takiguchi, Yusuke NakamuraAbstract:The authors have extended the authors mapping effort on human Chromosome 11 to encompass a total of 262 DNA markers, which have been mapped into 24 intervals on Chromosome 11; 123 of the markers reveal RFLPs. Theses clones are scattered throughout the Chromosome, although some clustering occurs in R-positive bands (p15.1, p11.2,q13, and q23.3). Fifty-two of the markers were found to contain DNA sequences conserved in Chinese hamster, and some of these 52 also cross-hybridized with DNA from other mammals and/or chicken. As the length of Chromosome 11 is estimated at nearly 130 cM, the average distance between RFLP markers is roughly 1 cM. The large panel of DNA markers on their map should contribute to investigations of hereditary diseases on this Chromosome, and it will also provide reagents for constructing either fine-scale linkage and physical maps or contig maps of cosmids or yeast artificial Chromosomes.
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isolation and mapping of 62 new rflp markers on human Chromosome 11
American Journal of Human Genetics, 1991Co-Authors: Takashi Tokino, Tadaaki Hori, Ei Ichi Takahashi, Masaki Mori, Akira Tanigami, Thomas M Glaser, J W Park, C Jones, Yusuke NakamuraAbstract:Abstract To obtain new RFLP markers on human Chromosome 11 for a high-resolution map, we constructed a cosmid library from a Chinese hamster x human somatic hybrid cell line that retains only human Chromosome 11 in a Chinese hamster genomic background. A total of 3,500 cosmids were isolated by colony hybridization with labeled human genomic DNA. DNA was prepared from 130 of these cosmid clones and examined for RFLP. In 62 of them, polymorphism was detected with one or more enzymes; four RFLPs were VNTR systems. All polymorphic clones were assigned to one of 22 intervals obtained by mapping on a deletion panel of 15 somatic hybrid cell lines containing parts of Chromosome 11; 11 clones were finely mapped by in situ hybridization. Although RFLP markers were scattered on the whole Chromosome, they were found predominantly in the regions of R-banding. These DNA markers will contribute to fine mapping of genes causing inherited disorders and tumor-suppressor genes that reside on Chromosome 11. Furthermore, as one-third of the cosmid clones revealed a band or bands in Chinese hamster DNA, indicating sequence conservation, this subset of clones may be useful for isolating biologically important genes on Chromosome 11.
Bernard E Weissman - One of the best experts on this subject based on the ideXlab platform.
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suppression of mda mb 435 breast carcinoma cell metastasis following the introduction of human Chromosome 11
Cancer Research, 1996Co-Authors: Karen K Phillips, Danny R Welch, Mary E Miele, Jeong Hyung Lee, Lisa L Wei, Bernard E WeissmanAbstract:Abstract To determine the relevance of genetic information on Chromosome 11 in the development of metastatic breast tumors, we introduced a normal human Chromosome 11 into the highly metastatic MDA-MB-435 breast carcinoma cell line via the microcell-mediated Chromosome transfer technique. Although the MDA-MB-435 recipient cell line and four randomly selected microcell hybrid clones remained tumorigenic in nude mice, the hybrids were >95% suppressed for metastasis to lung and regional lymph nodes (P
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human Chromosome 11 contains two different growth suppressor genes for embryonal rhabdomyosarcoma
Proceedings of the National Academy of Sciences of the United States of America, 1992Co-Authors: Heidi Scrable, Elizabeth Livanos, Marie J Arboleda, Webster K Cavenee, Bernard E WeissmanAbstract:Abstract The identification of acquired homozygosity in human cancers implies locations of tumor suppressor genes without providing functional evidence. The localization of a defect in embryonal rhabdomyosarcomas to chromosomal region 11p15 provides one such example. In this report, we show that transfer of a normal human Chromosome 11 into an embryonal rhabdomyosarcoma cell line elicited a dramatic loss of the proliferative capacity of the transferrants. Indeed, the majority of the viable microcell hybrids had either eliminated genetic information on the short arm of the transferred Chromosome 11 or increased the copy number of the rhabdomyosarcoma-derived Chromosomes 11. Cells that possessed only the long arm of Chromosome 11 also demonstrated a decreased growth rate. In contrast, all microcell hybrids retained the ability to form tumors upon inoculation into animals. These functional data support molecular studies indicating loss of genetic information on Chromosome 11p15 during the development of embryonal rhabdomyosarcoma. In addition, our studies demonstrate the existence of a second gene on the long arm, previously unrecognized by molecular analyses, which negatively regulates the growth of embryonal rhabdomyosarcoma cell lines.
Takashi Tokino - One of the best experts on this subject based on the ideXlab platform.
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A complete Not I restriction map covering the entire long arm of human Chromosome 11
Genes to cells : devoted to molecular & cellular mechanisms, 1997Co-Authors: Fumie Hosoda, Takashi Tokino, Yusuke Nakamura, Yasuhito Arai, Eiko Kitamura, Johji Inazawa, Michiyo Fukushima, Carol Jones, Naoki Kakazu, Tatsuo AbeAbstract:Background: Human Chromosome 11 is one of the autosomes on which many disease genes have been mapped. Many different types of map, including a radiation hybrid map, a genetic map, and an STS-content YAC map, have been constructed for the Chromosome. However, a physical map providing accurate physical distances has not yet been established. A Chromosome-wide Not I restriction map was constructed to understand the overall feature of the genome organization and to facilitate the positional cloning of disease genes. Results: A complete Not I restriction map of the entire long arm of human Chromosome 11 was constructed using linking-clone mapping. This physical map covers 77.6 Mb, from a pericentromeric Not I site to the terminus, and provides the most accurate ordering and distance estimation to date. We also mapped 138 sequence markers in the q13 region that have been poorly mapped previously. Conclusions: The restriction map of the entire long arm of human Chromosome 11 is the longest restriction map of the human genome. This mapping has disclosed unique features regarding the organization of the Chromosome, indicating that restriction sites of Not I, a CpG-recognition enzyme, are primarily distributed in R (or T) bands and that genetic distance is considerably longer in R (or T) bands than in G bands. The mapping, as well as the dense concentration of mapped markers within the q13 region, should help with positional cloning of the genes associated with various diseases.
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a high resolution cytogenetic map of 168 cosmid dna markers for human Chromosome 11
Genomics, 1992Co-Authors: Tadaaki Hori, Takashi Tokino, Ei Ichi Takahashi, Akira Tanigami, Yusuke NakamuraAbstract:We have constructed a high-resolution cytogenetic map with 168 DNA markers, including 90 RFLP markers for human Chromosome 11. The cosmid clones were mapped by fluorescence in situ suppression hybridization, in which discrete fluorescent signals can be detected directly on prometaphase R-banded Chromosomes. Although these cosmid clones were distributed throughout the Chromosome, they had some tendency to localize in the regions of R-positive band, such as 11p15, 11p11.2, 11q13, 11q23, and 11q25. Since these regions of Chromosome 11 are considered to contain genes responsible for certain genetic diseases, cancer breakpoints involved in Chromosome rearrangements, and tumor-suppressor genes, this high-resolution cytogenetic map will contribute to the molecular characterization of such genes. This map will also provide many landmarks essential for construction of the complete physical map with contigs of cosmid and YAC clones.
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mapping of 262 dna markers into 24 intervals on human Chromosome 11
American Journal of Human Genetics, 1992Co-Authors: Akira Tanigami, Takashi Tokino, Masaki Mori, Thomas M Glaser, J W Park, Carol Jones, Shuya Takiguchi, Yusuke NakamuraAbstract:The authors have extended the authors mapping effort on human Chromosome 11 to encompass a total of 262 DNA markers, which have been mapped into 24 intervals on Chromosome 11; 123 of the markers reveal RFLPs. Theses clones are scattered throughout the Chromosome, although some clustering occurs in R-positive bands (p15.1, p11.2,q13, and q23.3). Fifty-two of the markers were found to contain DNA sequences conserved in Chinese hamster, and some of these 52 also cross-hybridized with DNA from other mammals and/or chicken. As the length of Chromosome 11 is estimated at nearly 130 cM, the average distance between RFLP markers is roughly 1 cM. The large panel of DNA markers on their map should contribute to investigations of hereditary diseases on this Chromosome, and it will also provide reagents for constructing either fine-scale linkage and physical maps or contig maps of cosmids or yeast artificial Chromosomes.
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isolation and mapping of 62 new rflp markers on human Chromosome 11
American Journal of Human Genetics, 1991Co-Authors: Takashi Tokino, Tadaaki Hori, Ei Ichi Takahashi, Masaki Mori, Akira Tanigami, Thomas M Glaser, J W Park, C Jones, Yusuke NakamuraAbstract:Abstract To obtain new RFLP markers on human Chromosome 11 for a high-resolution map, we constructed a cosmid library from a Chinese hamster x human somatic hybrid cell line that retains only human Chromosome 11 in a Chinese hamster genomic background. A total of 3,500 cosmids were isolated by colony hybridization with labeled human genomic DNA. DNA was prepared from 130 of these cosmid clones and examined for RFLP. In 62 of them, polymorphism was detected with one or more enzymes; four RFLPs were VNTR systems. All polymorphic clones were assigned to one of 22 intervals obtained by mapping on a deletion panel of 15 somatic hybrid cell lines containing parts of Chromosome 11; 11 clones were finely mapped by in situ hybridization. Although RFLP markers were scattered on the whole Chromosome, they were found predominantly in the regions of R-banding. These DNA markers will contribute to fine mapping of genes causing inherited disorders and tumor-suppressor genes that reside on Chromosome 11. Furthermore, as one-third of the cosmid clones revealed a band or bands in Chinese hamster DNA, indicating sequence conservation, this subset of clones may be useful for isolating biologically important genes on Chromosome 11.
Tadayuki Takeda - One of the best experts on this subject based on the ideXlab platform.
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human Chromosome 11 dna sequence and analysis including novel gene identification
Nature, 2006Co-Authors: Todd D Taylor, Hideki Noguchi, Yasushi Totoki, Atsushi Toyoda, Yoko Kuroki, Ken Dewar, Christine Lloyd, Takehiko Itoh, Tadayuki TakedaAbstract:Chromosome 11, although average in size, is one of the most gene- and disease-rich Chromosomes in the human genome. Initial gene annotation indicates an average gene density of 11.6 genes per megabase, including 1,524 protein-coding genes, some of which were identified using novel methods, and 765 pseudogenes. One-quarter of the protein-coding genes shows overlap with other genes. Of the 856 olfactory receptor genes in the human genome, more than 40% are located in 28 single- and multi-gene clusters along this Chromosome. Out of the 171 disorders currently attributed to the Chromosome, 86 remain for which the underlying molecular basis is not yet known, including several mendelian traits, cancer and susceptibility loci. The high-quality data presented here—nearly 134.5 million base pairs representing 99.8% coverage of the euchromatic sequence—provide scientists with a solid foundation for understanding the genetic basis of these disorders and other biological phenomena. The Human Genome Project's analysis of Chromosome 11 is published this week. This is one of the most gene- and disease-rich Chromosomes in the human genome. It contains more than 40% of the olfactory receptor genes, the largest multi-gene family in any metazoan genome. It is also home to the β-globin gene cluster, which is responsible for several disorders including sickle-cell anaemia.
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human Chromosome 11 dna sequence and analysis including novel gene identification
Nature, 2006Co-Authors: Todd D Taylor, Hideki Noguchi, Yasushi Totoki, Atsushi Toyoda, Yoko Kuroki, Ken Dewar, Christine Lloyd, Takehiko Itoh, Tadayuki TakedaAbstract:Chromosome 11, although average in size, is one of the most gene- and disease-rich Chromosomes in the human genome. Initial gene annotation indicates an average gene density of 11.6 genes per megabase, including 1,524 protein-coding genes, some of which were identified using novel methods, and 765 pseudogenes. One-quarter of the protein-coding genes shows overlap with other genes. Of the 856 olfactory receptor genes in the human genome, more than 40% are located in 28 single- and multi-gene clusters along this Chromosome. Out of the 171 disorders currently attributed to the Chromosome, 86 remain for which the underlying molecular basis is not yet known, including several mendelian traits, cancer and susceptibility loci. The high-quality data presented here--nearly 134.5 million base pairs representing 99.8% coverage of the euchromatic sequence--provide scientists with a solid foundation for understanding the genetic basis of these disorders and other biological phenomena.
Eitan Friedman - One of the best experts on this subject based on the ideXlab platform.
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carcinoid tumors frequently display genetic abnormalities involving Chromosome 11
The Journal of Clinical Endocrinology and Metabolism, 1996Co-Authors: Orit Jakobovitz, Devora Nass, Luiz Demarco, Alfredo J A Barbosa, Frida Simoni, Gideon Rechavi, Eitan FriedmanAbstract:Carcinoid tumors are neuroendocrine neoplasms that are encountered either sporadically or as part of a familial syndrome, most notably-multiple endocrine neoplasia type 1 (MEN1). The MEN1 gene localizes to Chromosome 11 (11q13) and presumably functions as a tumor suppressor gene. The molecular mechanisms underlying carcinoid tumor development and their clonal composition remain largely unknown. To establish whether carcinoid tumors develop via a mechanism similar to other MEN1-associated tumors, and indirectly determine their clonal composition, we analyzed 36 sporadically occurring carcinoid tumors with 16 Chromosome 11 microsatellite markers, mostly from around the MEN1 region for loss of heterozygosity (LOH). Twenty one tumors (58%) displayed LOH of at least three markers, five lost almost an entire allele and the rest displayed a discontinuous pattern. Similar, but less extensive analysis was also carried out for 10 additional carcinoid tumors from Brazil, 6 of the 10 showed LOH with at least one marker. Overall, 36 of 46 tumors (78%) displayed LOH. In addition, 20 of 46 (43%) tumors exhibited a pattern of genomic instability. Thus, the majority of sporadically occurring carcinoid tumors are monoclonal whose tumorigenesis involves inactivation of a tumor suppressor gene on Chromosome 11 and DNA mismatch repair genes mutations.
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Allelic Loss from Chromosome 11 in Parathyroid Tumors
Cancer Research, 1992Co-Authors: Eitan Friedman, Luiz De Marco, Pablo V. Gejman, Jeffrey A. Norton, Allen E. Bale, Gerald D. Aurbach, Allen M. Spiegel, Stephen J. MarxAbstract:Parathyroid tumors may occur in a sporadic fashion or, more rarely, as part of a familial syndrome (such as familial multiple endocrine neoplasia type I). The MENI gene has been mapped by linkage analysis to Chromosome 11 at band q11-q13, and presumably acts as a tumor suppressor gene. In the present study, which is an extension of our previous studies, we examined 41 parathyroid tumors from patients with familial multiple endocrine neoplasia type I and 61 sporadic parathyroid tumors with markers on Chromosome 11, to assess the extent of allelic loss in those tumors. Twenty-four of the MENI -associated tumors (58%) and 16 of the sporadic parathyroid tumors (26%) displayed allelic loss from Chromosome 11. The region of overlap of the allelic losses in the MENI -associated tumors enables us to place the MENI gene between PGA centromerically and INT2 telomerically, a region spanning about 7.5 cM. Taken together with locus ordering by linkage analysis, this clearly localizes the MENI gene telomeric to the PGA locus. Our inability to detect allelic loss on Chromosome 11 in some parathyroid tumors suggests the existence of other genes involved in the development and/or progression of this subgroup of presumably monoclonal tumors; or that localized events involving the 11q tumor suppressor gene have occurred in some parathyroid tumors whose detection is beyond the sensitivity of our analysis; or that at least some of the specimens analyzed were in fact primarily hyperplastic parathyroid tissue.