3 Flanking Region

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Ikuko Mizuta - One of the best experts on this subject based on the ideXlab platform.

  • yy1 binds to α synuclein 3 Flanking Region snp and stimulates antisense noncoding rna expression
    Journal of Human Genetics, 2013
    Co-Authors: Ikuko Mizuta, Kazuaki Takafuji, Yuko Ando, Wataru Satake, Motoi Kanagawa, Kazuhiro Kobayashi, Shushi Nagamori, Takayuki Shinohara, Mitsutoshi Yamamoto
    Abstract:

    YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression

  • YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression
    Journal of Human Genetics, 2013
    Co-Authors: Ikuko Mizuta, Kazuaki Takafuji, Yuko Ando, Wataru Satake, Motoi Kanagawa, Kazuhiro Kobayashi, Shushi Nagamori, Takayuki Shinohara, Mitsutoshi Yamamoto, Nobutaka Hattori
    Abstract:

    α-synuclein ( SNCA ) is an established susceptibility gene for Parkinson’s disease (PD), one of the most common human neurodegenerative disorders. Increased SNCA is considered to lead to PD and dementia with Lewy bodies. Four single-nucleotide polymorphisms (SNPs) in SNCA 3Region were prominently associated with PD among different ethnic groups. To examine how these SNPs influence disease susceptibility, we analyzed their potential effects on SNCA gene expression. We found that rs356219 showed allele-specific features. Gel shift assay using nuclear extracts from SH-SY5Y cells showed binding of one or more proteins to the protective allele, rs356219-A. We purified the rs356219-A–protein complex with DNA affinity beads and identified a bound protein using mass spectrometry. This protein, YY1 (Yin Yang 1), is an ubiquitous transcription factor with multiple functions. We next investigated SNCA expression change in SH-SY5Y cells by YY1 transfection. We also analyzed the expression of antisense noncoding RNA (ncRNA) RP11-115D19.1 in SNCA 3′-Flanking Region, because rs356219 is located in intron of RP11-115D19.1 . Little change was observed in SNCA expression levels; however, RP11-115D19.1 expression was prominently stimulated by YY1. In autopsied cortices, positive correlation was observed among RP11-115D19.1 , SNCA and YY1 expression levels, suggesting their functional interactions in vivo . Knockdown of RP11-115D19.1 increased SNCA expression significantly in SH-SY5Y cells, suggesting its repressive effect on SNCA expression. Our findings of the protective allele-specific YY1 and antisense ncRNA raised a novel possible mechanism to regulate SNCA expression.

  • YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression
    Journal of Human Genetics, 2013
    Co-Authors: Ikuko Mizuta, Kazuaki Takafuji, Yuko Ando, Wataru Satake, Motoi Kanagawa, Kazuhiro Kobayashi, Shushi Nagamori, Takayuki Shinohara, Mitsutoshi Yamamoto
    Abstract:

    YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression

Mitsutoshi Yamamoto - One of the best experts on this subject based on the ideXlab platform.

  • yy1 binds to α synuclein 3 Flanking Region snp and stimulates antisense noncoding rna expression
    Journal of Human Genetics, 2013
    Co-Authors: Ikuko Mizuta, Kazuaki Takafuji, Yuko Ando, Wataru Satake, Motoi Kanagawa, Kazuhiro Kobayashi, Shushi Nagamori, Takayuki Shinohara, Mitsutoshi Yamamoto
    Abstract:

    YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression

  • YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression
    Journal of Human Genetics, 2013
    Co-Authors: Ikuko Mizuta, Kazuaki Takafuji, Yuko Ando, Wataru Satake, Motoi Kanagawa, Kazuhiro Kobayashi, Shushi Nagamori, Takayuki Shinohara, Mitsutoshi Yamamoto, Nobutaka Hattori
    Abstract:

    α-synuclein ( SNCA ) is an established susceptibility gene for Parkinson’s disease (PD), one of the most common human neurodegenerative disorders. Increased SNCA is considered to lead to PD and dementia with Lewy bodies. Four single-nucleotide polymorphisms (SNPs) in SNCA 3Region were prominently associated with PD among different ethnic groups. To examine how these SNPs influence disease susceptibility, we analyzed their potential effects on SNCA gene expression. We found that rs356219 showed allele-specific features. Gel shift assay using nuclear extracts from SH-SY5Y cells showed binding of one or more proteins to the protective allele, rs356219-A. We purified the rs356219-A–protein complex with DNA affinity beads and identified a bound protein using mass spectrometry. This protein, YY1 (Yin Yang 1), is an ubiquitous transcription factor with multiple functions. We next investigated SNCA expression change in SH-SY5Y cells by YY1 transfection. We also analyzed the expression of antisense noncoding RNA (ncRNA) RP11-115D19.1 in SNCA 3′-Flanking Region, because rs356219 is located in intron of RP11-115D19.1 . Little change was observed in SNCA expression levels; however, RP11-115D19.1 expression was prominently stimulated by YY1. In autopsied cortices, positive correlation was observed among RP11-115D19.1 , SNCA and YY1 expression levels, suggesting their functional interactions in vivo . Knockdown of RP11-115D19.1 increased SNCA expression significantly in SH-SY5Y cells, suggesting its repressive effect on SNCA expression. Our findings of the protective allele-specific YY1 and antisense ncRNA raised a novel possible mechanism to regulate SNCA expression.

  • YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression
    Journal of Human Genetics, 2013
    Co-Authors: Ikuko Mizuta, Kazuaki Takafuji, Yuko Ando, Wataru Satake, Motoi Kanagawa, Kazuhiro Kobayashi, Shushi Nagamori, Takayuki Shinohara, Mitsutoshi Yamamoto
    Abstract:

    YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression

Philip L Huang - One of the best experts on this subject based on the ideXlab platform.

  • the 3 Flanking Region of the human erythropoietin encoding gene contains nitrogen regulatory oxygen sensing consensus sequences and tissue specific transcriptional regulatory elements
    Gene, 1993
    Co-Authors: Leehuang Sylvia, Lin Jihjing, Kung Hsiangfu, Philip L Huang
    Abstract:

    Abstract We have reported the identification of a classical canonical CAAT box, TATA boxes and other transcriptional regulatory elements in the 5' Flanking Region of the human erythropoietin (hEp)-encoding gene [Lee-Huang et al., Gene 128 (1993) 227–236]. These elements were not found in the hEp genomic clones reported by others. Our genomic clone extends in both directions beyond any reported clones, by 3.9 kb on the 5' side and by 1.8 kb on the 3' side. Many important regulatory elements are found in these extended Flanking Regions. We report here the genomic structure of the extended 3' Flanking Region of hEp. This Region contains the following regulatory elements: nitrogen-regulatory/oxygen-sensing consensus sequences, 5'-TTTTGCA and 5'-CCCTGCA; tissue-specific regulatory elements, including binding sites for A-activator, 5'-GTGGTGCAA; for DBP, 5'-TGATTTTGT; for HNF, 5'-T(A/G)TTTGT; and for C/EBP, 5'-T(T/G) (T/G)TGCAAT; a lymphokine-responsive element, 5'-GTGAAACCCC (Rev), as well as binding sites for AP and Spl. In addition, the nucleotide (nt) sequence in this Region is rich in inverted repeats (palindromes) that allow the formation of hairpin loops. A total of 14 potential stem loops with a maximum loop size of 20 nt are found. The identification of these regulatory elements in hEp should provide further insight into the tissue-specific and inducible expression of hEp. Such knowledge should be useful in the clinical modulation of erythropoiesis under physiologic and pathologic conditions.

  • The 3'-Flanking Region of the human erythropoietin-encoding gene contains nitrogen-regulatory/oxygen-sensing consensus sequences and tissue-specific transcriptional regulatory elements
    Gene, 1993
    Co-Authors: Leehuang Sylvia, Philip L Huang, Lin Jih-jing, Kung Hsiang-fu
    Abstract:

    Abstract We have reported the identification of a classical canonical CAAT box, TATA boxes and other transcriptional regulatory elements in the 5' Flanking Region of the human erythropoietin (hEp)-encoding gene [Lee-Huang et al., Gene 128 (1993) 227–236]. These elements were not found in the hEp genomic clones reported by others. Our genomic clone extends in both directions beyond any reported clones, by 3.9 kb on the 5' side and by 1.8 kb on the 3' side. Many important regulatory elements are found in these extended Flanking Regions. We report here the genomic structure of the extended 3' Flanking Region of hEp. This Region contains the following regulatory elements: nitrogen-regulatory/oxygen-sensing consensus sequences, 5'-TTTTGCA and 5'-CCCTGCA; tissue-specific regulatory elements, including binding sites for A-activator, 5'-GTGGTGCAA; for DBP, 5'-TGATTTTGT; for HNF, 5'-T(A/G)TTTGT; and for C/EBP, 5'-T(T/G) (T/G)TGCAAT; a lymphokine-responsive element, 5'-GTGAAACCCC (Rev), as well as binding sites for AP and Spl. In addition, the nucleotide (nt) sequence in this Region is rich in inverted repeats (palindromes) that allow the formation of hairpin loops. A total of 14 potential stem loops with a maximum loop size of 20 nt are found. The identification of these regulatory elements in hEp should provide further insight into the tissue-specific and inducible expression of hEp. Such knowledge should be useful in the clinical modulation of erythropoiesis under physiologic and pathologic conditions.

Cristiano Ferlini - One of the best experts on this subject based on the ideXlab platform.

  • hypoxia induces class iii beta tubulin gene expression by hif 1α binding to its 3 Flanking Region
    Gene, 2008
    Co-Authors: Giuseppina Raspaglio, Flavia Filippetti, Silvia Prislei, Roberta Penci, Ilaria De Maria, Lucia Cicchillitti, Simona Mozzetti, Giovanni Scambia, Cristiano Ferlini
    Abstract:

    Abstract Class III β-tubulin (TUBB3) overexpression represents a major mechanism of drug resistance to microtubule interacting agents such as taxanes and Vinca alkaloids. Here, we tested hypoxia as a possible inducer of TUBB3. The effects of hypoxia on TUBB3 expression were monitored at mRNA and protein level in A2780, in its paclitaxel-resistant counterpart (TC1) and in HeLa cells. Hypoxia was a strong inducer of TUBB3 in A2780, but not in TC1 and HeLa cells. In A2780 HIF-1α was knocked down using RNA interference and TUBB3 expression was assessed in normoxia and hypoxia. The silencing abolished the hypoxia-dependent increase of TUBB3, thereby demonstrating that HIF-1α mediates TUBB3 induction in hypoxia. To investigate this phenomenon, the 5' Flanking Region of human TUBB3 was cloned upstream GFP as a reporter. This Region contained the promoter gene, but activity of the reporter was unaffected by hypoxia. Thus, we looked at the 3' Flanking Region and, at + 168 nucleotides from the stop codon, an HIF-1α binding site was proven to be active in hypoxia, using a construct in which the site was cloned downstream GFP as reporter gene. Deletion of the site in the construct abolished GFP enhancement upon hypoxia. Chromatin immunoprecipitation revealed the engagement by HIF-1α of this site in hypoxia. Methylation analysis of this 3' enhancer showed that it was free of methylation in 70% of cells in A2780, while in less than 16% in both TC1 and HeLa cells, thereby suggesting that TUBB3 increase upon hypoxia is abolished through methylation of the 3' enhancer.

  • Hypoxia induces class III beta-tubulin gene expression by HIF-1alpha binding to its 3' Flanking Region.
    Gene, 2007
    Co-Authors: Giuseppina Raspaglio, Flavia Filippetti, Silvia Prislei, Roberta Penci, Ilaria De Maria, Lucia Cicchillitti, Simona Mozzetti, Giovanni Scambia, Cristiano Ferlini
    Abstract:

    Class III beta-tubulin (TUBB3) overexpression represents a major mechanism of drug resistance to microtubule interacting agents such as taxanes and Vinca alkaloids. Here, we tested hypoxia as a possible inducer of TUBB3. The effects of hypoxia on TUBB3 expression were monitored at mRNA and protein level in A2780, in its paclitaxel-resistant counterpart (TC1) and in HeLa cells. Hypoxia was a strong inducer of TUBB3 in A2780, but not in TC1 and HeLa cells. In A2780 HIF-1alpha was knocked down using RNA interference and TUBB3 expression was assessed in normoxia and hypoxia. The silencing abolished the hypoxia-dependent increase of TUBB3, thereby demonstrating that HIF-1alpha mediates TUBB3 induction in hypoxia. To investigate this phenomenon, the 5' Flanking Region of human TUBB3 was cloned upstream GFP as a reporter. This Region contained the promoter gene, but activity of the reporter was unaffected by hypoxia. Thus, we looked at the 3' Flanking Region and, at +168 nucleotides from the stop codon, an HIF-1alpha binding site was proven to be active in hypoxia, using a construct in which the site was cloned downstream GFP as reporter gene. Deletion of the site in the construct abolished GFP enhancement upon hypoxia. Chromatin immunoprecipitation revealed the engagement by HIF-1alpha of this site in hypoxia. Methylation analysis of this 3' enhancer showed that it was free of methylation in 70% of cells in A2780, while in less than 16% in both TC1 and HeLa cells, thereby suggesting that TUBB3 increase upon hypoxia is abolished through methylation of the 3' enhancer.

Takayuki Shinohara - One of the best experts on this subject based on the ideXlab platform.

  • yy1 binds to α synuclein 3 Flanking Region snp and stimulates antisense noncoding rna expression
    Journal of Human Genetics, 2013
    Co-Authors: Ikuko Mizuta, Kazuaki Takafuji, Yuko Ando, Wataru Satake, Motoi Kanagawa, Kazuhiro Kobayashi, Shushi Nagamori, Takayuki Shinohara, Mitsutoshi Yamamoto
    Abstract:

    YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression

  • YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression
    Journal of Human Genetics, 2013
    Co-Authors: Ikuko Mizuta, Kazuaki Takafuji, Yuko Ando, Wataru Satake, Motoi Kanagawa, Kazuhiro Kobayashi, Shushi Nagamori, Takayuki Shinohara, Mitsutoshi Yamamoto, Nobutaka Hattori
    Abstract:

    α-synuclein ( SNCA ) is an established susceptibility gene for Parkinson’s disease (PD), one of the most common human neurodegenerative disorders. Increased SNCA is considered to lead to PD and dementia with Lewy bodies. Four single-nucleotide polymorphisms (SNPs) in SNCA 3Region were prominently associated with PD among different ethnic groups. To examine how these SNPs influence disease susceptibility, we analyzed their potential effects on SNCA gene expression. We found that rs356219 showed allele-specific features. Gel shift assay using nuclear extracts from SH-SY5Y cells showed binding of one or more proteins to the protective allele, rs356219-A. We purified the rs356219-A–protein complex with DNA affinity beads and identified a bound protein using mass spectrometry. This protein, YY1 (Yin Yang 1), is an ubiquitous transcription factor with multiple functions. We next investigated SNCA expression change in SH-SY5Y cells by YY1 transfection. We also analyzed the expression of antisense noncoding RNA (ncRNA) RP11-115D19.1 in SNCA 3′-Flanking Region, because rs356219 is located in intron of RP11-115D19.1 . Little change was observed in SNCA expression levels; however, RP11-115D19.1 expression was prominently stimulated by YY1. In autopsied cortices, positive correlation was observed among RP11-115D19.1 , SNCA and YY1 expression levels, suggesting their functional interactions in vivo . Knockdown of RP11-115D19.1 increased SNCA expression significantly in SH-SY5Y cells, suggesting its repressive effect on SNCA expression. Our findings of the protective allele-specific YY1 and antisense ncRNA raised a novel possible mechanism to regulate SNCA expression.

  • YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression
    Journal of Human Genetics, 2013
    Co-Authors: Ikuko Mizuta, Kazuaki Takafuji, Yuko Ando, Wataru Satake, Motoi Kanagawa, Kazuhiro Kobayashi, Shushi Nagamori, Takayuki Shinohara, Mitsutoshi Yamamoto
    Abstract:

    YY1 binds to α-synuclein 3′-Flanking Region SNP and stimulates antisense noncoding RNA expression