The Experts below are selected from a list of 948 Experts worldwide ranked by ideXlab platform
Michel Simonneau - One of the best experts on this subject based on the ideXlab platform.
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p 698 analysis of smarca2 and genes encoding interactors of swi snf smarca2 BRM Protein in schizophrenia patients from an algerian trio cohort
European Psychiatry, 2012Co-Authors: D Benmessaoud, A M L Bestel, M Delepine, J Hager, J M Moalic, P Gorwood, F Kacha, Michel SimonneauAbstract:The genetic architecture of schizophrenia (SZ) is based on common variants identified by Genome Wide Association Studies (GWIS) and on rare variants. We found that the SZ-GWIS genes are part of an interacting network centered on SMARCA2 (Loe-Mie et al., HMG, 2010). Both rare and common variants have been identified in SMARCA2 gene (Koga et al., HMG, 2009; Walsh et al., Science, 2008). Taking advantage of an Algerian trio cohort of one hundred SZ patients (Benmessaoud et al., BMC Psychiatry, 2008), we replicated the association of SNP rs2296212 localized in exon 33, resulting in D1546E amino acid change. We found that exon 33 displays a signature of positive evolution in the primate lineage, with an excess of rare variants in SZ-patients compared to their parents (p = 0.038, Fisher test) and a higher proportion of rare variants in the primate-accelerated exons compared with the non-evolutionary exon in SZ-patients (p = 0.032, Fisher test). As SMARCA2/BRM Protein is part of a large SWI/SNF Protein complex involved in epigenetics regulation of synaptic plasticity (Lepagnol-Bestel et al., in preparation), this raises the question of possible rare variants in SMARCA2 gene and in genes encoding SMARCA2/BRM interactors, in particular for those displaying a signature of primate-accelerated evolution. A total of 17 genes have been selected: MEECP2, SMARCA2, DNMT1, SMARCA4, SMARCE1, EHMT2, SMARCC1, HDAC2, SIN3A, RCOR2, CSF2RA, TCF4, PGBD1, RBM9, UTP11L, DDX5, EWRS1. The sequencing data obtained from Roche 454 device will be presented. Altogether, these results are expected to give new insights into the genetic architecture of SZ.
Joshua D Liao - One of the best experts on this subject based on the ideXlab platform.
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Journal of Cancer Complex Alternative Splicing of the Smarca2 Gene Suggests the Importance of Smarca2-B Variants
2013Co-Authors: Min Yang, Yuan Sun, Chenguang Wang, Joshua D LiaoAbstract:licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. Received: 2011.04.11; Accepted: 2011.06.22; Published: 2011.07.06 BRM is an ATPase component of the SWI/SNF complex that regulates chromatin remodeling and cell proliferation and is considered a tumor suppressor. In this study we characterized transcripts from the Smarca2 gene that encodes the BRM Protein. We found that the human Smarca2 gene (hSmarca2), like its mouse counterpart (mSmarca2), also initiated a short transcript from intron 27 of the long transcript. We name the long and short transcripts as Smarca2-a and Smarca2-b, respectively. Like its human counterpart, mSmarca2-a also underwent alternative splicing at the 54-bp exon 29. The hSmarca2-b had two alternative initiation sites and underwent alternative splicing at three different 3 ’ sites of exon 1 and at exons 2, 3 and/or 5. We identified nine hSmarca2-b mRNA variants that might produce five different Proteins. mSmarca2-b also underwent alternative splicing at exon 3 and/or exon 5, besides alternatively retaining part of intron 1 in exon 1. Smarca2-b was expressed more abundantly than Smarca2-a in many cell lines and wa
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complex alternative splicing of the smarca2 gene suggests the importance of smarca2 b variants
Journal of Cancer, 2011Co-Authors: Min Yang, Yuan Sun, Chenguang Wang, Joshua D LiaoAbstract:BRM is an ATPase component of the SWI/SNF complex that regulates chromatin remodeling and cell proliferation and is considered a tumor suppressor. In this study we characterized transcripts from the Smarca2 gene that encodes the BRM Protein. We found that the human Smarca2 gene (hSmarca2), like its mouse counterpart (mSmarca2), also initiated a short transcript from intron 27 of the long transcript. We name the long and short transcripts as Smarca2-a and Smarca2-b, respectively. Like its human counterpart, mSmarca2-a also underwent alternative splicing at the 54-bp exon 29. The hSmarca2-b had two alternative initiation sites and underwent alternative splicing at three different 3’ sites of exon 1 and at exons 2, 3 and/or 5. We identified nine hSmarca2-b mRNA variants that might produce five different Proteins. mSmarca2-b also underwent alternative splicing at exon 3 and/or exon 5, besides alternatively retaining part of intron 1 in exon 1. Smarca2-b was expressed more abundantly than Smarca2-a in many cell lines and was more sensitive to serum starvation. Moreover, cyclin D1 also regulated the expression of both Smarca2-a and Smarca2-b in a complex manner. These data suggest that the functions of the Smarca2 gene may be very complex, not just simply inhibiting cell proliferation, and in certain situations may be elicited mainly by expressing the much less known Smarca2-b, not the better studied Smarca2-a and its products BRM Proteins.
D Benmessaoud - One of the best experts on this subject based on the ideXlab platform.
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p 698 analysis of smarca2 and genes encoding interactors of swi snf smarca2 BRM Protein in schizophrenia patients from an algerian trio cohort
European Psychiatry, 2012Co-Authors: D Benmessaoud, A M L Bestel, M Delepine, J Hager, J M Moalic, P Gorwood, F Kacha, Michel SimonneauAbstract:The genetic architecture of schizophrenia (SZ) is based on common variants identified by Genome Wide Association Studies (GWIS) and on rare variants. We found that the SZ-GWIS genes are part of an interacting network centered on SMARCA2 (Loe-Mie et al., HMG, 2010). Both rare and common variants have been identified in SMARCA2 gene (Koga et al., HMG, 2009; Walsh et al., Science, 2008). Taking advantage of an Algerian trio cohort of one hundred SZ patients (Benmessaoud et al., BMC Psychiatry, 2008), we replicated the association of SNP rs2296212 localized in exon 33, resulting in D1546E amino acid change. We found that exon 33 displays a signature of positive evolution in the primate lineage, with an excess of rare variants in SZ-patients compared to their parents (p = 0.038, Fisher test) and a higher proportion of rare variants in the primate-accelerated exons compared with the non-evolutionary exon in SZ-patients (p = 0.032, Fisher test). As SMARCA2/BRM Protein is part of a large SWI/SNF Protein complex involved in epigenetics regulation of synaptic plasticity (Lepagnol-Bestel et al., in preparation), this raises the question of possible rare variants in SMARCA2 gene and in genes encoding SMARCA2/BRM interactors, in particular for those displaying a signature of primate-accelerated evolution. A total of 17 genes have been selected: MEECP2, SMARCA2, DNMT1, SMARCA4, SMARCE1, EHMT2, SMARCC1, HDAC2, SIN3A, RCOR2, CSF2RA, TCF4, PGBD1, RBM9, UTP11L, DDX5, EWRS1. The sequencing data obtained from Roche 454 device will be presented. Altogether, these results are expected to give new insights into the genetic architecture of SZ.
Min Yang - One of the best experts on this subject based on the ideXlab platform.
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Journal of Cancer Complex Alternative Splicing of the Smarca2 Gene Suggests the Importance of Smarca2-B Variants
2013Co-Authors: Min Yang, Yuan Sun, Chenguang Wang, Joshua D LiaoAbstract:licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. Received: 2011.04.11; Accepted: 2011.06.22; Published: 2011.07.06 BRM is an ATPase component of the SWI/SNF complex that regulates chromatin remodeling and cell proliferation and is considered a tumor suppressor. In this study we characterized transcripts from the Smarca2 gene that encodes the BRM Protein. We found that the human Smarca2 gene (hSmarca2), like its mouse counterpart (mSmarca2), also initiated a short transcript from intron 27 of the long transcript. We name the long and short transcripts as Smarca2-a and Smarca2-b, respectively. Like its human counterpart, mSmarca2-a also underwent alternative splicing at the 54-bp exon 29. The hSmarca2-b had two alternative initiation sites and underwent alternative splicing at three different 3 ’ sites of exon 1 and at exons 2, 3 and/or 5. We identified nine hSmarca2-b mRNA variants that might produce five different Proteins. mSmarca2-b also underwent alternative splicing at exon 3 and/or exon 5, besides alternatively retaining part of intron 1 in exon 1. Smarca2-b was expressed more abundantly than Smarca2-a in many cell lines and wa
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complex alternative splicing of the smarca2 gene suggests the importance of smarca2 b variants
Journal of Cancer, 2011Co-Authors: Min Yang, Yuan Sun, Chenguang Wang, Joshua D LiaoAbstract:BRM is an ATPase component of the SWI/SNF complex that regulates chromatin remodeling and cell proliferation and is considered a tumor suppressor. In this study we characterized transcripts from the Smarca2 gene that encodes the BRM Protein. We found that the human Smarca2 gene (hSmarca2), like its mouse counterpart (mSmarca2), also initiated a short transcript from intron 27 of the long transcript. We name the long and short transcripts as Smarca2-a and Smarca2-b, respectively. Like its human counterpart, mSmarca2-a also underwent alternative splicing at the 54-bp exon 29. The hSmarca2-b had two alternative initiation sites and underwent alternative splicing at three different 3’ sites of exon 1 and at exons 2, 3 and/or 5. We identified nine hSmarca2-b mRNA variants that might produce five different Proteins. mSmarca2-b also underwent alternative splicing at exon 3 and/or exon 5, besides alternatively retaining part of intron 1 in exon 1. Smarca2-b was expressed more abundantly than Smarca2-a in many cell lines and was more sensitive to serum starvation. Moreover, cyclin D1 also regulated the expression of both Smarca2-a and Smarca2-b in a complex manner. These data suggest that the functions of the Smarca2 gene may be very complex, not just simply inhibiting cell proliferation, and in certain situations may be elicited mainly by expressing the much less known Smarca2-b, not the better studied Smarca2-a and its products BRM Proteins.
J Hager - One of the best experts on this subject based on the ideXlab platform.
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p 698 analysis of smarca2 and genes encoding interactors of swi snf smarca2 BRM Protein in schizophrenia patients from an algerian trio cohort
European Psychiatry, 2012Co-Authors: D Benmessaoud, A M L Bestel, M Delepine, J Hager, J M Moalic, P Gorwood, F Kacha, Michel SimonneauAbstract:The genetic architecture of schizophrenia (SZ) is based on common variants identified by Genome Wide Association Studies (GWIS) and on rare variants. We found that the SZ-GWIS genes are part of an interacting network centered on SMARCA2 (Loe-Mie et al., HMG, 2010). Both rare and common variants have been identified in SMARCA2 gene (Koga et al., HMG, 2009; Walsh et al., Science, 2008). Taking advantage of an Algerian trio cohort of one hundred SZ patients (Benmessaoud et al., BMC Psychiatry, 2008), we replicated the association of SNP rs2296212 localized in exon 33, resulting in D1546E amino acid change. We found that exon 33 displays a signature of positive evolution in the primate lineage, with an excess of rare variants in SZ-patients compared to their parents (p = 0.038, Fisher test) and a higher proportion of rare variants in the primate-accelerated exons compared with the non-evolutionary exon in SZ-patients (p = 0.032, Fisher test). As SMARCA2/BRM Protein is part of a large SWI/SNF Protein complex involved in epigenetics regulation of synaptic plasticity (Lepagnol-Bestel et al., in preparation), this raises the question of possible rare variants in SMARCA2 gene and in genes encoding SMARCA2/BRM interactors, in particular for those displaying a signature of primate-accelerated evolution. A total of 17 genes have been selected: MEECP2, SMARCA2, DNMT1, SMARCA4, SMARCE1, EHMT2, SMARCC1, HDAC2, SIN3A, RCOR2, CSF2RA, TCF4, PGBD1, RBM9, UTP11L, DDX5, EWRS1. The sequencing data obtained from Roche 454 device will be presented. Altogether, these results are expected to give new insights into the genetic architecture of SZ.