A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis

Background The genetic background to bipolar disorder (BPD) has been attributed to different genetic and genomic risk factors. In the present study we hypothesized that inherited copy number variations (CNVs) contribute to susceptibility of BPD. We screened 637 BP-pedigrees from the NIMH Genetic Ini...
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Autor*in:	Lekman, Magnus [verfasserIn] Karlsson, Robert Graae, Lisette Hössjer, Ola Kockum, Ingrid

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Schlagwörter:	Bipolar disorder Genome-wide Linkage analysis Copy number variation

Anmerkung:	© Lekman et al. 2015

Übergeordnetes Werk:	Enthalten in: BioData Mining - London : BioMed Central, 2008, 8(2015), 1 vom: 18. Dez.
Übergeordnetes Werk:	volume:8 ; year:2015 ; number:1 ; day:18 ; month:12

Links:	Volltext

DOI / URN:	10.1186/s13040-015-0076-y

Katalog-ID:	SPR029587271

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520			\|a Background The genetic background to bipolar disorder (BPD) has been attributed to different genetic and genomic risk factors. In the present study we hypothesized that inherited copy number variations (CNVs) contribute to susceptibility of BPD. We screened 637 BP-pedigrees from the NIMH Genetic Initiative and gave priority to 46 pedigrees. In this subsample we performed parametric and non-parametric genome-wide linkage analyses using ~21,000 SNP-markers. We developed an algorithm to test for linkage restricted to regions with CNVs that are shared within and across families. Results For the combined CNV and linkage analysis, one region on 19q13 survived correction for multiple comparisons and replicates a previous BPD risk locus. The shared CNV map to the pregnancy-specific glycoprotein (PSG) gene, a gene-family not previously implicated in BPD etiology. Two SNPs in the shared CNV are likely transcription factor binding sites and are linked to expression of an F-box binding gene, a key regulator of neuronal pathways suggested to be involved in BPD etiology. Conclusions Our CNV-weighted linkage approach identifies a risk locus for BPD on 19q13 and forms a useful tool to future studies to unravel part of the genetic vulnerability to BPD.
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allfields	10.1186/s13040-015-0076-y doi (DE-627)SPR029587271 (SPR)s13040-015-0076-y-e DE-627 ger DE-627 rakwb eng Lekman, Magnus verfasserin aut A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Lekman et al. 2015 Background The genetic background to bipolar disorder (BPD) has been attributed to different genetic and genomic risk factors. In the present study we hypothesized that inherited copy number variations (CNVs) contribute to susceptibility of BPD. We screened 637 BP-pedigrees from the NIMH Genetic Initiative and gave priority to 46 pedigrees. In this subsample we performed parametric and non-parametric genome-wide linkage analyses using ~21,000 SNP-markers. We developed an algorithm to test for linkage restricted to regions with CNVs that are shared within and across families. Results For the combined CNV and linkage analysis, one region on 19q13 survived correction for multiple comparisons and replicates a previous BPD risk locus. The shared CNV map to the pregnancy-specific glycoprotein (PSG) gene, a gene-family not previously implicated in BPD etiology. Two SNPs in the shared CNV are likely transcription factor binding sites and are linked to expression of an F-box binding gene, a key regulator of neuronal pathways suggested to be involved in BPD etiology. Conclusions Our CNV-weighted linkage approach identifies a risk locus for BPD on 19q13 and forms a useful tool to future studies to unravel part of the genetic vulnerability to BPD. Bipolar disorder (dpeaa)DE-He213 Genome-wide (dpeaa)DE-He213 Linkage analysis (dpeaa)DE-He213 Copy number variation (dpeaa)DE-He213 Karlsson, Robert aut Graae, Lisette aut Hössjer, Ola aut Kockum, Ingrid aut Enthalten in BioData Mining London : BioMed Central, 2008 8(2015), 1 vom: 18. Dez. (DE-627)572421893 (DE-600)2438773-3 1756-0381 nnns volume:8 year:2015 number:1 day:18 month:12 https://dx.doi.org/10.1186/s13040-015-0076-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2015 1 18 12
spelling	10.1186/s13040-015-0076-y doi (DE-627)SPR029587271 (SPR)s13040-015-0076-y-e DE-627 ger DE-627 rakwb eng Lekman, Magnus verfasserin aut A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Lekman et al. 2015 Background The genetic background to bipolar disorder (BPD) has been attributed to different genetic and genomic risk factors. In the present study we hypothesized that inherited copy number variations (CNVs) contribute to susceptibility of BPD. We screened 637 BP-pedigrees from the NIMH Genetic Initiative and gave priority to 46 pedigrees. In this subsample we performed parametric and non-parametric genome-wide linkage analyses using ~21,000 SNP-markers. We developed an algorithm to test for linkage restricted to regions with CNVs that are shared within and across families. Results For the combined CNV and linkage analysis, one region on 19q13 survived correction for multiple comparisons and replicates a previous BPD risk locus. The shared CNV map to the pregnancy-specific glycoprotein (PSG) gene, a gene-family not previously implicated in BPD etiology. Two SNPs in the shared CNV are likely transcription factor binding sites and are linked to expression of an F-box binding gene, a key regulator of neuronal pathways suggested to be involved in BPD etiology. Conclusions Our CNV-weighted linkage approach identifies a risk locus for BPD on 19q13 and forms a useful tool to future studies to unravel part of the genetic vulnerability to BPD. Bipolar disorder (dpeaa)DE-He213 Genome-wide (dpeaa)DE-He213 Linkage analysis (dpeaa)DE-He213 Copy number variation (dpeaa)DE-He213 Karlsson, Robert aut Graae, Lisette aut Hössjer, Ola aut Kockum, Ingrid aut Enthalten in BioData Mining London : BioMed Central, 2008 8(2015), 1 vom: 18. Dez. (DE-627)572421893 (DE-600)2438773-3 1756-0381 nnns volume:8 year:2015 number:1 day:18 month:12 https://dx.doi.org/10.1186/s13040-015-0076-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2015 1 18 12
allfields_unstemmed	10.1186/s13040-015-0076-y doi (DE-627)SPR029587271 (SPR)s13040-015-0076-y-e DE-627 ger DE-627 rakwb eng Lekman, Magnus verfasserin aut A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Lekman et al. 2015 Background The genetic background to bipolar disorder (BPD) has been attributed to different genetic and genomic risk factors. In the present study we hypothesized that inherited copy number variations (CNVs) contribute to susceptibility of BPD. We screened 637 BP-pedigrees from the NIMH Genetic Initiative and gave priority to 46 pedigrees. In this subsample we performed parametric and non-parametric genome-wide linkage analyses using ~21,000 SNP-markers. We developed an algorithm to test for linkage restricted to regions with CNVs that are shared within and across families. Results For the combined CNV and linkage analysis, one region on 19q13 survived correction for multiple comparisons and replicates a previous BPD risk locus. The shared CNV map to the pregnancy-specific glycoprotein (PSG) gene, a gene-family not previously implicated in BPD etiology. Two SNPs in the shared CNV are likely transcription factor binding sites and are linked to expression of an F-box binding gene, a key regulator of neuronal pathways suggested to be involved in BPD etiology. Conclusions Our CNV-weighted linkage approach identifies a risk locus for BPD on 19q13 and forms a useful tool to future studies to unravel part of the genetic vulnerability to BPD. Bipolar disorder (dpeaa)DE-He213 Genome-wide (dpeaa)DE-He213 Linkage analysis (dpeaa)DE-He213 Copy number variation (dpeaa)DE-He213 Karlsson, Robert aut Graae, Lisette aut Hössjer, Ola aut Kockum, Ingrid aut Enthalten in BioData Mining London : BioMed Central, 2008 8(2015), 1 vom: 18. Dez. (DE-627)572421893 (DE-600)2438773-3 1756-0381 nnns volume:8 year:2015 number:1 day:18 month:12 https://dx.doi.org/10.1186/s13040-015-0076-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2015 1 18 12
allfieldsGer	10.1186/s13040-015-0076-y doi (DE-627)SPR029587271 (SPR)s13040-015-0076-y-e DE-627 ger DE-627 rakwb eng Lekman, Magnus verfasserin aut A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Lekman et al. 2015 Background The genetic background to bipolar disorder (BPD) has been attributed to different genetic and genomic risk factors. In the present study we hypothesized that inherited copy number variations (CNVs) contribute to susceptibility of BPD. We screened 637 BP-pedigrees from the NIMH Genetic Initiative and gave priority to 46 pedigrees. In this subsample we performed parametric and non-parametric genome-wide linkage analyses using ~21,000 SNP-markers. We developed an algorithm to test for linkage restricted to regions with CNVs that are shared within and across families. Results For the combined CNV and linkage analysis, one region on 19q13 survived correction for multiple comparisons and replicates a previous BPD risk locus. The shared CNV map to the pregnancy-specific glycoprotein (PSG) gene, a gene-family not previously implicated in BPD etiology. Two SNPs in the shared CNV are likely transcription factor binding sites and are linked to expression of an F-box binding gene, a key regulator of neuronal pathways suggested to be involved in BPD etiology. Conclusions Our CNV-weighted linkage approach identifies a risk locus for BPD on 19q13 and forms a useful tool to future studies to unravel part of the genetic vulnerability to BPD. Bipolar disorder (dpeaa)DE-He213 Genome-wide (dpeaa)DE-He213 Linkage analysis (dpeaa)DE-He213 Copy number variation (dpeaa)DE-He213 Karlsson, Robert aut Graae, Lisette aut Hössjer, Ola aut Kockum, Ingrid aut Enthalten in BioData Mining London : BioMed Central, 2008 8(2015), 1 vom: 18. Dez. (DE-627)572421893 (DE-600)2438773-3 1756-0381 nnns volume:8 year:2015 number:1 day:18 month:12 https://dx.doi.org/10.1186/s13040-015-0076-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2015 1 18 12
allfieldsSound	10.1186/s13040-015-0076-y doi (DE-627)SPR029587271 (SPR)s13040-015-0076-y-e DE-627 ger DE-627 rakwb eng Lekman, Magnus verfasserin aut A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Lekman et al. 2015 Background The genetic background to bipolar disorder (BPD) has been attributed to different genetic and genomic risk factors. In the present study we hypothesized that inherited copy number variations (CNVs) contribute to susceptibility of BPD. We screened 637 BP-pedigrees from the NIMH Genetic Initiative and gave priority to 46 pedigrees. In this subsample we performed parametric and non-parametric genome-wide linkage analyses using ~21,000 SNP-markers. We developed an algorithm to test for linkage restricted to regions with CNVs that are shared within and across families. Results For the combined CNV and linkage analysis, one region on 19q13 survived correction for multiple comparisons and replicates a previous BPD risk locus. The shared CNV map to the pregnancy-specific glycoprotein (PSG) gene, a gene-family not previously implicated in BPD etiology. Two SNPs in the shared CNV are likely transcription factor binding sites and are linked to expression of an F-box binding gene, a key regulator of neuronal pathways suggested to be involved in BPD etiology. Conclusions Our CNV-weighted linkage approach identifies a risk locus for BPD on 19q13 and forms a useful tool to future studies to unravel part of the genetic vulnerability to BPD. Bipolar disorder (dpeaa)DE-He213 Genome-wide (dpeaa)DE-He213 Linkage analysis (dpeaa)DE-He213 Copy number variation (dpeaa)DE-He213 Karlsson, Robert aut Graae, Lisette aut Hössjer, Ola aut Kockum, Ingrid aut Enthalten in BioData Mining London : BioMed Central, 2008 8(2015), 1 vom: 18. Dez. (DE-627)572421893 (DE-600)2438773-3 1756-0381 nnns volume:8 year:2015 number:1 day:18 month:12 https://dx.doi.org/10.1186/s13040-015-0076-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2015 1 18 12
language	English
source	Enthalten in BioData Mining 8(2015), 1 vom: 18. Dez. volume:8 year:2015 number:1 day:18 month:12
sourceStr	Enthalten in BioData Mining 8(2015), 1 vom: 18. Dez. volume:8 year:2015 number:1 day:18 month:12
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Bipolar disorder Genome-wide Linkage analysis Copy number variation
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container_title	BioData Mining
authorswithroles_txt_mv	Lekman, Magnus @@aut@@ Karlsson, Robert @@aut@@ Graae, Lisette @@aut@@ Hössjer, Ola @@aut@@ Kockum, Ingrid @@aut@@
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author	Lekman, Magnus
spellingShingle	Lekman, Magnus misc Bipolar disorder misc Genome-wide misc Linkage analysis misc Copy number variation A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis
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topic_title	A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis Bipolar disorder (dpeaa)DE-He213 Genome-wide (dpeaa)DE-He213 Linkage analysis (dpeaa)DE-He213 Copy number variation (dpeaa)DE-He213
topic	misc Bipolar disorder misc Genome-wide misc Linkage analysis misc Copy number variation
topic_unstemmed	misc Bipolar disorder misc Genome-wide misc Linkage analysis misc Copy number variation
topic_browse	misc Bipolar disorder misc Genome-wide misc Linkage analysis misc Copy number variation
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title	A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis
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title_full	A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis
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author_browse	Lekman, Magnus Karlsson, Robert Graae, Lisette Hössjer, Ola Kockum, Ingrid
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author-letter	Lekman, Magnus
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title_sort	significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis
title_auth	A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis
abstract	Background The genetic background to bipolar disorder (BPD) has been attributed to different genetic and genomic risk factors. In the present study we hypothesized that inherited copy number variations (CNVs) contribute to susceptibility of BPD. We screened 637 BP-pedigrees from the NIMH Genetic Initiative and gave priority to 46 pedigrees. In this subsample we performed parametric and non-parametric genome-wide linkage analyses using ~21,000 SNP-markers. We developed an algorithm to test for linkage restricted to regions with CNVs that are shared within and across families. Results For the combined CNV and linkage analysis, one region on 19q13 survived correction for multiple comparisons and replicates a previous BPD risk locus. The shared CNV map to the pregnancy-specific glycoprotein (PSG) gene, a gene-family not previously implicated in BPD etiology. Two SNPs in the shared CNV are likely transcription factor binding sites and are linked to expression of an F-box binding gene, a key regulator of neuronal pathways suggested to be involved in BPD etiology. Conclusions Our CNV-weighted linkage approach identifies a risk locus for BPD on 19q13 and forms a useful tool to future studies to unravel part of the genetic vulnerability to BPD. © Lekman et al. 2015
abstractGer	Background The genetic background to bipolar disorder (BPD) has been attributed to different genetic and genomic risk factors. In the present study we hypothesized that inherited copy number variations (CNVs) contribute to susceptibility of BPD. We screened 637 BP-pedigrees from the NIMH Genetic Initiative and gave priority to 46 pedigrees. In this subsample we performed parametric and non-parametric genome-wide linkage analyses using ~21,000 SNP-markers. We developed an algorithm to test for linkage restricted to regions with CNVs that are shared within and across families. Results For the combined CNV and linkage analysis, one region on 19q13 survived correction for multiple comparisons and replicates a previous BPD risk locus. The shared CNV map to the pregnancy-specific glycoprotein (PSG) gene, a gene-family not previously implicated in BPD etiology. Two SNPs in the shared CNV are likely transcription factor binding sites and are linked to expression of an F-box binding gene, a key regulator of neuronal pathways suggested to be involved in BPD etiology. Conclusions Our CNV-weighted linkage approach identifies a risk locus for BPD on 19q13 and forms a useful tool to future studies to unravel part of the genetic vulnerability to BPD. © Lekman et al. 2015
abstract_unstemmed	Background The genetic background to bipolar disorder (BPD) has been attributed to different genetic and genomic risk factors. In the present study we hypothesized that inherited copy number variations (CNVs) contribute to susceptibility of BPD. We screened 637 BP-pedigrees from the NIMH Genetic Initiative and gave priority to 46 pedigrees. In this subsample we performed parametric and non-parametric genome-wide linkage analyses using ~21,000 SNP-markers. We developed an algorithm to test for linkage restricted to regions with CNVs that are shared within and across families. Results For the combined CNV and linkage analysis, one region on 19q13 survived correction for multiple comparisons and replicates a previous BPD risk locus. The shared CNV map to the pregnancy-specific glycoprotein (PSG) gene, a gene-family not previously implicated in BPD etiology. Two SNPs in the shared CNV are likely transcription factor binding sites and are linked to expression of an F-box binding gene, a key regulator of neuronal pathways suggested to be involved in BPD etiology. Conclusions Our CNV-weighted linkage approach identifies a risk locus for BPD on 19q13 and forms a useful tool to future studies to unravel part of the genetic vulnerability to BPD. © Lekman et al. 2015
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title_short	A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis
url	https://dx.doi.org/10.1186/s13040-015-0076-y
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author2	Karlsson, Robert Graae, Lisette Hössjer, Ola Kockum, Ingrid
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up_date	2024-07-04T01:35:34.470Z
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A significant risk locus on 19q13 for bipolar disorder identified using a combined genome-wide linkage and copy number variation analysis

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