The DLX1and DLX2 genes and susceptibility to autism spectrum disorders
An imbalance between excitation and inhibition in the cerebral cortex has been suggested as a possible etiology of autism. The DLX genes encode homeodomain-containing transcription factors controlling the generation of GABAergic cortical interneurons. The DLX1 and DLX2 genes lie head-to-head in 2q32...
Gespeichert in:
| Veröffentlicht in: | European journal of human genetics : EJHG 2009-02, Vol.17 (2), p.228-235 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 235 |
|---|---|
| container_issue | 2 |
| container_start_page | 228 |
| container_title | European journal of human genetics : EJHG |
| container_volume | 17 |
| creator | Liu, Xudong Novosedlik, Natalia Wang, Ami Hudson, Melissa L Cohen, Ira L Chudley, Albert E Forster-Gibson, Cynthia J Lewis, Suzanne M E Holden, Jeanette J A |
| description | An imbalance between excitation and inhibition in the cerebral cortex has been suggested as a possible etiology of autism. The
DLX
genes encode homeodomain-containing transcription factors controlling the generation of GABAergic cortical interneurons. The
DLX1
and
DLX2
genes lie head-to-head in 2q32, a region associated with autism susceptibility. We investigated 6 Tag SNPs within the
DLX1/2
genes in two cohorts of multiplex (MPX) and one of simplex (SPX) families for association with autism. Family-based association tests showed strong association with five of the SNPs. The common alleles of
rs743605
and
rs4519482
were significantly associated with autism (
P |
| doi_str_mv | 10.1038/ejhg.2008.148 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2986060</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1627726261</sourcerecordid><originalsourceid>FETCH-LOGICAL-c578t-ad222d7d802cf03f26f2a4178ca60202600288409e19ee3d74010a97568ca4993</originalsourceid><addsrcrecordid>eNqFkcuLFDEQxoMo7svjXqUR9NZj5TFJ-iIsq7srDHjZBW8hm66eydCPMdUt7H9vmhn2IYKnSqgfX31VH2PnHBYcpP2M2816IQDsgiv7ih1zZXS5VNK-zm_gtlSWyyN2QrQFyE3D37Ijbo2wupLH7Op2g8XX1U_u-3quolhjj1TMX5oo4G6M97GN40MxDoWfxkhdQTsMY5q6oo40pBoTnbE3jW8J3x3qKbu7-nZ7eVOuflx_v7xYlWFp7Fj6WghRm9qCCA3IRuhGeMWNDV6DAKEBhLUKKuQVoqyNAg6-MkudCVVV8pR92evupvsO64D9mHzrdil2Pj24wUf3stPHjVsPv52orAYNWeDTQSANvyak0XUxb9m2vsdhIqe1FTrP-y-Y3Rorpcrgh7_A7TClPl_BibyZ4rwyGSr3UEgDUcLm0TIHN-fo5hzdnKPLOWb-_fM9n-hDcBn4eAA8Bd82yfch0iMnOGgjYR682HOUW_0a05O7f0_-A47Ds9Y</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>217841197</pqid></control><display><type>article</type><title>The DLX1and DLX2 genes and susceptibility to autism spectrum disorders</title><source>MEDLINE</source><source>SpringerLink Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Liu, Xudong ; Novosedlik, Natalia ; Wang, Ami ; Hudson, Melissa L ; Cohen, Ira L ; Chudley, Albert E ; Forster-Gibson, Cynthia J ; Lewis, Suzanne M E ; Holden, Jeanette J A</creator><creatorcontrib>Liu, Xudong ; Novosedlik, Natalia ; Wang, Ami ; Hudson, Melissa L ; Cohen, Ira L ; Chudley, Albert E ; Forster-Gibson, Cynthia J ; Lewis, Suzanne M E ; Holden, Jeanette J A</creatorcontrib><description>An imbalance between excitation and inhibition in the cerebral cortex has been suggested as a possible etiology of autism. The
DLX
genes encode homeodomain-containing transcription factors controlling the generation of GABAergic cortical interneurons. The
DLX1
and
DLX2
genes lie head-to-head in 2q32, a region associated with autism susceptibility. We investigated 6 Tag SNPs within the
DLX1/2
genes in two cohorts of multiplex (MPX) and one of simplex (SPX) families for association with autism. Family-based association tests showed strong association with five of the SNPs. The common alleles of
rs743605
and
rs4519482
were significantly associated with autism (
P
<0.012) in the first sample of 138 MPX families, with the latter remaining significant after correction for multiple testing (
P
cor
=0.0046). Findings in a second sample of 169 MPX families not only confirmed the association at
rs4519482
(
P
=0.034) but also showed strong allelic association of the common alleles at
rs788172
,
rs788173
and
rs813720
(
P
cor
=0.0003–0.04). In the combined MPX families, the common alleles were all significantly associated with autism (
P
cor
=0.0005–0.016). The GGGTG haplotype was over transmitted in the two MPX cohorts and the combined samples [
P
cor
<0.05:
P
cor
=0.00007 for the combined MPX families, Odds Ratio: 1.75 (95% CI: 1.33–2.30)]. Further testing in 306 SPX families replicated the association at
rs4519482
(
P
=0.033) and the over transmission of the haplotype GGGTG (
P
=0.012) although
P
-values were not significant after correction for multiple testing. The findings support the presence of two functional polymorphisms, one in or near each of the
DLX
genes that increase susceptibility to, or cause, autism in MPX families where there is a greater genetic component for these conditions.</description><identifier>ISSN: 1018-4813</identifier><identifier>EISSN: 1476-5438</identifier><identifier>DOI: 10.1038/ejhg.2008.148</identifier><identifier>PMID: 18728693</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Alleles ; Autism ; Autistic Disorder - genetics ; Bioinformatics ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Brain research ; Child clinical studies ; Chromosome 2 ; Cohort Studies ; Cortex ; Cytogenetics ; Developmental disorders ; Epilepsy ; Etiology ; Family ; Fundamental and applied biological sciences. Psychology ; Gene Expression ; General aspects. Genetic counseling ; Genes ; Genetic Predisposition to Disease ; Genetics ; Genetics of eukaryotes. Biological and molecular evolution ; Haplotypes ; Homeobox ; Homeodomain Proteins - genetics ; Human Genetics ; Humans ; Hypotheses ; Infantile autism ; Interneurons ; Medical genetics ; Medical sciences ; Molecular and cellular biology ; Mutation ; Neurobiology ; Physiology ; Polymorphism, Single Nucleotide ; Psychiatry ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Single-nucleotide polymorphism ; Transcription factors ; Transcription Factors - genetics ; γ-Aminobutyric acid</subject><ispartof>European journal of human genetics : EJHG, 2009-02, Vol.17 (2), p.228-235</ispartof><rights>Springer Nature Switzerland AG 2009</rights><rights>2009 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Feb 2009</rights><rights>Copyright © 2009 Nature Publishing Group 2009 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c578t-ad222d7d802cf03f26f2a4178ca60202600288409e19ee3d74010a97568ca4993</citedby><cites>FETCH-LOGICAL-c578t-ad222d7d802cf03f26f2a4178ca60202600288409e19ee3d74010a97568ca4993</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2986060/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2986060/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21067307$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18728693$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Xudong</creatorcontrib><creatorcontrib>Novosedlik, Natalia</creatorcontrib><creatorcontrib>Wang, Ami</creatorcontrib><creatorcontrib>Hudson, Melissa L</creatorcontrib><creatorcontrib>Cohen, Ira L</creatorcontrib><creatorcontrib>Chudley, Albert E</creatorcontrib><creatorcontrib>Forster-Gibson, Cynthia J</creatorcontrib><creatorcontrib>Lewis, Suzanne M E</creatorcontrib><creatorcontrib>Holden, Jeanette J A</creatorcontrib><title>The DLX1and DLX2 genes and susceptibility to autism spectrum disorders</title><title>European journal of human genetics : EJHG</title><addtitle>Eur J Hum Genet</addtitle><addtitle>Eur J Hum Genet</addtitle><description>An imbalance between excitation and inhibition in the cerebral cortex has been suggested as a possible etiology of autism. The
DLX
genes encode homeodomain-containing transcription factors controlling the generation of GABAergic cortical interneurons. The
DLX1
and
DLX2
genes lie head-to-head in 2q32, a region associated with autism susceptibility. We investigated 6 Tag SNPs within the
DLX1/2
genes in two cohorts of multiplex (MPX) and one of simplex (SPX) families for association with autism. Family-based association tests showed strong association with five of the SNPs. The common alleles of
rs743605
and
rs4519482
were significantly associated with autism (
P
<0.012) in the first sample of 138 MPX families, with the latter remaining significant after correction for multiple testing (
P
cor
=0.0046). Findings in a second sample of 169 MPX families not only confirmed the association at
rs4519482
(
P
=0.034) but also showed strong allelic association of the common alleles at
rs788172
,
rs788173
and
rs813720
(
P
cor
=0.0003–0.04). In the combined MPX families, the common alleles were all significantly associated with autism (
P
cor
=0.0005–0.016). The GGGTG haplotype was over transmitted in the two MPX cohorts and the combined samples [
P
cor
<0.05:
P
cor
=0.00007 for the combined MPX families, Odds Ratio: 1.75 (95% CI: 1.33–2.30)]. Further testing in 306 SPX families replicated the association at
rs4519482
(
P
=0.033) and the over transmission of the haplotype GGGTG (
P
=0.012) although
P
-values were not significant after correction for multiple testing. The findings support the presence of two functional polymorphisms, one in or near each of the
DLX
genes that increase susceptibility to, or cause, autism in MPX families where there is a greater genetic component for these conditions.</description><subject>Alleles</subject><subject>Autism</subject><subject>Autistic Disorder - genetics</subject><subject>Bioinformatics</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain research</subject><subject>Child clinical studies</subject><subject>Chromosome 2</subject><subject>Cohort Studies</subject><subject>Cortex</subject><subject>Cytogenetics</subject><subject>Developmental disorders</subject><subject>Epilepsy</subject><subject>Etiology</subject><subject>Family</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression</subject><subject>General aspects. Genetic counseling</subject><subject>Genes</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetics</subject><subject>Genetics of eukaryotes. Biological and molecular evolution</subject><subject>Haplotypes</subject><subject>Homeobox</subject><subject>Homeodomain Proteins - genetics</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Infantile autism</subject><subject>Interneurons</subject><subject>Medical genetics</subject><subject>Medical sciences</subject><subject>Molecular and cellular biology</subject><subject>Mutation</subject><subject>Neurobiology</subject><subject>Physiology</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Psychiatry</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Single-nucleotide polymorphism</subject><subject>Transcription factors</subject><subject>Transcription Factors - genetics</subject><subject>γ-Aminobutyric acid</subject><issn>1018-4813</issn><issn>1476-5438</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkcuLFDEQxoMo7svjXqUR9NZj5TFJ-iIsq7srDHjZBW8hm66eydCPMdUt7H9vmhn2IYKnSqgfX31VH2PnHBYcpP2M2816IQDsgiv7ih1zZXS5VNK-zm_gtlSWyyN2QrQFyE3D37Ijbo2wupLH7Op2g8XX1U_u-3quolhjj1TMX5oo4G6M97GN40MxDoWfxkhdQTsMY5q6oo40pBoTnbE3jW8J3x3qKbu7-nZ7eVOuflx_v7xYlWFp7Fj6WghRm9qCCA3IRuhGeMWNDV6DAKEBhLUKKuQVoqyNAg6-MkudCVVV8pR92evupvsO64D9mHzrdil2Pj24wUf3stPHjVsPv52orAYNWeDTQSANvyak0XUxb9m2vsdhIqe1FTrP-y-Y3Rorpcrgh7_A7TClPl_BibyZ4rwyGSr3UEgDUcLm0TIHN-fo5hzdnKPLOWb-_fM9n-hDcBn4eAA8Bd82yfch0iMnOGgjYR682HOUW_0a05O7f0_-A47Ds9Y</recordid><startdate>20090201</startdate><enddate>20090201</enddate><creator>Liu, Xudong</creator><creator>Novosedlik, Natalia</creator><creator>Wang, Ami</creator><creator>Hudson, Melissa L</creator><creator>Cohen, Ira L</creator><creator>Chudley, Albert E</creator><creator>Forster-Gibson, Cynthia J</creator><creator>Lewis, Suzanne M E</creator><creator>Holden, Jeanette J A</creator><general>Springer International Publishing</general><general>Nature Publishing Group</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090201</creationdate><title>The DLX1and DLX2 genes and susceptibility to autism spectrum disorders</title><author>Liu, Xudong ; Novosedlik, Natalia ; Wang, Ami ; Hudson, Melissa L ; Cohen, Ira L ; Chudley, Albert E ; Forster-Gibson, Cynthia J ; Lewis, Suzanne M E ; Holden, Jeanette J A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c578t-ad222d7d802cf03f26f2a4178ca60202600288409e19ee3d74010a97568ca4993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Alleles</topic><topic>Autism</topic><topic>Autistic Disorder - genetics</topic><topic>Bioinformatics</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain research</topic><topic>Child clinical studies</topic><topic>Chromosome 2</topic><topic>Cohort Studies</topic><topic>Cortex</topic><topic>Cytogenetics</topic><topic>Developmental disorders</topic><topic>Epilepsy</topic><topic>Etiology</topic><topic>Family</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression</topic><topic>General aspects. Genetic counseling</topic><topic>Genes</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetics</topic><topic>Genetics of eukaryotes. Biological and molecular evolution</topic><topic>Haplotypes</topic><topic>Homeobox</topic><topic>Homeodomain Proteins - genetics</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Infantile autism</topic><topic>Interneurons</topic><topic>Medical genetics</topic><topic>Medical sciences</topic><topic>Molecular and cellular biology</topic><topic>Mutation</topic><topic>Neurobiology</topic><topic>Physiology</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Psychiatry</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Single-nucleotide polymorphism</topic><topic>Transcription factors</topic><topic>Transcription Factors - genetics</topic><topic>γ-Aminobutyric acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Xudong</creatorcontrib><creatorcontrib>Novosedlik, Natalia</creatorcontrib><creatorcontrib>Wang, Ami</creatorcontrib><creatorcontrib>Hudson, Melissa L</creatorcontrib><creatorcontrib>Cohen, Ira L</creatorcontrib><creatorcontrib>Chudley, Albert E</creatorcontrib><creatorcontrib>Forster-Gibson, Cynthia J</creatorcontrib><creatorcontrib>Lewis, Suzanne M E</creatorcontrib><creatorcontrib>Holden, Jeanette J A</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>European journal of human genetics : EJHG</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Xudong</au><au>Novosedlik, Natalia</au><au>Wang, Ami</au><au>Hudson, Melissa L</au><au>Cohen, Ira L</au><au>Chudley, Albert E</au><au>Forster-Gibson, Cynthia J</au><au>Lewis, Suzanne M E</au><au>Holden, Jeanette J A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The DLX1and DLX2 genes and susceptibility to autism spectrum disorders</atitle><jtitle>European journal of human genetics : EJHG</jtitle><stitle>Eur J Hum Genet</stitle><addtitle>Eur J Hum Genet</addtitle><date>2009-02-01</date><risdate>2009</risdate><volume>17</volume><issue>2</issue><spage>228</spage><epage>235</epage><pages>228-235</pages><issn>1018-4813</issn><eissn>1476-5438</eissn><abstract>An imbalance between excitation and inhibition in the cerebral cortex has been suggested as a possible etiology of autism. The
DLX
genes encode homeodomain-containing transcription factors controlling the generation of GABAergic cortical interneurons. The
DLX1
and
DLX2
genes lie head-to-head in 2q32, a region associated with autism susceptibility. We investigated 6 Tag SNPs within the
DLX1/2
genes in two cohorts of multiplex (MPX) and one of simplex (SPX) families for association with autism. Family-based association tests showed strong association with five of the SNPs. The common alleles of
rs743605
and
rs4519482
were significantly associated with autism (
P
<0.012) in the first sample of 138 MPX families, with the latter remaining significant after correction for multiple testing (
P
cor
=0.0046). Findings in a second sample of 169 MPX families not only confirmed the association at
rs4519482
(
P
=0.034) but also showed strong allelic association of the common alleles at
rs788172
,
rs788173
and
rs813720
(
P
cor
=0.0003–0.04). In the combined MPX families, the common alleles were all significantly associated with autism (
P
cor
=0.0005–0.016). The GGGTG haplotype was over transmitted in the two MPX cohorts and the combined samples [
P
cor
<0.05:
P
cor
=0.00007 for the combined MPX families, Odds Ratio: 1.75 (95% CI: 1.33–2.30)]. Further testing in 306 SPX families replicated the association at
rs4519482
(
P
=0.033) and the over transmission of the haplotype GGGTG (
P
=0.012) although
P
-values were not significant after correction for multiple testing. The findings support the presence of two functional polymorphisms, one in or near each of the
DLX
genes that increase susceptibility to, or cause, autism in MPX families where there is a greater genetic component for these conditions.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>18728693</pmid><doi>10.1038/ejhg.2008.148</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1018-4813 |
| ispartof | European journal of human genetics : EJHG, 2009-02, Vol.17 (2), p.228-235 |
| issn | 1018-4813 1476-5438 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2986060 |
| source | MEDLINE; SpringerLink Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Alleles Autism Autistic Disorder - genetics Bioinformatics Biological and medical sciences Biomedical and Life Sciences Biomedicine Brain research Child clinical studies Chromosome 2 Cohort Studies Cortex Cytogenetics Developmental disorders Epilepsy Etiology Family Fundamental and applied biological sciences. Psychology Gene Expression General aspects. Genetic counseling Genes Genetic Predisposition to Disease Genetics Genetics of eukaryotes. Biological and molecular evolution Haplotypes Homeobox Homeodomain Proteins - genetics Human Genetics Humans Hypotheses Infantile autism Interneurons Medical genetics Medical sciences Molecular and cellular biology Mutation Neurobiology Physiology Polymorphism, Single Nucleotide Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Single-nucleotide polymorphism Transcription factors Transcription Factors - genetics γ-Aminobutyric acid |
| title | The DLX1and DLX2 genes and susceptibility to autism spectrum disorders |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T05%3A23%3A43IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20DLX1and%20DLX2%20genes%20and%20susceptibility%20to%20autism%20spectrum%20disorders&rft.jtitle=European%20journal%20of%20human%20genetics%20:%20EJHG&rft.au=Liu,%20Xudong&rft.date=2009-02-01&rft.volume=17&rft.issue=2&rft.spage=228&rft.epage=235&rft.pages=228-235&rft.issn=1018-4813&rft.eissn=1476-5438&rft_id=info:doi/10.1038/ejhg.2008.148&rft_dat=%3Cproquest_pubme%3E1627726261%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=217841197&rft_id=info:pmid/18728693&rfr_iscdi=true |