Genetic Variation in the Promoter Region of Chitinase 3-Like 1 Is Associated with Atopy
Atopy or atopic syndrome is an allergic hypersensitivity subject to hereditary influences. Aberrant expression of chitinase 3-like 1 (CHI3L1), also known as YKL-40 or HC gp-39, is involved in the pathogenesis of inflammatory and allergic diseases. The genetic contribution of CHI3L1 gene to atopic su...
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| Veröffentlicht in: | American journal of respiratory and critical care medicine 2009-03, Vol.179 (6), p.449-456 |
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| creator | Sohn, Myung Hyun Lee, Ji Hyun Kim, Kyung Won Kim, So Won Lee, Sung Hee Kim, Kyu-Earn Kim, Kyung Hwan Lee, Chun Geun Elias, Jack A Lee, Min Goo |
| description | Atopy or atopic syndrome is an allergic hypersensitivity subject to hereditary influences. Aberrant expression of chitinase 3-like 1 (CHI3L1), also known as YKL-40 or HC gp-39, is involved in the pathogenesis of inflammatory and allergic diseases.
The genetic contribution of CHI3L1 gene to atopic susceptibility was investigated using an integrated population genetic and molecular analysis.
Genetic variations in CHI3L1 were identified and genotyped in 295 unrelated patients with atopy and 180 control subjects. Serum YKL-40 and IgE levels were analyzed according to genotype. The effects of a promoter polymorphism (g.-247C/T) on promoter activity were examined in reporter and protein binding assays.
In the case-control association analysis, the g.-247C/T polymorphism at the promoter region (rs10399805; P = 0.0062) and the IVS7+82C/T polymorphism at intron 7 (rs2275353; P = 0.0056) of CHI3L1 showed a significant association with atopy. Subjects with the g.-247T risk allele had significantly higher serum YKL-40 (P < 0.0001) and IgE (P = 0.012) levels. An in vitro promoter assay using THP-1 human monocyte cells revealed that the C to T conversion at g.-247 induced a more than twofold increase of reporter gene expression. Moreover, the g.-247T allele showed an increased affinity for CCAAT enhancer-binding protein, a well known transcriptional activator, by electrophoretic mobility shift assay. Accordingly, subjects with the g.-247TT genotype showed a 2.5-fold increase in CHI3L1 mRNA expression in peripheral blood cells compared with those with the g.-247CC genotype.
These results strongly suggest that the g.-247C/T polymorphism in the CHI3L1 promoter region is associated with the risk of atopy. |
| doi_str_mv | 10.1164/rccm.200809-1422OC |
| format | Article |
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The genetic contribution of CHI3L1 gene to atopic susceptibility was investigated using an integrated population genetic and molecular analysis.
Genetic variations in CHI3L1 were identified and genotyped in 295 unrelated patients with atopy and 180 control subjects. Serum YKL-40 and IgE levels were analyzed according to genotype. The effects of a promoter polymorphism (g.-247C/T) on promoter activity were examined in reporter and protein binding assays.
In the case-control association analysis, the g.-247C/T polymorphism at the promoter region (rs10399805; P = 0.0062) and the IVS7+82C/T polymorphism at intron 7 (rs2275353; P = 0.0056) of CHI3L1 showed a significant association with atopy. Subjects with the g.-247T risk allele had significantly higher serum YKL-40 (P < 0.0001) and IgE (P = 0.012) levels. An in vitro promoter assay using THP-1 human monocyte cells revealed that the C to T conversion at g.-247 induced a more than twofold increase of reporter gene expression. Moreover, the g.-247T allele showed an increased affinity for CCAAT enhancer-binding protein, a well known transcriptional activator, by electrophoretic mobility shift assay. Accordingly, subjects with the g.-247TT genotype showed a 2.5-fold increase in CHI3L1 mRNA expression in peripheral blood cells compared with those with the g.-247CC genotype.
These results strongly suggest that the g.-247C/T polymorphism in the CHI3L1 promoter region is associated with the risk of atopy.</description><identifier>ISSN: 1073-449X</identifier><identifier>EISSN: 1535-4970</identifier><identifier>DOI: 10.1164/rccm.200809-1422OC</identifier><identifier>PMID: 19106306</identifier><language>eng</language><publisher>New York, NY: Am Thoracic Soc</publisher><subject>Adipokines ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Asthma ; Biological and medical sciences ; Case-Control Studies ; CCAAT-Enhancer-Binding Proteins ; Child ; Chitinase ; Chitinase-3-Like Protein 1 ; Digestive system ; Electrophoretic Mobility Shift Assay ; Female ; Genotype ; Genotype & phenotype ; Glycoproteins ; Glycoproteins - blood ; Glycoproteins - genetics ; Haplotypes ; Humans ; Hypersensitivity, Immediate - genetics ; Immunoglobulin E - blood ; Intensive care medicine ; Investigative techniques, diagnostic techniques (general aspects) ; Korea ; Lectins ; Male ; Medical sciences ; Pathogenesis ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Polymerase Chain Reaction ; Polymorphism ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; Proteins ; Risk Factors ; RNA, Messenger - metabolism ; Skin</subject><ispartof>American journal of respiratory and critical care medicine, 2009-03, Vol.179 (6), p.449-456</ispartof><rights>2009 INIST-CNRS</rights><rights>Copyright American Thoracic Society Mar 15, 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-1077e968d4f165ae73f2e09d1fb8790cb3332aba37a7cc8e0fd1c3b1b900434b3</citedby><cites>FETCH-LOGICAL-c423t-1077e968d4f165ae73f2e09d1fb8790cb3332aba37a7cc8e0fd1c3b1b900434b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4023,4024,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21253251$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19106306$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sohn, Myung Hyun</creatorcontrib><creatorcontrib>Lee, Ji Hyun</creatorcontrib><creatorcontrib>Kim, Kyung Won</creatorcontrib><creatorcontrib>Kim, So Won</creatorcontrib><creatorcontrib>Lee, Sung Hee</creatorcontrib><creatorcontrib>Kim, Kyu-Earn</creatorcontrib><creatorcontrib>Kim, Kyung Hwan</creatorcontrib><creatorcontrib>Lee, Chun Geun</creatorcontrib><creatorcontrib>Elias, Jack A</creatorcontrib><creatorcontrib>Lee, Min Goo</creatorcontrib><title>Genetic Variation in the Promoter Region of Chitinase 3-Like 1 Is Associated with Atopy</title><title>American journal of respiratory and critical care medicine</title><addtitle>Am J Respir Crit Care Med</addtitle><description>Atopy or atopic syndrome is an allergic hypersensitivity subject to hereditary influences. Aberrant expression of chitinase 3-like 1 (CHI3L1), also known as YKL-40 or HC gp-39, is involved in the pathogenesis of inflammatory and allergic diseases.
The genetic contribution of CHI3L1 gene to atopic susceptibility was investigated using an integrated population genetic and molecular analysis.
Genetic variations in CHI3L1 were identified and genotyped in 295 unrelated patients with atopy and 180 control subjects. Serum YKL-40 and IgE levels were analyzed according to genotype. The effects of a promoter polymorphism (g.-247C/T) on promoter activity were examined in reporter and protein binding assays.
In the case-control association analysis, the g.-247C/T polymorphism at the promoter region (rs10399805; P = 0.0062) and the IVS7+82C/T polymorphism at intron 7 (rs2275353; P = 0.0056) of CHI3L1 showed a significant association with atopy. Subjects with the g.-247T risk allele had significantly higher serum YKL-40 (P < 0.0001) and IgE (P = 0.012) levels. An in vitro promoter assay using THP-1 human monocyte cells revealed that the C to T conversion at g.-247 induced a more than twofold increase of reporter gene expression. Moreover, the g.-247T allele showed an increased affinity for CCAAT enhancer-binding protein, a well known transcriptional activator, by electrophoretic mobility shift assay. Accordingly, subjects with the g.-247TT genotype showed a 2.5-fold increase in CHI3L1 mRNA expression in peripheral blood cells compared with those with the g.-247CC genotype.
These results strongly suggest that the g.-247C/T polymorphism in the CHI3L1 promoter region is associated with the risk of atopy.</description><subject>Adipokines</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Asthma</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>CCAAT-Enhancer-Binding Proteins</subject><subject>Child</subject><subject>Chitinase</subject><subject>Chitinase-3-Like Protein 1</subject><subject>Digestive system</subject><subject>Electrophoretic Mobility Shift Assay</subject><subject>Female</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Glycoproteins</subject><subject>Glycoproteins - blood</subject><subject>Glycoproteins - genetics</subject><subject>Haplotypes</subject><subject>Humans</subject><subject>Hypersensitivity, Immediate - genetics</subject><subject>Immunoglobulin E - blood</subject><subject>Intensive care medicine</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Korea</subject><subject>Lectins</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pathogenesis</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>Polymerase Chain Reaction</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Promoter Regions, Genetic</subject><subject>Proteins</subject><subject>Risk Factors</subject><subject>RNA, Messenger - metabolism</subject><subject>Skin</subject><issn>1073-449X</issn><issn>1535-4970</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkV2L1DAUhoso7rr6B7yQICh40fWcJG2ay2HQdWFgRfy6C2l6upOxbWaTDsv-ezN0UPDGq4TwvG9O8hTFS4RLxFq-j86NlxygAV2i5Pxm_ag4x0pUpdQKHuc9KFFKqX-eFc9S2gEgbxCeFmeoEWoB9Xnx44ommr1j3230dvZhYn5i85bY5xjGMFNkX-j2eBx6tt762U82ERPlxv8ihuw6sVVKweUsdezez1u2msP-4XnxpLdDohen9aL49vHD1_WncnNzdb1ebUonuZjLPKEiXTed7LGuLCnRcwLdYd82SoNrhRDctlYoq5xrCPoOnWix1QBSyFZcFG-X3n0MdwdKsxl9cjQMdqJwSKZWACDyP_wP5CAVohYZfP0PuAuHOOVHGNS6FrKpdIb4ArkYUorUm330o40PBsEc5ZijHLPIMYucHHp1aj60I3V_IycbGXhzAmxyduijnZxPfziOvBK8wsy9W7itv93e-0gmjXYYci0auzvejEqb2mT14jemvaRy</recordid><startdate>20090315</startdate><enddate>20090315</enddate><creator>Sohn, Myung Hyun</creator><creator>Lee, Ji Hyun</creator><creator>Kim, Kyung Won</creator><creator>Kim, So Won</creator><creator>Lee, Sung Hee</creator><creator>Kim, Kyu-Earn</creator><creator>Kim, Kyung Hwan</creator><creator>Lee, Chun Geun</creator><creator>Elias, Jack A</creator><creator>Lee, Min Goo</creator><general>Am Thoracic Soc</general><general>American Thoracic Society</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>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20090315</creationdate><title>Genetic Variation in the Promoter Region of Chitinase 3-Like 1 Is Associated with Atopy</title><author>Sohn, Myung Hyun ; Lee, Ji Hyun ; Kim, Kyung Won ; Kim, So Won ; Lee, Sung Hee ; Kim, Kyu-Earn ; Kim, Kyung Hwan ; Lee, Chun Geun ; Elias, Jack A ; Lee, Min Goo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-1077e968d4f165ae73f2e09d1fb8790cb3332aba37a7cc8e0fd1c3b1b900434b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adipokines</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Asthma</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>CCAAT-Enhancer-Binding Proteins</topic><topic>Child</topic><topic>Chitinase</topic><topic>Chitinase-3-Like Protein 1</topic><topic>Digestive system</topic><topic>Electrophoretic Mobility Shift Assay</topic><topic>Female</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Glycoproteins</topic><topic>Glycoproteins - blood</topic><topic>Glycoproteins - genetics</topic><topic>Haplotypes</topic><topic>Humans</topic><topic>Hypersensitivity, Immediate - genetics</topic><topic>Immunoglobulin E - blood</topic><topic>Intensive care medicine</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Korea</topic><topic>Lectins</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pathogenesis</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>Polymerase Chain Reaction</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Promoter Regions, Genetic</topic><topic>Proteins</topic><topic>Risk Factors</topic><topic>RNA, Messenger - metabolism</topic><topic>Skin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sohn, Myung Hyun</creatorcontrib><creatorcontrib>Lee, Ji Hyun</creatorcontrib><creatorcontrib>Kim, Kyung Won</creatorcontrib><creatorcontrib>Kim, So Won</creatorcontrib><creatorcontrib>Lee, Sung Hee</creatorcontrib><creatorcontrib>Kim, Kyu-Earn</creatorcontrib><creatorcontrib>Kim, Kyung Hwan</creatorcontrib><creatorcontrib>Lee, Chun Geun</creatorcontrib><creatorcontrib>Elias, Jack A</creatorcontrib><creatorcontrib>Lee, Min Goo</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>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of respiratory and critical care medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sohn, Myung Hyun</au><au>Lee, Ji Hyun</au><au>Kim, Kyung Won</au><au>Kim, So Won</au><au>Lee, Sung Hee</au><au>Kim, Kyu-Earn</au><au>Kim, Kyung Hwan</au><au>Lee, Chun Geun</au><au>Elias, Jack A</au><au>Lee, Min Goo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic Variation in the Promoter Region of Chitinase 3-Like 1 Is Associated with Atopy</atitle><jtitle>American journal of respiratory and critical care medicine</jtitle><addtitle>Am J Respir Crit Care Med</addtitle><date>2009-03-15</date><risdate>2009</risdate><volume>179</volume><issue>6</issue><spage>449</spage><epage>456</epage><pages>449-456</pages><issn>1073-449X</issn><eissn>1535-4970</eissn><abstract>Atopy or atopic syndrome is an allergic hypersensitivity subject to hereditary influences. Aberrant expression of chitinase 3-like 1 (CHI3L1), also known as YKL-40 or HC gp-39, is involved in the pathogenesis of inflammatory and allergic diseases.
The genetic contribution of CHI3L1 gene to atopic susceptibility was investigated using an integrated population genetic and molecular analysis.
Genetic variations in CHI3L1 were identified and genotyped in 295 unrelated patients with atopy and 180 control subjects. Serum YKL-40 and IgE levels were analyzed according to genotype. The effects of a promoter polymorphism (g.-247C/T) on promoter activity were examined in reporter and protein binding assays.
In the case-control association analysis, the g.-247C/T polymorphism at the promoter region (rs10399805; P = 0.0062) and the IVS7+82C/T polymorphism at intron 7 (rs2275353; P = 0.0056) of CHI3L1 showed a significant association with atopy. Subjects with the g.-247T risk allele had significantly higher serum YKL-40 (P < 0.0001) and IgE (P = 0.012) levels. An in vitro promoter assay using THP-1 human monocyte cells revealed that the C to T conversion at g.-247 induced a more than twofold increase of reporter gene expression. Moreover, the g.-247T allele showed an increased affinity for CCAAT enhancer-binding protein, a well known transcriptional activator, by electrophoretic mobility shift assay. Accordingly, subjects with the g.-247TT genotype showed a 2.5-fold increase in CHI3L1 mRNA expression in peripheral blood cells compared with those with the g.-247CC genotype.
These results strongly suggest that the g.-247C/T polymorphism in the CHI3L1 promoter region is associated with the risk of atopy.</abstract><cop>New York, NY</cop><pub>Am Thoracic Soc</pub><pmid>19106306</pmid><doi>10.1164/rccm.200809-1422OC</doi><tpages>8</tpages></addata></record> |
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| ispartof | American journal of respiratory and critical care medicine, 2009-03, Vol.179 (6), p.449-456 |
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| subjects | Adipokines Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Asthma Biological and medical sciences Case-Control Studies CCAAT-Enhancer-Binding Proteins Child Chitinase Chitinase-3-Like Protein 1 Digestive system Electrophoretic Mobility Shift Assay Female Genotype Genotype & phenotype Glycoproteins Glycoproteins - blood Glycoproteins - genetics Haplotypes Humans Hypersensitivity, Immediate - genetics Immunoglobulin E - blood Intensive care medicine Investigative techniques, diagnostic techniques (general aspects) Korea Lectins Male Medical sciences Pathogenesis Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Polymerase Chain Reaction Polymorphism Polymorphism, Single Nucleotide Promoter Regions, Genetic Proteins Risk Factors RNA, Messenger - metabolism Skin |
| title | Genetic Variation in the Promoter Region of Chitinase 3-Like 1 Is Associated with Atopy |
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