CD209 (DC-SIGN) −336A>G promoter polymorphism and severe acute respiratory syndrome in Hong Kong Chinese
Abstract CD209 (DC-SIGN) is an important C-type lectin which acts a receptor of many pathogens. The single nucleotide polymorphism (SNP) −336A>G in the CD209 promoter has been demonstrated to regulate promoter activity and to be associated with several important infectious diseases, such as human...
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| Veröffentlicht in: | Human immunology 2010-07, Vol.71 (7), p.702-707 |
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| creator | Chan, Kelvin Yuen Kwong Xu, Mei-Shu Ching, Johannes Chi Yun So, Thomas Man Kit Lai, Sik-To Chu, Chung-Ming Yam, Loretta Y.C Wong, Andrew T.Y Chung, Pui Hong Chan, Vera Sau Fong Lin, Chen Lung Steve Sham, Pak Chung Leung, Gabriel M Peiris, Joseph S.M Khoo, Ui-Soon |
| description | Abstract CD209 (DC-SIGN) is an important C-type lectin which acts a receptor of many pathogens. The single nucleotide polymorphism (SNP) −336A>G in the CD209 promoter has been demonstrated to regulate promoter activity and to be associated with several important infectious diseases, such as human immunodeficiency virus–1 (HIV-1), Mycobacterium tuberculosis , and Dengue fever. CD209 facilitates severe acute respiratory syndrome (SARS)–coronavirus spike protein-bearing pseudotype driven infection of permissive cells in vitro . In keeping with previously published findings, our in vitro studies confirmed that this SNP modulates gene promoter activity. Genetic association analysis of this SNP with clinico-pathologic outcomes in 824 serologic confirmed SARS patients showed that the −336AG/GG genotype SARS patients was associated with lower standardized lactate-dehydrogenase (LDH) levels compared with the −336AA patients ( p = 0.014, odds ratio = 0.40). High LDH levels are known to be an independent predictor for poor clinical outcome, probably related to tissue destruction from immune hyperactivity. Hence, SARS patients with the CD209 −336 AA genotype carry a 60% chance of having a poorer prognosis. This association is in keeping with the role of CD209 in modulating immune response to viral infection. The relevance of these findings for other infectious diseases and inflammatory conditions would be worth investigating. |
| doi_str_mv | 10.1016/j.humimm.2010.03.006 |
| format | Article |
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The single nucleotide polymorphism (SNP) −336A>G in the CD209 promoter has been demonstrated to regulate promoter activity and to be associated with several important infectious diseases, such as human immunodeficiency virus–1 (HIV-1), Mycobacterium tuberculosis , and Dengue fever. CD209 facilitates severe acute respiratory syndrome (SARS)–coronavirus spike protein-bearing pseudotype driven infection of permissive cells in vitro . In keeping with previously published findings, our in vitro studies confirmed that this SNP modulates gene promoter activity. Genetic association analysis of this SNP with clinico-pathologic outcomes in 824 serologic confirmed SARS patients showed that the −336AG/GG genotype SARS patients was associated with lower standardized lactate-dehydrogenase (LDH) levels compared with the −336AA patients ( p = 0.014, odds ratio = 0.40). High LDH levels are known to be an independent predictor for poor clinical outcome, probably related to tissue destruction from immune hyperactivity. Hence, SARS patients with the CD209 −336 AA genotype carry a 60% chance of having a poorer prognosis. This association is in keeping with the role of CD209 in modulating immune response to viral infection. The relevance of these findings for other infectious diseases and inflammatory conditions would be worth investigating.</description><identifier>ISSN: 0198-8859</identifier><identifier>EISSN: 1879-1166</identifier><identifier>DOI: 10.1016/j.humimm.2010.03.006</identifier><identifier>PMID: 20359516</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adult ; Allergy and Immunology ; Antigens, CD - genetics ; Asian Continental Ancestry Group - genetics ; CD209 ; Cell Adhesion Molecules - genetics ; Cell Adhesion Molecules - metabolism ; DC-SIGN ; DNA - metabolism ; DNA Probes - genetics ; Electrophoretic Mobility Shift Assay ; Female ; Gene Frequency - genetics ; Genotype ; HeLa Cells ; Heterozygote ; Homozygote ; Hong Kong ; Humans ; L-Lactate Dehydrogenase - blood ; Lactate dehydrogenase ; Lectins, C-Type - genetics ; Lectins, C-Type - metabolism ; Male ; Middle Aged ; Nuclear Proteins - metabolism ; Polymorphism, Single Nucleotide - genetics ; Promoter Regions, Genetic - genetics ; Protein Binding - genetics ; Receptors, Cell Surface - genetics ; Receptors, Cell Surface - metabolism ; SARS ; Severe Acute Respiratory Syndrome - blood ; Severe Acute Respiratory Syndrome - genetics ; SNP ; Sp1 Transcription Factor - genetics ; Transcription Factor AP-2 - genetics ; Transfection</subject><ispartof>Human immunology, 2010-07, Vol.71 (7), p.702-707</ispartof><rights>American Society for Histocompatibility and Immunogenetics</rights><rights>2010 American Society for Histocompatibility and Immunogenetics</rights><rights>Copyright 2010 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.</rights><rights>Copyright © 2010 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved. 2010 American Society for Histocompatibility and Immunogenetics</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c517t-de85ee3cc90921b431cb86d85ec0d607289858361fbd8bf8c7a752529469c2e93</citedby><cites>FETCH-LOGICAL-c517t-de85ee3cc90921b431cb86d85ec0d607289858361fbd8bf8c7a752529469c2e93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.humimm.2010.03.006$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,315,781,785,886,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20359516$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chan, Kelvin Yuen Kwong</creatorcontrib><creatorcontrib>Xu, Mei-Shu</creatorcontrib><creatorcontrib>Ching, Johannes Chi Yun</creatorcontrib><creatorcontrib>So, Thomas Man Kit</creatorcontrib><creatorcontrib>Lai, Sik-To</creatorcontrib><creatorcontrib>Chu, Chung-Ming</creatorcontrib><creatorcontrib>Yam, Loretta Y.C</creatorcontrib><creatorcontrib>Wong, Andrew T.Y</creatorcontrib><creatorcontrib>Chung, Pui Hong</creatorcontrib><creatorcontrib>Chan, Vera Sau Fong</creatorcontrib><creatorcontrib>Lin, Chen Lung Steve</creatorcontrib><creatorcontrib>Sham, Pak Chung</creatorcontrib><creatorcontrib>Leung, Gabriel M</creatorcontrib><creatorcontrib>Peiris, Joseph S.M</creatorcontrib><creatorcontrib>Khoo, Ui-Soon</creatorcontrib><title>CD209 (DC-SIGN) −336A>G promoter polymorphism and severe acute respiratory syndrome in Hong Kong Chinese</title><title>Human immunology</title><addtitle>Hum Immunol</addtitle><description>Abstract CD209 (DC-SIGN) is an important C-type lectin which acts a receptor of many pathogens. The single nucleotide polymorphism (SNP) −336A>G in the CD209 promoter has been demonstrated to regulate promoter activity and to be associated with several important infectious diseases, such as human immunodeficiency virus–1 (HIV-1), Mycobacterium tuberculosis , and Dengue fever. CD209 facilitates severe acute respiratory syndrome (SARS)–coronavirus spike protein-bearing pseudotype driven infection of permissive cells in vitro . In keeping with previously published findings, our in vitro studies confirmed that this SNP modulates gene promoter activity. Genetic association analysis of this SNP with clinico-pathologic outcomes in 824 serologic confirmed SARS patients showed that the −336AG/GG genotype SARS patients was associated with lower standardized lactate-dehydrogenase (LDH) levels compared with the −336AA patients ( p = 0.014, odds ratio = 0.40). High LDH levels are known to be an independent predictor for poor clinical outcome, probably related to tissue destruction from immune hyperactivity. Hence, SARS patients with the CD209 −336 AA genotype carry a 60% chance of having a poorer prognosis. This association is in keeping with the role of CD209 in modulating immune response to viral infection. The relevance of these findings for other infectious diseases and inflammatory conditions would be worth investigating.</description><subject>Adult</subject><subject>Allergy and Immunology</subject><subject>Antigens, CD - genetics</subject><subject>Asian Continental Ancestry Group - genetics</subject><subject>CD209</subject><subject>Cell Adhesion Molecules - genetics</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>DC-SIGN</subject><subject>DNA - metabolism</subject><subject>DNA Probes - genetics</subject><subject>Electrophoretic Mobility Shift Assay</subject><subject>Female</subject><subject>Gene Frequency - genetics</subject><subject>Genotype</subject><subject>HeLa Cells</subject><subject>Heterozygote</subject><subject>Homozygote</subject><subject>Hong Kong</subject><subject>Humans</subject><subject>L-Lactate Dehydrogenase - blood</subject><subject>Lactate dehydrogenase</subject><subject>Lectins, C-Type - genetics</subject><subject>Lectins, C-Type - metabolism</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Nuclear Proteins - metabolism</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Protein Binding - genetics</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>SARS</subject><subject>Severe Acute Respiratory Syndrome - blood</subject><subject>Severe Acute Respiratory Syndrome - genetics</subject><subject>SNP</subject><subject>Sp1 Transcription Factor - genetics</subject><subject>Transcription Factor AP-2 - genetics</subject><subject>Transfection</subject><issn>0198-8859</issn><issn>1879-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks1u1DAUhS0EokPhDRDyDlhkuI4Tx95UqlKYVlSwKKytxLnT8ZDYwU5Gyhuw5hF5EhJNKT8bNrZ0fe85tr9DyHMGawZMvNmvd2Nnu26dwlwCvgYQD8iKyUIljAnxkKyAKZlImasT8iTGPQAUUGSPyUkKPFc5EyuyLy9SUPTVRZncXG0-vKY_vn3nXJyfbWgffOcHDLT37dT50O9s7GjlGhrxgAFpZcYBacDY21ANPkw0Tq6Zp5BaRy-9u6Xvl6XcWYcRn5JH26qN-OxuPyWf3739VF4m1x83V-X5dWJyVgxJgzJH5MYoUCmrM85MLUUzFw00AopUKplLLti2bmS9laaoijzNU5UJZVJU_JScHXX7se6wMeiGULW6D7arwqR9ZfXfJ87u9K0_6IKxPAM2C7y8Ewj-64hx0J2NBtu2cujHqAvOlZzdxNyZHTtN8DEG3N67MNALJb3XR0p6oaSB65nSPPbizxveD_3C8vsJOP_TwWLQ0Vh0Bhsb0Ay68fZ_Dv8KmNY6a6r2C04Y934MbmagmY6pBn2zJGUJCoMlJFLxn7GfutA</recordid><startdate>20100701</startdate><enddate>20100701</enddate><creator>Chan, Kelvin Yuen Kwong</creator><creator>Xu, Mei-Shu</creator><creator>Ching, Johannes Chi Yun</creator><creator>So, Thomas Man Kit</creator><creator>Lai, Sik-To</creator><creator>Chu, Chung-Ming</creator><creator>Yam, Loretta Y.C</creator><creator>Wong, Andrew T.Y</creator><creator>Chung, Pui Hong</creator><creator>Chan, Vera Sau Fong</creator><creator>Lin, Chen Lung Steve</creator><creator>Sham, Pak Chung</creator><creator>Leung, Gabriel M</creator><creator>Peiris, Joseph S.M</creator><creator>Khoo, Ui-Soon</creator><general>Elsevier Inc</general><general>American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc</general><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100701</creationdate><title>CD209 (DC-SIGN) −336A>G promoter polymorphism and severe acute respiratory syndrome in Hong Kong Chinese</title><author>Chan, Kelvin Yuen Kwong ; Xu, Mei-Shu ; Ching, Johannes Chi Yun ; So, Thomas Man Kit ; Lai, Sik-To ; Chu, Chung-Ming ; Yam, Loretta Y.C ; Wong, Andrew T.Y ; Chung, Pui Hong ; Chan, Vera Sau Fong ; Lin, Chen Lung Steve ; Sham, Pak Chung ; Leung, Gabriel M ; Peiris, Joseph S.M ; Khoo, Ui-Soon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c517t-de85ee3cc90921b431cb86d85ec0d607289858361fbd8bf8c7a752529469c2e93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adult</topic><topic>Allergy and Immunology</topic><topic>Antigens, CD - genetics</topic><topic>Asian Continental Ancestry Group - genetics</topic><topic>CD209</topic><topic>Cell Adhesion Molecules - genetics</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>DC-SIGN</topic><topic>DNA - metabolism</topic><topic>DNA Probes - genetics</topic><topic>Electrophoretic Mobility Shift Assay</topic><topic>Female</topic><topic>Gene Frequency - genetics</topic><topic>Genotype</topic><topic>HeLa Cells</topic><topic>Heterozygote</topic><topic>Homozygote</topic><topic>Hong Kong</topic><topic>Humans</topic><topic>L-Lactate Dehydrogenase - blood</topic><topic>Lactate dehydrogenase</topic><topic>Lectins, C-Type - genetics</topic><topic>Lectins, C-Type - metabolism</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Nuclear Proteins - metabolism</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Protein Binding - genetics</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>SARS</topic><topic>Severe Acute Respiratory Syndrome - blood</topic><topic>Severe Acute Respiratory Syndrome - genetics</topic><topic>SNP</topic><topic>Sp1 Transcription Factor - genetics</topic><topic>Transcription Factor AP-2 - genetics</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chan, Kelvin Yuen Kwong</creatorcontrib><creatorcontrib>Xu, Mei-Shu</creatorcontrib><creatorcontrib>Ching, Johannes Chi Yun</creatorcontrib><creatorcontrib>So, Thomas Man Kit</creatorcontrib><creatorcontrib>Lai, Sik-To</creatorcontrib><creatorcontrib>Chu, Chung-Ming</creatorcontrib><creatorcontrib>Yam, Loretta Y.C</creatorcontrib><creatorcontrib>Wong, Andrew T.Y</creatorcontrib><creatorcontrib>Chung, Pui Hong</creatorcontrib><creatorcontrib>Chan, Vera Sau Fong</creatorcontrib><creatorcontrib>Lin, Chen Lung Steve</creatorcontrib><creatorcontrib>Sham, Pak Chung</creatorcontrib><creatorcontrib>Leung, Gabriel M</creatorcontrib><creatorcontrib>Peiris, Joseph S.M</creatorcontrib><creatorcontrib>Khoo, Ui-Soon</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Human immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chan, Kelvin Yuen Kwong</au><au>Xu, Mei-Shu</au><au>Ching, Johannes Chi Yun</au><au>So, Thomas Man Kit</au><au>Lai, Sik-To</au><au>Chu, Chung-Ming</au><au>Yam, Loretta Y.C</au><au>Wong, Andrew T.Y</au><au>Chung, Pui Hong</au><au>Chan, Vera Sau Fong</au><au>Lin, Chen Lung Steve</au><au>Sham, Pak Chung</au><au>Leung, Gabriel M</au><au>Peiris, Joseph S.M</au><au>Khoo, Ui-Soon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CD209 (DC-SIGN) −336A>G promoter polymorphism and severe acute respiratory syndrome in Hong Kong Chinese</atitle><jtitle>Human immunology</jtitle><addtitle>Hum Immunol</addtitle><date>2010-07-01</date><risdate>2010</risdate><volume>71</volume><issue>7</issue><spage>702</spage><epage>707</epage><pages>702-707</pages><issn>0198-8859</issn><eissn>1879-1166</eissn><abstract>Abstract CD209 (DC-SIGN) is an important C-type lectin which acts a receptor of many pathogens. The single nucleotide polymorphism (SNP) −336A>G in the CD209 promoter has been demonstrated to regulate promoter activity and to be associated with several important infectious diseases, such as human immunodeficiency virus–1 (HIV-1), Mycobacterium tuberculosis , and Dengue fever. CD209 facilitates severe acute respiratory syndrome (SARS)–coronavirus spike protein-bearing pseudotype driven infection of permissive cells in vitro . In keeping with previously published findings, our in vitro studies confirmed that this SNP modulates gene promoter activity. Genetic association analysis of this SNP with clinico-pathologic outcomes in 824 serologic confirmed SARS patients showed that the −336AG/GG genotype SARS patients was associated with lower standardized lactate-dehydrogenase (LDH) levels compared with the −336AA patients ( p = 0.014, odds ratio = 0.40). High LDH levels are known to be an independent predictor for poor clinical outcome, probably related to tissue destruction from immune hyperactivity. Hence, SARS patients with the CD209 −336 AA genotype carry a 60% chance of having a poorer prognosis. This association is in keeping with the role of CD209 in modulating immune response to viral infection. The relevance of these findings for other infectious diseases and inflammatory conditions would be worth investigating.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>20359516</pmid><doi>10.1016/j.humimm.2010.03.006</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Allergy and Immunology Antigens, CD - genetics Asian Continental Ancestry Group - genetics CD209 Cell Adhesion Molecules - genetics Cell Adhesion Molecules - metabolism DC-SIGN DNA - metabolism DNA Probes - genetics Electrophoretic Mobility Shift Assay Female Gene Frequency - genetics Genotype HeLa Cells Heterozygote Homozygote Hong Kong Humans L-Lactate Dehydrogenase - blood Lactate dehydrogenase Lectins, C-Type - genetics Lectins, C-Type - metabolism Male Middle Aged Nuclear Proteins - metabolism Polymorphism, Single Nucleotide - genetics Promoter Regions, Genetic - genetics Protein Binding - genetics Receptors, Cell Surface - genetics Receptors, Cell Surface - metabolism SARS Severe Acute Respiratory Syndrome - blood Severe Acute Respiratory Syndrome - genetics SNP Sp1 Transcription Factor - genetics Transcription Factor AP-2 - genetics Transfection |
| title | CD209 (DC-SIGN) −336A>G promoter polymorphism and severe acute respiratory syndrome in Hong Kong Chinese |
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