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Platelet Glycoprotein Ib α‐Chain as a Putative Therapeutic Target for Juvenile Idiopathic Arthritis: A Mendelian Randomization Study
Objective To ascertain the role of platelet glycoprotein Ib α‐chain (GPIbα) plasma protein levels in cardiovascular, autoimmune, and autoinflammatory diseases and whether its effects are mediated by platelet count. Methods We performed a two‐sample Mendelian randomization (MR) study, using both a ci...
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| Published in: | Arthritis & rheumatology (Hoboken, N.J.) N.J.), 2021-04, Vol.73 (4), p.693-701 |
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| container_title | Arthritis & rheumatology (Hoboken, N.J.) |
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| creator | Luo, Shan Clarke, Sarah L. N. Ramanan, Athimalaipet V. Thompson, Susan D. Langefeld, Carl D. Marion, Miranda C. Grom, Alexei A. Schooling, C. Mary Gaunt, Tom R. Yeung, Shiu Lun Au Zheng, Jie |
| description | Objective
To ascertain the role of platelet glycoprotein Ib α‐chain (GPIbα) plasma protein levels in cardiovascular, autoimmune, and autoinflammatory diseases and whether its effects are mediated by platelet count.
Methods
We performed a two‐sample Mendelian randomization (MR) study, using both a cis‐acting protein quantitative trait locus (cis‐pQTL) and trans‐pQTL near the GP1BA and BRAP genes as instruments. To assess if platelet count mediated the effect, we then performed a two‐step MR study. Putative associations (GPIbα/platelet count/disease) detected by MR analyses were subsequently assessed using multiple‐trait colocalization analyses.
Results
After correction for multiple testing (Bonferroni‐corrected threshold P ≤ 2 × 10−3), GPIbα, instrumented by either cis‐pQTL or trans‐pQTL, was causally implicated with an increased risk of oligoarticular and rheumatoid factor (RF)–negative polyarticular juvenile idiopathic arthritis (JIA). These effects of GPIbα appeared to be mediated by platelet count and were supported by strong evidence of colocalization (probability of all 3 traits sharing a common causal variant ≥0.80). GPIbα instrumented by cis‐pQTL did not appear to affect cardiovascular risk, although the GPIbα trans‐pQTL was associated with an increased risk of cardiovascular diseases and autoimmune diseases but a decreased risk of autoinflammatory diseases, suggesting that this trans‐acting instrument operates through other pathways.
Conclusion
The role of platelets in thrombosis is well‐established; however, our findings provide some novel genetic evidence that platelets may be causally implicated in the development of oligoarticular and RF‐negative polyarticular JIA, and indicate that GPIbα may serve as a putative therapeutic target for these JIA subtypes. |
| doi_str_mv | 10.1002/art.41561 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8048917</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2509261780</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4101-5da718479a6799a57b0ca26bc7fcc80058092b71cc9cd26bfe027079dc298b723</originalsourceid><addsrcrecordid>eNp1kcFu1DAQhi0EolXpgRdAljhx2HbsjeOYA9JqBWVREVVZztbEcRpXWTs4zqLlxI0rr8KL8BA8CYZtKzjgy9gzn_8Z-yfkMYMTBsBPMaaTgomS3SOHfM7LmeAg7t_umWIH5HgcryEvJaEE8ZAczOcgVVGIQ_L1osdke5voWb8zYYghWefpqqY_vv_88m3ZYT7hSJFeTAmT21q67mzEwU7JGbrGeJXvtiHSN9PWetdbumpcGDB1ubyIqYsuufE5XdC31je2d-jpJfombNznrBc8fZ-mZveIPGixH-3xTTwiH169XC9fz87fna2Wi_OZKRiwmWhQsqqQCkupFApZg0Fe1ka2xlQAogLFa8mMUabJ-dYCl_mtjeGqqiWfH5EXe91hqje2MdaniL0eottg3OmATv9b8a7TV2GrKygqxWQWeHojEMPHyY5JX4cp-jyz5iI3L5msIFPP9pSJYRyjbe86MNC_bdPZNv3Htsw--XukO_LWpAyc7oFP-Xt3_1fSi8v1XvIXrqOlSA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2509261780</pqid></control><display><type>article</type><title>Platelet Glycoprotein Ib α‐Chain as a Putative Therapeutic Target for Juvenile Idiopathic Arthritis: A Mendelian Randomization Study</title><source>Wiley-Blackwell Read & Publish Collection</source><creator>Luo, Shan ; Clarke, Sarah L. N. ; Ramanan, Athimalaipet V. ; Thompson, Susan D. ; Langefeld, Carl D. ; Marion, Miranda C. ; Grom, Alexei A. ; Schooling, C. Mary ; Gaunt, Tom R. ; Yeung, Shiu Lun Au ; Zheng, Jie</creator><creatorcontrib>Luo, Shan ; Clarke, Sarah L. N. ; Ramanan, Athimalaipet V. ; Thompson, Susan D. ; Langefeld, Carl D. ; Marion, Miranda C. ; Grom, Alexei A. ; Schooling, C. Mary ; Gaunt, Tom R. ; Yeung, Shiu Lun Au ; Zheng, Jie</creatorcontrib><description>Objective
To ascertain the role of platelet glycoprotein Ib α‐chain (GPIbα) plasma protein levels in cardiovascular, autoimmune, and autoinflammatory diseases and whether its effects are mediated by platelet count.
Methods
We performed a two‐sample Mendelian randomization (MR) study, using both a cis‐acting protein quantitative trait locus (cis‐pQTL) and trans‐pQTL near the GP1BA and BRAP genes as instruments. To assess if platelet count mediated the effect, we then performed a two‐step MR study. Putative associations (GPIbα/platelet count/disease) detected by MR analyses were subsequently assessed using multiple‐trait colocalization analyses.
Results
After correction for multiple testing (Bonferroni‐corrected threshold P ≤ 2 × 10−3), GPIbα, instrumented by either cis‐pQTL or trans‐pQTL, was causally implicated with an increased risk of oligoarticular and rheumatoid factor (RF)–negative polyarticular juvenile idiopathic arthritis (JIA). These effects of GPIbα appeared to be mediated by platelet count and were supported by strong evidence of colocalization (probability of all 3 traits sharing a common causal variant ≥0.80). GPIbα instrumented by cis‐pQTL did not appear to affect cardiovascular risk, although the GPIbα trans‐pQTL was associated with an increased risk of cardiovascular diseases and autoimmune diseases but a decreased risk of autoinflammatory diseases, suggesting that this trans‐acting instrument operates through other pathways.
Conclusion
The role of platelets in thrombosis is well‐established; however, our findings provide some novel genetic evidence that platelets may be causally implicated in the development of oligoarticular and RF‐negative polyarticular JIA, and indicate that GPIbα may serve as a putative therapeutic target for these JIA subtypes.</description><identifier>ISSN: 2326-5191</identifier><identifier>EISSN: 2326-5205</identifier><identifier>DOI: 10.1002/art.41561</identifier><identifier>PMID: 33079445</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Arthritis ; Arthritis, Juvenile - genetics ; Arthritis, Juvenile - immunology ; Autoimmune diseases ; Cardiovascular diseases ; Chains ; Female ; Full Length ; Gene mapping ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotype ; Glycoproteins ; Health risks ; Humans ; Inflammatory diseases ; Male ; Mendelian Randomization Analysis ; Pediatric Rheumatology ; Phenotype ; Platelet Glycoprotein GPIb-IX Complex - genetics ; Platelets ; Proteins ; Quantitative Trait Loci ; Randomization ; Rheumatoid factor ; Risk ; Therapeutic applications ; Therapeutic targets ; Thromboembolism ; Thrombosis</subject><ispartof>Arthritis & rheumatology (Hoboken, N.J.), 2021-04, Vol.73 (4), p.693-701</ispartof><rights>2020 The Authors. published by Wiley Periodicals LLC on behalf of American College of Rheumatology.</rights><rights>2020 The Authors. Arthritis & Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology.</rights><rights>2020. This article is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4101-5da718479a6799a57b0ca26bc7fcc80058092b71cc9cd26bfe027079dc298b723</citedby><cites>FETCH-LOGICAL-c4101-5da718479a6799a57b0ca26bc7fcc80058092b71cc9cd26bfe027079dc298b723</cites><orcidid>0000-0001-8663-2401 ; 0000-0003-4130-2796 ; 0000-0002-6623-6839 ; 0000-0003-3368-9935 ; 0000-0001-6136-1836 ; 0000-0003-0924-3247 ; 0000-0001-9933-5887 ; 0000-0002-4266-6949 ; 0000-0002-7385-6307</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,783,787,888,27936,27937</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33079445$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Luo, Shan</creatorcontrib><creatorcontrib>Clarke, Sarah L. N.</creatorcontrib><creatorcontrib>Ramanan, Athimalaipet V.</creatorcontrib><creatorcontrib>Thompson, Susan D.</creatorcontrib><creatorcontrib>Langefeld, Carl D.</creatorcontrib><creatorcontrib>Marion, Miranda C.</creatorcontrib><creatorcontrib>Grom, Alexei A.</creatorcontrib><creatorcontrib>Schooling, C. Mary</creatorcontrib><creatorcontrib>Gaunt, Tom R.</creatorcontrib><creatorcontrib>Yeung, Shiu Lun Au</creatorcontrib><creatorcontrib>Zheng, Jie</creatorcontrib><title>Platelet Glycoprotein Ib α‐Chain as a Putative Therapeutic Target for Juvenile Idiopathic Arthritis: A Mendelian Randomization Study</title><title>Arthritis & rheumatology (Hoboken, N.J.)</title><addtitle>Arthritis Rheumatol</addtitle><description>Objective
To ascertain the role of platelet glycoprotein Ib α‐chain (GPIbα) plasma protein levels in cardiovascular, autoimmune, and autoinflammatory diseases and whether its effects are mediated by platelet count.
Methods
We performed a two‐sample Mendelian randomization (MR) study, using both a cis‐acting protein quantitative trait locus (cis‐pQTL) and trans‐pQTL near the GP1BA and BRAP genes as instruments. To assess if platelet count mediated the effect, we then performed a two‐step MR study. Putative associations (GPIbα/platelet count/disease) detected by MR analyses were subsequently assessed using multiple‐trait colocalization analyses.
Results
After correction for multiple testing (Bonferroni‐corrected threshold P ≤ 2 × 10−3), GPIbα, instrumented by either cis‐pQTL or trans‐pQTL, was causally implicated with an increased risk of oligoarticular and rheumatoid factor (RF)–negative polyarticular juvenile idiopathic arthritis (JIA). These effects of GPIbα appeared to be mediated by platelet count and were supported by strong evidence of colocalization (probability of all 3 traits sharing a common causal variant ≥0.80). GPIbα instrumented by cis‐pQTL did not appear to affect cardiovascular risk, although the GPIbα trans‐pQTL was associated with an increased risk of cardiovascular diseases and autoimmune diseases but a decreased risk of autoinflammatory diseases, suggesting that this trans‐acting instrument operates through other pathways.
Conclusion
The role of platelets in thrombosis is well‐established; however, our findings provide some novel genetic evidence that platelets may be causally implicated in the development of oligoarticular and RF‐negative polyarticular JIA, and indicate that GPIbα may serve as a putative therapeutic target for these JIA subtypes.</description><subject>Arthritis</subject><subject>Arthritis, Juvenile - genetics</subject><subject>Arthritis, Juvenile - immunology</subject><subject>Autoimmune diseases</subject><subject>Cardiovascular diseases</subject><subject>Chains</subject><subject>Female</subject><subject>Full Length</subject><subject>Gene mapping</subject><subject>Genetic Predisposition to Disease</subject><subject>Genome-Wide Association Study</subject><subject>Genotype</subject><subject>Glycoproteins</subject><subject>Health risks</subject><subject>Humans</subject><subject>Inflammatory diseases</subject><subject>Male</subject><subject>Mendelian Randomization Analysis</subject><subject>Pediatric Rheumatology</subject><subject>Phenotype</subject><subject>Platelet Glycoprotein GPIb-IX Complex - genetics</subject><subject>Platelets</subject><subject>Proteins</subject><subject>Quantitative Trait Loci</subject><subject>Randomization</subject><subject>Rheumatoid factor</subject><subject>Risk</subject><subject>Therapeutic applications</subject><subject>Therapeutic targets</subject><subject>Thromboembolism</subject><subject>Thrombosis</subject><issn>2326-5191</issn><issn>2326-5205</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><recordid>eNp1kcFu1DAQhi0EolXpgRdAljhx2HbsjeOYA9JqBWVREVVZztbEcRpXWTs4zqLlxI0rr8KL8BA8CYZtKzjgy9gzn_8Z-yfkMYMTBsBPMaaTgomS3SOHfM7LmeAg7t_umWIH5HgcryEvJaEE8ZAczOcgVVGIQ_L1osdke5voWb8zYYghWefpqqY_vv_88m3ZYT7hSJFeTAmT21q67mzEwU7JGbrGeJXvtiHSN9PWetdbumpcGDB1ubyIqYsuufE5XdC31je2d-jpJfombNznrBc8fZ-mZveIPGixH-3xTTwiH169XC9fz87fna2Wi_OZKRiwmWhQsqqQCkupFApZg0Fe1ka2xlQAogLFa8mMUabJ-dYCl_mtjeGqqiWfH5EXe91hqje2MdaniL0eottg3OmATv9b8a7TV2GrKygqxWQWeHojEMPHyY5JX4cp-jyz5iI3L5msIFPP9pSJYRyjbe86MNC_bdPZNv3Htsw--XukO_LWpAyc7oFP-Xt3_1fSi8v1XvIXrqOlSA</recordid><startdate>202104</startdate><enddate>202104</enddate><creator>Luo, Shan</creator><creator>Clarke, Sarah L. N.</creator><creator>Ramanan, Athimalaipet V.</creator><creator>Thompson, Susan D.</creator><creator>Langefeld, Carl D.</creator><creator>Marion, Miranda C.</creator><creator>Grom, Alexei A.</creator><creator>Schooling, C. Mary</creator><creator>Gaunt, Tom R.</creator><creator>Yeung, Shiu Lun Au</creator><creator>Zheng, Jie</creator><general>Wiley Subscription Services, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TM</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8663-2401</orcidid><orcidid>https://orcid.org/0000-0003-4130-2796</orcidid><orcidid>https://orcid.org/0000-0002-6623-6839</orcidid><orcidid>https://orcid.org/0000-0003-3368-9935</orcidid><orcidid>https://orcid.org/0000-0001-6136-1836</orcidid><orcidid>https://orcid.org/0000-0003-0924-3247</orcidid><orcidid>https://orcid.org/0000-0001-9933-5887</orcidid><orcidid>https://orcid.org/0000-0002-4266-6949</orcidid><orcidid>https://orcid.org/0000-0002-7385-6307</orcidid></search><sort><creationdate>202104</creationdate><title>Platelet Glycoprotein Ib α‐Chain as a Putative Therapeutic Target for Juvenile Idiopathic Arthritis: A Mendelian Randomization Study</title><author>Luo, Shan ; Clarke, Sarah L. N. ; Ramanan, Athimalaipet V. ; Thompson, Susan D. ; Langefeld, Carl D. ; Marion, Miranda C. ; Grom, Alexei A. ; Schooling, C. Mary ; Gaunt, Tom R. ; Yeung, Shiu Lun Au ; Zheng, Jie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4101-5da718479a6799a57b0ca26bc7fcc80058092b71cc9cd26bfe027079dc298b723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Arthritis</topic><topic>Arthritis, Juvenile - genetics</topic><topic>Arthritis, Juvenile - immunology</topic><topic>Autoimmune diseases</topic><topic>Cardiovascular diseases</topic><topic>Chains</topic><topic>Female</topic><topic>Full Length</topic><topic>Gene mapping</topic><topic>Genetic Predisposition to Disease</topic><topic>Genome-Wide Association Study</topic><topic>Genotype</topic><topic>Glycoproteins</topic><topic>Health risks</topic><topic>Humans</topic><topic>Inflammatory diseases</topic><topic>Male</topic><topic>Mendelian Randomization Analysis</topic><topic>Pediatric Rheumatology</topic><topic>Phenotype</topic><topic>Platelet Glycoprotein GPIb-IX Complex - genetics</topic><topic>Platelets</topic><topic>Proteins</topic><topic>Quantitative Trait Loci</topic><topic>Randomization</topic><topic>Rheumatoid factor</topic><topic>Risk</topic><topic>Therapeutic applications</topic><topic>Therapeutic targets</topic><topic>Thromboembolism</topic><topic>Thrombosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luo, Shan</creatorcontrib><creatorcontrib>Clarke, Sarah L. 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Mary</creatorcontrib><creatorcontrib>Gaunt, Tom R.</creatorcontrib><creatorcontrib>Yeung, Shiu Lun Au</creatorcontrib><creatorcontrib>Zheng, Jie</creatorcontrib><collection>Wiley Online Library</collection><collection>Wiley Unsubscribed Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Luo, Shan</au><au>Clarke, Sarah L. N.</au><au>Ramanan, Athimalaipet V.</au><au>Thompson, Susan D.</au><au>Langefeld, Carl D.</au><au>Marion, Miranda C.</au><au>Grom, Alexei A.</au><au>Schooling, C. Mary</au><au>Gaunt, Tom R.</au><au>Yeung, Shiu Lun Au</au><au>Zheng, Jie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet Glycoprotein Ib α‐Chain as a Putative Therapeutic Target for Juvenile Idiopathic Arthritis: A Mendelian Randomization Study</atitle><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle><addtitle>Arthritis Rheumatol</addtitle><date>2021-04</date><risdate>2021</risdate><volume>73</volume><issue>4</issue><spage>693</spage><epage>701</epage><pages>693-701</pages><issn>2326-5191</issn><eissn>2326-5205</eissn><abstract>Objective
To ascertain the role of platelet glycoprotein Ib α‐chain (GPIbα) plasma protein levels in cardiovascular, autoimmune, and autoinflammatory diseases and whether its effects are mediated by platelet count.
Methods
We performed a two‐sample Mendelian randomization (MR) study, using both a cis‐acting protein quantitative trait locus (cis‐pQTL) and trans‐pQTL near the GP1BA and BRAP genes as instruments. To assess if platelet count mediated the effect, we then performed a two‐step MR study. Putative associations (GPIbα/platelet count/disease) detected by MR analyses were subsequently assessed using multiple‐trait colocalization analyses.
Results
After correction for multiple testing (Bonferroni‐corrected threshold P ≤ 2 × 10−3), GPIbα, instrumented by either cis‐pQTL or trans‐pQTL, was causally implicated with an increased risk of oligoarticular and rheumatoid factor (RF)–negative polyarticular juvenile idiopathic arthritis (JIA). These effects of GPIbα appeared to be mediated by platelet count and were supported by strong evidence of colocalization (probability of all 3 traits sharing a common causal variant ≥0.80). GPIbα instrumented by cis‐pQTL did not appear to affect cardiovascular risk, although the GPIbα trans‐pQTL was associated with an increased risk of cardiovascular diseases and autoimmune diseases but a decreased risk of autoinflammatory diseases, suggesting that this trans‐acting instrument operates through other pathways.
Conclusion
The role of platelets in thrombosis is well‐established; however, our findings provide some novel genetic evidence that platelets may be causally implicated in the development of oligoarticular and RF‐negative polyarticular JIA, and indicate that GPIbα may serve as a putative therapeutic target for these JIA subtypes.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>33079445</pmid><doi>10.1002/art.41561</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-8663-2401</orcidid><orcidid>https://orcid.org/0000-0003-4130-2796</orcidid><orcidid>https://orcid.org/0000-0002-6623-6839</orcidid><orcidid>https://orcid.org/0000-0003-3368-9935</orcidid><orcidid>https://orcid.org/0000-0001-6136-1836</orcidid><orcidid>https://orcid.org/0000-0003-0924-3247</orcidid><orcidid>https://orcid.org/0000-0001-9933-5887</orcidid><orcidid>https://orcid.org/0000-0002-4266-6949</orcidid><orcidid>https://orcid.org/0000-0002-7385-6307</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Arthritis & rheumatology (Hoboken, N.J.), 2021-04, Vol.73 (4), p.693-701 |
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| subjects | Arthritis Arthritis, Juvenile - genetics Arthritis, Juvenile - immunology Autoimmune diseases Cardiovascular diseases Chains Female Full Length Gene mapping Genetic Predisposition to Disease Genome-Wide Association Study Genotype Glycoproteins Health risks Humans Inflammatory diseases Male Mendelian Randomization Analysis Pediatric Rheumatology Phenotype Platelet Glycoprotein GPIb-IX Complex - genetics Platelets Proteins Quantitative Trait Loci Randomization Rheumatoid factor Risk Therapeutic applications Therapeutic targets Thromboembolism Thrombosis |
| title | Platelet Glycoprotein Ib α‐Chain as a Putative Therapeutic Target for Juvenile Idiopathic Arthritis: A Mendelian Randomization Study |
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