Human genetic evidence that OX40 is implicated in myocardial infarction
We recently showed that genetic variants in OX40L are associated with myocardial infarction (MI) and severity of coronary artery disease in human. A number of studies also suggest a possible role for OX40 (the OX40L receptor) as a factor contributing to atherosclerosis. In the present study, the OX4...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2006-01, Vol.339 (3), p.1001-1006 |
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| container_title | Biochemical and biophysical research communications |
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| creator | Ria, Massimiliano Eriksson, Per Boquist, Susanna Ericsson, Carl-Göran Hamsten, Anders Lagercrantz, Jacob |
| description | We recently showed that genetic variants in
OX40L are associated with myocardial infarction (MI) and severity of coronary artery disease in human. A number of studies also suggest a possible role for OX40 (the OX40L receptor) as a factor contributing to atherosclerosis. In the present study, the
OX40 gene was screened for variants associated with precocious MI, using individuals with MI before the age of 60 and controls. Despite the fact that the
OX40 gene is highly conserved between species and that relatively few common genetic variants were encountered, an association with MI was seen for a polymorphism in intron 5 (rs2298212). In silico investigation suggested that genetic variation (rs2298211), linked to this intronic variant, is possibly affecting spliceosome function. Our results provide evidence that variants in human
OX40 might influence susceptibility to MI. The relevance of these findings is supported by the vital functions fulfilled by
OX40 in mammals as reflected by the high level of evolutionary conservation. |
| doi_str_mv | 10.1016/j.bbrc.2005.11.092 |
| format | Article |
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OX40L are associated with myocardial infarction (MI) and severity of coronary artery disease in human. A number of studies also suggest a possible role for OX40 (the OX40L receptor) as a factor contributing to atherosclerosis. In the present study, the
OX40 gene was screened for variants associated with precocious MI, using individuals with MI before the age of 60 and controls. Despite the fact that the
OX40 gene is highly conserved between species and that relatively few common genetic variants were encountered, an association with MI was seen for a polymorphism in intron 5 (rs2298212). In silico investigation suggested that genetic variation (rs2298211), linked to this intronic variant, is possibly affecting spliceosome function. Our results provide evidence that variants in human
OX40 might influence susceptibility to MI. The relevance of these findings is supported by the vital functions fulfilled by
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OX40L are associated with myocardial infarction (MI) and severity of coronary artery disease in human. A number of studies also suggest a possible role for OX40 (the OX40L receptor) as a factor contributing to atherosclerosis. In the present study, the
OX40 gene was screened for variants associated with precocious MI, using individuals with MI before the age of 60 and controls. Despite the fact that the
OX40 gene is highly conserved between species and that relatively few common genetic variants were encountered, an association with MI was seen for a polymorphism in intron 5 (rs2298212). In silico investigation suggested that genetic variation (rs2298211), linked to this intronic variant, is possibly affecting spliceosome function. Our results provide evidence that variants in human
OX40 might influence susceptibility to MI. The relevance of these findings is supported by the vital functions fulfilled by
OX40 in mammals as reflected by the high level of evolutionary conservation.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Association study</subject><subject>Atherosclerosis</subject><subject>Candidate gene</subject><subject>Comorbidity</subject><subject>DNA Mutational Analysis</subject><subject>Evidence-Based Medicine</subject><subject>Female</subject><subject>Genetic Predisposition to Disease - epidemiology</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genetic Testing - methods</subject><subject>Genotype</subject><subject>Haplotype blocks</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Male</subject><subject>Medicin och hälsovetenskap</subject><subject>Middle Aged</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - epidemiology</subject><subject>Myocardial Infarction - metabolism</subject><subject>OX40</subject><subject>OX40L</subject><subject>Polymorphism, Genetic</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Prevalence</subject><subject>Receptors, OX40</subject><subject>Receptors, Tumor Necrosis Factor - genetics</subject><subject>Risk Assessment - methods</subject><subject>Risk Factors</subject><subject>Single nucleotide polymorphism</subject><subject>Sweden - epidemiology</subject><subject>T cells</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi0EokvhD3BAOXFLmPE6TixxQRW0SJV66aE3yxlPwEs-Fjsp6r_Hyy70BJz8oed5NZpXiNcIFQLqd7uq6yJVEqCuECsw8onYIBgoJYJ6KjYAoEtp8O5MvEhpB4CotHkuzlBvpTGm2YjLq3V0U_GFJ14CFXwfPE_ExfLVLcXNnYIipCKM-yGQW9gXYSrGh5lc9MEN-dW7SEuYp5fiWe-GxK9O57m4_fTx9uKqvL65_Hzx4bok1WyXUmvXe5CsyDFqlFL5vle1bIEYe0PUAnvCHj0TSO3rmpVrqas1KKB2ey7KY2z6wfu1s_sYRhcf7OyCPX19yze2ddO0us68-Su_j7N_lH6LiBqkzEvL7tujm8HvK6fFjiERD4ObeF6TbUCCQrX9L4iNqlvzC5RHkOKcUuT-zzwI9lCp3dlDpfZQaZ7E5kqz9OaUvnYj-0fl1GEG3h8Bznu_DxxtonAo0YfItFg_h3_l_wR3w7N1</recordid><startdate>20060120</startdate><enddate>20060120</enddate><creator>Ria, Massimiliano</creator><creator>Eriksson, Per</creator><creator>Boquist, Susanna</creator><creator>Ericsson, Carl-Göran</creator><creator>Hamsten, Anders</creator><creator>Lagercrantz, Jacob</creator><general>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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>20060120</creationdate><title>Human genetic evidence that OX40 is implicated in myocardial infarction</title><author>Ria, Massimiliano ; 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OX40L are associated with myocardial infarction (MI) and severity of coronary artery disease in human. A number of studies also suggest a possible role for OX40 (the OX40L receptor) as a factor contributing to atherosclerosis. In the present study, the
OX40 gene was screened for variants associated with precocious MI, using individuals with MI before the age of 60 and controls. Despite the fact that the
OX40 gene is highly conserved between species and that relatively few common genetic variants were encountered, an association with MI was seen for a polymorphism in intron 5 (rs2298212). In silico investigation suggested that genetic variation (rs2298211), linked to this intronic variant, is possibly affecting spliceosome function. Our results provide evidence that variants in human
OX40 might influence susceptibility to MI. The relevance of these findings is supported by the vital functions fulfilled by
OX40 in mammals as reflected by the high level of evolutionary conservation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16329997</pmid><doi>10.1016/j.bbrc.2005.11.092</doi><tpages>6</tpages></addata></record> |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Adolescent Adult Association study Atherosclerosis Candidate gene Comorbidity DNA Mutational Analysis Evidence-Based Medicine Female Genetic Predisposition to Disease - epidemiology Genetic Predisposition to Disease - genetics Genetic Testing - methods Genotype Haplotype blocks Humans Inflammation Male Medicin och hälsovetenskap Middle Aged Myocardial infarction Myocardial Infarction - epidemiology Myocardial Infarction - metabolism OX40 OX40L Polymorphism, Genetic Polymorphism, Single Nucleotide - genetics Prevalence Receptors, OX40 Receptors, Tumor Necrosis Factor - genetics Risk Assessment - methods Risk Factors Single nucleotide polymorphism Sweden - epidemiology T cells |
| title | Human genetic evidence that OX40 is implicated in myocardial infarction |
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