Schizophrenia-associated Risk and Protective Variants of c-Fos Encoding Gene

<!DOCTYPE html> <html lang="en"> <head> <meta charset="utf-8"> <title> Schizophrenia-associated Risk and Protective Variants of c-Fos Encoding Gene | Bentham Science </title> <meta content="IE=edge" http-equiv="X-UA-Compatible"> <meta content="width=device-width, initial-scale=1" name="viewport">  <meta content="4RtnG8Gb9swGdke2lTXa5LHPreg5Xgq7JKlr9jiO" name="csrf-token">  <meta name="description" content="Defects in synaptic plasticity play a key role in pathophysiology of schizophrenia. Pathomechanisms responsible for synaptic plasticity alterations in sch" /> <meta name="keywords" content="Schizophrenia-associated Risk and Protective Variants of c-Fos Encoding Gene"> <meta property="og:type" content="website" /> <meta property="og:title" content="Schizophrenia-associated Risk and Protective Variants of c-Fos Encoding Gene" /> <meta property="og:url" content="https://www.benthamscience.com/article/65357" /> <meta property="og:image" content="http://www.benthamscience.com/images/bentham/radnag-journal-cover.gif" /> <meta property="og:description" content="Defects in synaptic plasticity play a key role in pathophysiology of schizophrenia. Pathomechanisms responsible for synaptic plasticity alterations in schizophrenia are very complicated and not well defined. Transcription factor c-Fos plays an important role in regulation of synaptic plasticity. In the present study we evaluated the association of rs7101 and rs1063169 single nucleotide polymorphisms (SNPs) of c-Fos encoding gene (FOS) with schizophrenia. A total of 604 DNA samples of schizophrenia-affected and healthy subjects of Armenian ancestry were genotyped using polymerase chain reaction with sequence-specific primers. Also, comparative determination of the blood levels of c-Fos protein in schizophrenia patients and controls was performed using the enzyme-linked immunosorbent assay. Potential interaction between protein level and genotypes as well as relationships between genotypes/protein level and clinical-demographic characteristics of schizophrenia patients were assessed. The results obtained demonstrated that mutant allele of FOS rs1063169 SNP is negatively associated with schizophrenia and may be nominated as a protective factor for this disorder. On the other hand, according to our results, the FOS rs7101T mutant allele is positively associated with schizophrenia and, therefore, may be considered as a risk factor for this disorder. In addition, decreased c-Fos plasma levels in schizophrenia patients compared to controls were found. In conclusion, the results of this study suggest that FOS is among the candidate genes of schizophrenia and that changes in the expression of c-Fos protein may contribute to molecular pathomechanisms of schizophrenia-related alterations in synaptic plasticity." /> <meta property="og:site_name" content="http://www.benthamscience.com" /> <meta name="citation_title" content="Schizophrenia-associated Risk and Protective Variants of c-Fos Encoding Gene" /> <meta name="citation_author" content="Anna Boyajyan" /> <meta name="citation_author" content="Roksana Zakharyan" /> <meta name="citation_author" content="Sofi Atshemyan" /> <meta name="citation_author" content="Andranik Chavushyan" /> <meta name="citation_author" content="Gohar Mkrtchyan" /> <meta name="citation_publish_on" content="2015-02-23 " /> <meta name="citation_journal_title" content="Recent Advances in DNA & Gene Sequences (Discontinued)"> <meta name="citation_volume" content="9"> <meta name="citation_issue" content="1"> <meta name="citation_firstpage" content="51"> <meta name="citation_lastpage" content="57"> <meta name="citation_pdf_url" content="http://www.benthamscience.com/article/65357"> <meta name="citation_doi" content="10.2174/2352092209666150223113334" /> <script defer="" src="https://www.benthamscience.com/js/app.js"></script> <script type="text/javascript" src="https://www.benthamscience.com/js/jquery.min.js"></script>  <script src="https://www.benthamscience.com/js/all.min.js"></script>   <link href="https://www.benthamscience.com/css/bootstrap.min.css" rel="stylesheet"> <link href="https://www.benthamscience.com/css/style.css" media="all" rel="stylesheet" type="text/css"> <link href="https://www.benthamscience.com/plugins/animate-hover/hover-min.css" rel="stylesheet" type="text/css"> <link href="https://www.benthamscience.com/plugins/wow-animate/animate.css" rel="stylesheet" type="text/css"> <link href="https://www.benthamscience.com/assets/vendors/select2/css/select2.min.css" rel="stylesheet" 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data-content="<p><strong>Editor-in-Chief:</strong><br>Christian Bronner  <br>Institute of Genetics and Molecular and Cellular Biology<br>University of Strasboug<br>France</p>">Editor-in-Chief <i class="fas fa-angle-double-right"></i></a> <p>ISSN (Print): 2352-0922 <br> ISSN (Online): 2352-0930 </p> </div> </div> </div> <div class="col-md-12 mt-3"> <a href="https://www.benthamscience.com" class="btn btn-outline-light btn-sm">Back</a> <div class="dropdown d-inline"> <button class="btn btn-light btn-sm dropdown-toggle" type="button" id="dropdownMenuButton" data-toggle="dropdown" aria-haspopup="true" aria-expanded="false"> Journal </button> <div class="dropdown-menu" aria-labelledby="dropdownMenuButton"> <a class="dropdown-item" href="https://www.benthamscience.com/journal/154">Journal Home</a> <a class="dropdown-item" href="/journal/154/about-journal">About Journal</a> <a class="dropdown-item" href="/journal/154/editorial-board">Editorial Board</a> <a class="dropdown-item" href="/journal/154/current-issue">Current Issue </a> <a class="dropdown-item" href="https://www.benthamscience.com/journal/154">Volumes/Issues</a> </div> </div> <a href="https://benthamscience.com/subscribe-to-this-journal/154" class="btn btn-light btn-sm">Subscribe</a> </div> </div> </div> <div id="side-b" class="col-md-7"> <span class="badge badge-pill badge-info mb-2"></span> <h1>Schizophrenia-associated Risk and Protective Variants of c-Fos Encoding Gene</h1> <span class="l-h-3"><strong>Author(s):</strong> <a href="javascript:void(0)" class="text-secondary" title="Affiliation" data-html="true" data-toggle="popover" data-placement="bottom" data-trigger="hover" data-content="<ul><li>Laboratory of Human Genomics and Immunomics, Department of Applied Molecular Biology, Institute of Molecular Biology NAS RA, Zip code: 0014, Yerevan, Republic of Armenia,Armenia </li></ul>">Anna Boyajyan</a>, Roksana Zakharyan, Sofi Atshemyan, Andranik Chavushyan and Gohar Mkrtchyan </span> <div class="row"> <div class="col-md-8"> <p>Volume 9, Issue 1, 2015 </p>  <p><strong>Page:</strong> [51 - 57] <span class="float-right"><strong>Pages:</strong> 7 </span></p> <p><strong>DOI:</strong> <a href="http://dx.doi.org/10.2174/2352092209666150223113334" class="btn-link">10.2174/2352092209666150223113334</a></p> <p><strong>Price:</strong> $65</a></p> </div> <form method="POST" action="https://www.benthamscience.com/cart" id="addtocartForm"> <input type="hidden" name="_token" value="4RtnG8Gb9swGdke2lTXa5LHPreg5Xgq7JKlr9jiO" autocomplete="off"> <input type="hidden" name="param" value="eyJpdiI6IkFUWDhIenZvVm4yNTJGWGhKbmFPMHc9PSIsInZhbHVlIjoiWHkxU2VYbWR1Sy9WQzNnT3RQMFU1UT09IiwibWFjIjoiNmFkYjM5NmJhYzAyOWJkZmI4ZTE4OTNkMjViYzQ1YWQ2ZjQ5MmZlM2M5NjVkNDc3ZmRmM2MzMzc0NTAzYjM5YyIsInRhZyI6IiJ9"> <div class="col-md-4 text-right"> <button type="submit" id="addcartbtn" class="btn btn-download hvr-icon-hang">Purchase<br>PDF<br><i class="fas fa-cart-plus hvr-icon"></i></button> </div> </form> </div> </div> </div> </div> </section>   <main id="article"> <section> <div class="container"> <div class="row"> <div class="col-md-8">   <div id="abstract" class="card bigbox-hvr-slow"> <div class="card-header"> <h5>Abstract</h5> </div> <div class="card-body"> <p class="text-justify"> Defects in synaptic plasticity play a key role in pathophysiology of schizophrenia. Pathomechanisms responsible for synaptic plasticity alterations in schizophrenia are very complicated and not well defined. Transcription factor c-Fos plays an important role in regulation of synaptic plasticity. In the present study we evaluated the association of rs7101 and rs1063169 single nucleotide polymorphisms (SNPs) of c-Fos encoding gene (FOS) with schizophrenia. A total of 604 DNA samples of schizophrenia-affected and healthy subjects of Armenian ancestry were genotyped using polymerase chain reaction with sequence-specific primers. Also, comparative determination of the blood levels of c-Fos protein in schizophrenia patients and controls was performed using the enzyme-linked immunosorbent assay. Potential interaction between protein level and genotypes as well as relationships between genotypes/protein level and clinical-demographic characteristics of schizophrenia patients were assessed. The results obtained demonstrated that mutant allele of FOS rs1063169 SNP is negatively associated with schizophrenia and may be nominated as a protective factor for this disorder. On the other hand, according to our results, the FOS rs7101T mutant allele is positively associated with schizophrenia and, therefore, may be considered as a risk factor for this disorder. In addition, decreased c-Fos plasma levels in schizophrenia patients compared to controls were found. In conclusion, the results of this study suggest that FOS is among the candidate genes of schizophrenia and that changes in the expression of c-Fos protein may contribute to molecular pathomechanisms of schizophrenia-related alterations in synaptic plasticity. </p> <p><strong>Keywords: </strong> <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue=c-Fos protein">c-Fos protein</a>, <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue= FOS gene"> FOS gene</a>, <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue= genetic polymorphisms"> genetic polymorphisms</a>, <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue= plasma levels"> plasma levels</a>, <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue= schizophrenia"> schizophrenia</a>, <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue= synaptic plasticity."> synaptic plasticity.</a> </p> </div> </div> <div class="card-body"> <a href="https://www.benthamscience.com/article/72496" class="float-left btn btn-primary btn-sm active" data-mdb-toggle="button" autocomplete="off" aria-pressed="true">« Previous</a> <a href="https://www.benthamscience.com/article/65134" class="float-right btn btn-primary btn-sm active" data-mdb-toggle="button" autocomplete="off" aria-pressed="true">Next »</a> </div> <div id="abstract" class="card bigbox-hvr-slow mt-4"> <div class="card-header"> <h5>Graphical Abstract</h5> </div> <div class="card-body"> <p class="text-center"> <a href="javascript:void(0);" title="Click to enlarge"><img src="https://www.eurekaselect.com/images/graphical-abstract/radnag/9/1/2.jpg" data-high-res-src="https://www.eurekaselect.com/images/graphical-abstract/radnag/9/1/big-2.jpg" alt="" class="gallery-items img-thumbnail"> </a> <p> </div> </div> <br>  <div class="row mx-0"> <div class="col-lg-auto download-bar 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<p><strong>Title:</strong>Schizophrenia-associated Risk and Protective Variants of c-Fos Encoding Gene</p> <p><strong>Volume:</strong> 9 <strong>Issue:</strong> 1 </p> <p><strong>Author(s): </strong>Anna Boyajyan, Roksana Zakharyan, Sofi Atshemyan, Andranik Chavushyan and Gohar Mkrtchyan</p> <p><strong>Affiliation: </strong><ul></ul><ul></ul><ul></ul><ul></ul><ul></ul></p> <p><strong>Keywords:</strong> <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue=c-Fos protein">c-Fos protein</a>, <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue= FOS gene"> FOS gene</a>, <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue= genetic polymorphisms"> genetic polymorphisms</a>, <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue= plasma levels"> plasma levels</a>, <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue= schizophrenia"> schizophrenia</a>, <a target="_blank" class="btn-link" href="https://eurekaselect.com/search?searchvalue= synaptic plasticity."> synaptic plasticity.</a> </p> <p><strong>Abstract:</strong> Defects in synaptic plasticity play a key role in pathophysiology of schizophrenia. Pathomechanisms responsible for synaptic plasticity alterations in schizophrenia are very complicated and not well defined. Transcription factor c-Fos plays an important role in regulation of synaptic plasticity. In the present study we evaluated the association of rs7101 and rs1063169 single nucleotide polymorphisms (SNPs) of c-Fos encoding gene (FOS) with schizophrenia. A total of 604 DNA samples of schizophrenia-affected and healthy subjects of Armenian ancestry were genotyped using polymerase chain reaction with sequence-specific primers. Also, comparative determination of the blood levels of c-Fos protein in schizophrenia patients and controls was performed using the enzyme-linked immunosorbent assay. Potential interaction between protein level and genotypes as well as relationships between genotypes/protein level and clinical-demographic characteristics of schizophrenia patients were assessed. The results obtained demonstrated that mutant allele of FOS rs1063169 SNP is negatively associated with schizophrenia and may be nominated as a protective factor for this disorder. On the other hand, according to our results, the FOS rs7101T mutant allele is positively associated with schizophrenia and, therefore, may be considered as a risk factor for this disorder. In addition, decreased c-Fos plasma levels in schizophrenia patients compared to controls were found. In conclusion, the results of this study suggest that FOS is among the candidate genes of schizophrenia and that changes in the expression of c-Fos protein may contribute to molecular pathomechanisms of schizophrenia-related alterations in synaptic plasticity.</p> </div> <div class="modal-footer"> <button type="button" class="btn btn-outline-dark" data-dismiss="modal">Close</button> <button type="button" class="btn btn-outline-primary" data-dismiss="modal" onclick="SendForPrint()">Print this page</button> </div> </div> </div> </div>   <div class="modal fade" id="ExportWindow" role="dialog"> <div class="modal-dialog"> <div class="modal-content"> <div class="modal-header"> <h4 class="modal-title">Export Options</h4> <button type="button" class="close" data-dismiss="modal" aria-label="Close"><span aria-hidden="true">×</span></button> </div> <div class="modal-body"> <form method="post" action="https://www.benthamscience.com/citation" enctype="multipart/form-data" accept-charset="UTF-8" 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