Protein interaction for an interferon-inducible systemic lupus associated gene, IFIT1
Objective. To identify disease-related genes and immune-regulatory pathways in the pathogenesis of systemic lupus erythematosus (SLE) by using gene expression profiling and protein–protein interaction analysis. Methods. Peripheral white blood cell gene expression profiles of 10 SLE patients were det...
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creator | Ye, S. Pang, H. Gu, Y.-Y. Hua, J. Chen, X.-G. Bao, C.-D. Wang, Y. Zhang, W. Qian, J. Tsao, B. P. Hahn, B. H. Chen, S.-L. Rao, Z.-H. Shen, N. |
description | Objective. To identify disease-related genes and immune-regulatory pathways in the pathogenesis of systemic lupus erythematosus (SLE) by using gene expression profiling and protein–protein interaction analysis. Methods. Peripheral white blood cell gene expression profiles of 10 SLE patients were determined by oligonucleotide microarray analysis. Clustering of the gene expression profile was compared with the clinical immune phenotype. SLE-induced genes that were over- or under-expressed were determined and independently validated using a real-time polymerase chain reaction (PCR) method. To study their potential function and the possible pathways involved, a candidate gene was cloned and a GST (glutathione S-transferase) fusion protein was expressed in Escherichia coli. The fusion protein was further purified using the glutathione Sepharose 4B system, and was treated as bait to capture prey from SLE peripheral white blood cell lysate. MALDI-TOF (matrix-assisted laser desorption/ionization–time-of-flight) mass spectrometry was then performed to determine the prey protein. Results. Similarity was found between the gene expression profile and the immune phenotype clusters of the SLE patients. More than 20 disease-associated genes were identified, some of which have not been related to SLE previously. Of these genes, a cluster of interferon-induced genes were highly correlated. IFIT1 (interferon-induced with tetratricopeptide repeats 1) was one of these genes, and overexpression of its mRNA was confirmed independently by real-time PCR in a larger population (40 SLE patients and 29 normal controls). An IFIT1 protein– protein interaction study showed that IFIT1 may interact with Rho/Rac guanine nucleotide exchange factor. Conclusion. The gene expression profile seems to be the molecular basis of the diverse immune phenotype of SLE. On the basis of the SLE-related genes found in this study, we suggest that the interferon-related immune pathway is important in the pathogenesis of SLE. IFIT1 is the first gene described as a candidate gene for SLE, and may function by activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factor. IFIT1 and the interferon-related pathway may provide potential targets for novel interventions in the treatment of SLE. |
doi_str_mv | 10.1093/rheumatology/keg315 |
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P. ; Hahn, B. H. ; Chen, S.-L. ; Rao, Z.-H. ; Shen, N.</creator><creatorcontrib>Ye, S. ; Pang, H. ; Gu, Y.-Y. ; Hua, J. ; Chen, X.-G. ; Bao, C.-D. ; Wang, Y. ; Zhang, W. ; Qian, J. ; Tsao, B. P. ; Hahn, B. H. ; Chen, S.-L. ; Rao, Z.-H. ; Shen, N.</creatorcontrib><description>Objective. To identify disease-related genes and immune-regulatory pathways in the pathogenesis of systemic lupus erythematosus (SLE) by using gene expression profiling and protein–protein interaction analysis. Methods. Peripheral white blood cell gene expression profiles of 10 SLE patients were determined by oligonucleotide microarray analysis. Clustering of the gene expression profile was compared with the clinical immune phenotype. SLE-induced genes that were over- or under-expressed were determined and independently validated using a real-time polymerase chain reaction (PCR) method. To study their potential function and the possible pathways involved, a candidate gene was cloned and a GST (glutathione S-transferase) fusion protein was expressed in Escherichia coli. The fusion protein was further purified using the glutathione Sepharose 4B system, and was treated as bait to capture prey from SLE peripheral white blood cell lysate. MALDI-TOF (matrix-assisted laser desorption/ionization–time-of-flight) mass spectrometry was then performed to determine the prey protein. Results. Similarity was found between the gene expression profile and the immune phenotype clusters of the SLE patients. More than 20 disease-associated genes were identified, some of which have not been related to SLE previously. Of these genes, a cluster of interferon-induced genes were highly correlated. IFIT1 (interferon-induced with tetratricopeptide repeats 1) was one of these genes, and overexpression of its mRNA was confirmed independently by real-time PCR in a larger population (40 SLE patients and 29 normal controls). An IFIT1 protein– protein interaction study showed that IFIT1 may interact with Rho/Rac guanine nucleotide exchange factor. Conclusion. The gene expression profile seems to be the molecular basis of the diverse immune phenotype of SLE. On the basis of the SLE-related genes found in this study, we suggest that the interferon-related immune pathway is important in the pathogenesis of SLE. IFIT1 is the first gene described as a candidate gene for SLE, and may function by activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factor. IFIT1 and the interferon-related pathway may provide potential targets for novel interventions in the treatment of SLE.</description><identifier>ISSN: 1462-0324</identifier><identifier>ISSN: 1460-2172</identifier><identifier>EISSN: 1462-0332</identifier><identifier>EISSN: 1460-2172</identifier><identifier>DOI: 10.1093/rheumatology/keg315</identifier><identifier>PMID: 12777642</identifier><identifier>CODEN: BJRHDF</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Biological and medical sciences ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; Escherichia coli ; Female ; Gene expression profile ; Gene Expression Profiling - methods ; Genetic Predisposition to Disease ; Glutathione Transferase - metabolism ; Humans ; Immunophenotyping ; Interferon ; Interferon-induced protein with tetratricopeptide repeats 1 ; Lupus Erythematosus, Systemic - genetics ; Lupus Erythematosus, Systemic - immunology ; Lupus Erythematosus, Systemic - metabolism ; Male ; Medical sciences ; Multigene Family ; Oligonucleotide Array Sequence Analysis ; Polymerase Chain Reaction - methods ; Protein Binding - genetics ; Protein–protein interaction ; Recombinant Fusion Proteins - metabolism ; RNA, Messenger - genetics ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Systemic lupus erythematosus ; Up-Regulation</subject><ispartof>British journal of rheumatology, 2003-10, Vol.42 (10), p.1155-1163</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Oct 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c538t-3b232da7e41a6e105e592d63cc446ad71884ba8b197339b8400f95ef0a0013873</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15165956$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12777642$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ye, S.</creatorcontrib><creatorcontrib>Pang, H.</creatorcontrib><creatorcontrib>Gu, Y.-Y.</creatorcontrib><creatorcontrib>Hua, J.</creatorcontrib><creatorcontrib>Chen, X.-G.</creatorcontrib><creatorcontrib>Bao, C.-D.</creatorcontrib><creatorcontrib>Wang, Y.</creatorcontrib><creatorcontrib>Zhang, W.</creatorcontrib><creatorcontrib>Qian, J.</creatorcontrib><creatorcontrib>Tsao, B. P.</creatorcontrib><creatorcontrib>Hahn, B. H.</creatorcontrib><creatorcontrib>Chen, S.-L.</creatorcontrib><creatorcontrib>Rao, Z.-H.</creatorcontrib><creatorcontrib>Shen, N.</creatorcontrib><title>Protein interaction for an interferon-inducible systemic lupus associated gene, IFIT1</title><title>British journal of rheumatology</title><addtitle>Rheumatology</addtitle><description>Objective. To identify disease-related genes and immune-regulatory pathways in the pathogenesis of systemic lupus erythematosus (SLE) by using gene expression profiling and protein–protein interaction analysis. Methods. Peripheral white blood cell gene expression profiles of 10 SLE patients were determined by oligonucleotide microarray analysis. Clustering of the gene expression profile was compared with the clinical immune phenotype. SLE-induced genes that were over- or under-expressed were determined and independently validated using a real-time polymerase chain reaction (PCR) method. To study their potential function and the possible pathways involved, a candidate gene was cloned and a GST (glutathione S-transferase) fusion protein was expressed in Escherichia coli. The fusion protein was further purified using the glutathione Sepharose 4B system, and was treated as bait to capture prey from SLE peripheral white blood cell lysate. MALDI-TOF (matrix-assisted laser desorption/ionization–time-of-flight) mass spectrometry was then performed to determine the prey protein. Results. Similarity was found between the gene expression profile and the immune phenotype clusters of the SLE patients. More than 20 disease-associated genes were identified, some of which have not been related to SLE previously. Of these genes, a cluster of interferon-induced genes were highly correlated. IFIT1 (interferon-induced with tetratricopeptide repeats 1) was one of these genes, and overexpression of its mRNA was confirmed independently by real-time PCR in a larger population (40 SLE patients and 29 normal controls). An IFIT1 protein– protein interaction study showed that IFIT1 may interact with Rho/Rac guanine nucleotide exchange factor. Conclusion. The gene expression profile seems to be the molecular basis of the diverse immune phenotype of SLE. On the basis of the SLE-related genes found in this study, we suggest that the interferon-related immune pathway is important in the pathogenesis of SLE. IFIT1 is the first gene described as a candidate gene for SLE, and may function by activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factor. IFIT1 and the interferon-related pathway may provide potential targets for novel interventions in the treatment of SLE.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - metabolism</subject><subject>Escherichia coli</subject><subject>Female</subject><subject>Gene expression profile</subject><subject>Gene Expression Profiling - methods</subject><subject>Genetic Predisposition to Disease</subject><subject>Glutathione Transferase - metabolism</subject><subject>Humans</subject><subject>Immunophenotyping</subject><subject>Interferon</subject><subject>Interferon-induced protein with tetratricopeptide repeats 1</subject><subject>Lupus Erythematosus, Systemic - genetics</subject><subject>Lupus Erythematosus, Systemic - immunology</subject><subject>Lupus Erythematosus, Systemic - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Multigene Family</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Polymerase Chain Reaction - methods</subject><subject>Protein Binding - genetics</subject><subject>Protein–protein interaction</subject><subject>Recombinant Fusion Proteins - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>Systemic lupus erythematosus</subject><subject>Up-Regulation</subject><issn>1462-0324</issn><issn>1460-2172</issn><issn>1462-0332</issn><issn>1460-2172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1rFTEUhoMotl79BYIMgl05Np-TZCm1HxcLdtGCdBMymTPXtDPJbTID3n9vyh1aceMqIXnOe3LyIPSe4C8Ea3acfsE82ikOcbM7vocNI-IFOiS8oTVmjL582lN-gN7kfIcxFoSp1-iAUCllw-khurlKcQIfKh8mSNZNPoaqj6myy1EPKYbah252vh2gyrs8wehdNczbOVc25-i8naCrNhDgc7U-W1-Tt-hVb4cM75Z1hW7OTq9PLurLH-frk6-XtRNMTTVrKaOdlcCJbYBgAULTrmHOcd7YThKleGtVS7RkTLeKY9xrAT22GJdBJFuho33uNsWHGfJkRp8dDIMNEOdspJBUaUX_CxJd0lj5nRX6-A94F-cUyhCFEY1iWj-2ZXvIpZhzgt5skx9t2hmCzaMb87cbs3dTqj4s0XM7Qvdcs8gowKcFsNnZoU82OJ-fOUEaUd5QuHrP-aLi99O9TfemkUwKc_Hz1tziq2_fpeDmnP0BfSWqIw</recordid><startdate>20031001</startdate><enddate>20031001</enddate><creator>Ye, S.</creator><creator>Pang, H.</creator><creator>Gu, Y.-Y.</creator><creator>Hua, J.</creator><creator>Chen, X.-G.</creator><creator>Bao, C.-D.</creator><creator>Wang, Y.</creator><creator>Zhang, W.</creator><creator>Qian, J.</creator><creator>Tsao, B. P.</creator><creator>Hahn, B. H.</creator><creator>Chen, S.-L.</creator><creator>Rao, Z.-H.</creator><creator>Shen, N.</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><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>7QP</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7QL</scope><scope>7T5</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20031001</creationdate><title>Protein interaction for an interferon-inducible systemic lupus associated gene, IFIT1</title><author>Ye, S. ; Pang, H. ; Gu, Y.-Y. ; Hua, J. ; Chen, X.-G. ; Bao, C.-D. ; Wang, Y. ; Zhang, W. ; Qian, J. ; Tsao, B. P. ; Hahn, B. H. ; Chen, S.-L. ; Rao, Z.-H. ; Shen, N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c538t-3b232da7e41a6e105e592d63cc446ad71884ba8b197339b8400f95ef0a0013873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - metabolism</topic><topic>Escherichia coli</topic><topic>Female</topic><topic>Gene expression profile</topic><topic>Gene Expression Profiling - methods</topic><topic>Genetic Predisposition to Disease</topic><topic>Glutathione Transferase - metabolism</topic><topic>Humans</topic><topic>Immunophenotyping</topic><topic>Interferon</topic><topic>Interferon-induced protein with tetratricopeptide repeats 1</topic><topic>Lupus Erythematosus, Systemic - genetics</topic><topic>Lupus Erythematosus, Systemic - immunology</topic><topic>Lupus Erythematosus, Systemic - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Multigene Family</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Polymerase Chain Reaction - methods</topic><topic>Protein Binding - genetics</topic><topic>Protein–protein interaction</topic><topic>Recombinant Fusion Proteins - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><topic>Systemic lupus erythematosus</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ye, S.</creatorcontrib><creatorcontrib>Pang, H.</creatorcontrib><creatorcontrib>Gu, Y.-Y.</creatorcontrib><creatorcontrib>Hua, J.</creatorcontrib><creatorcontrib>Chen, X.-G.</creatorcontrib><creatorcontrib>Bao, C.-D.</creatorcontrib><creatorcontrib>Wang, Y.</creatorcontrib><creatorcontrib>Zhang, W.</creatorcontrib><creatorcontrib>Qian, J.</creatorcontrib><creatorcontrib>Tsao, B. P.</creatorcontrib><creatorcontrib>Hahn, B. H.</creatorcontrib><creatorcontrib>Chen, S.-L.</creatorcontrib><creatorcontrib>Rao, Z.-H.</creatorcontrib><creatorcontrib>Shen, N.</creatorcontrib><collection>Istex</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of rheumatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ye, S.</au><au>Pang, H.</au><au>Gu, Y.-Y.</au><au>Hua, J.</au><au>Chen, X.-G.</au><au>Bao, C.-D.</au><au>Wang, Y.</au><au>Zhang, W.</au><au>Qian, J.</au><au>Tsao, B. P.</au><au>Hahn, B. H.</au><au>Chen, S.-L.</au><au>Rao, Z.-H.</au><au>Shen, N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protein interaction for an interferon-inducible systemic lupus associated gene, IFIT1</atitle><jtitle>British journal of rheumatology</jtitle><addtitle>Rheumatology</addtitle><date>2003-10-01</date><risdate>2003</risdate><volume>42</volume><issue>10</issue><spage>1155</spage><epage>1163</epage><pages>1155-1163</pages><issn>1462-0324</issn><issn>1460-2172</issn><eissn>1462-0332</eissn><eissn>1460-2172</eissn><coden>BJRHDF</coden><abstract>Objective. To identify disease-related genes and immune-regulatory pathways in the pathogenesis of systemic lupus erythematosus (SLE) by using gene expression profiling and protein–protein interaction analysis. Methods. Peripheral white blood cell gene expression profiles of 10 SLE patients were determined by oligonucleotide microarray analysis. Clustering of the gene expression profile was compared with the clinical immune phenotype. SLE-induced genes that were over- or under-expressed were determined and independently validated using a real-time polymerase chain reaction (PCR) method. To study their potential function and the possible pathways involved, a candidate gene was cloned and a GST (glutathione S-transferase) fusion protein was expressed in Escherichia coli. The fusion protein was further purified using the glutathione Sepharose 4B system, and was treated as bait to capture prey from SLE peripheral white blood cell lysate. MALDI-TOF (matrix-assisted laser desorption/ionization–time-of-flight) mass spectrometry was then performed to determine the prey protein. Results. Similarity was found between the gene expression profile and the immune phenotype clusters of the SLE patients. More than 20 disease-associated genes were identified, some of which have not been related to SLE previously. Of these genes, a cluster of interferon-induced genes were highly correlated. IFIT1 (interferon-induced with tetratricopeptide repeats 1) was one of these genes, and overexpression of its mRNA was confirmed independently by real-time PCR in a larger population (40 SLE patients and 29 normal controls). An IFIT1 protein– protein interaction study showed that IFIT1 may interact with Rho/Rac guanine nucleotide exchange factor. Conclusion. The gene expression profile seems to be the molecular basis of the diverse immune phenotype of SLE. On the basis of the SLE-related genes found in this study, we suggest that the interferon-related immune pathway is important in the pathogenesis of SLE. IFIT1 is the first gene described as a candidate gene for SLE, and may function by activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factor. IFIT1 and the interferon-related pathway may provide potential targets for novel interventions in the treatment of SLE.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>12777642</pmid><doi>10.1093/rheumatology/keg315</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Biological and medical sciences Carrier Proteins - genetics Carrier Proteins - metabolism Escherichia coli Female Gene expression profile Gene Expression Profiling - methods Genetic Predisposition to Disease Glutathione Transferase - metabolism Humans Immunophenotyping Interferon Interferon-induced protein with tetratricopeptide repeats 1 Lupus Erythematosus, Systemic - genetics Lupus Erythematosus, Systemic - immunology Lupus Erythematosus, Systemic - metabolism Male Medical sciences Multigene Family Oligonucleotide Array Sequence Analysis Polymerase Chain Reaction - methods Protein Binding - genetics Protein–protein interaction Recombinant Fusion Proteins - metabolism RNA, Messenger - genetics Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Systemic lupus erythematosus Up-Regulation |
title | Protein interaction for an interferon-inducible systemic lupus associated gene, IFIT1 |
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