External suppression causes the low expression of the Cosmc gene in IgA nephropathy
Objective. IgA1 aberrant O-glycosylation is one of the main pathogeneses of IgA nephropathy (IgAN), and the core I β3-Gal-T-specific molecular chaperone (Cosmc) mRNA expression of IgAN patients was significantly decreased. This study tried to clarify whether the down-regulation was a result of genet...
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| creator | Qin, Wei Zhong, Xiang Fan, Jun Ming Zhang, Ying Juan Liu, Xian Rong Ma, Xing Yi |
| description | Objective. IgA1 aberrant O-glycosylation is one of the main pathogeneses of IgA nephropathy (IgAN), and the core I β3-Gal-T-specific molecular chaperone (Cosmc) mRNA expression of IgAN patients was significantly decreased. This study tried to clarify whether the down-regulation was a result of genetic disorders or external suppressions. Method. Sixty-five IgAN patients, 23 non-IgAN glomerulonephritis patients and 21 normal controls were recruited. Genomic DNA was extracted and the Cosmc gene was PCR amplified and directly sequenced. Peripheral B lymphocytes of IgAN patients and normal controls were isolated, and cultured with RPMI-1640 alone or with lipopolysaccharide (LPS) for 72 h. The Cosmc mRNA expression levels at baseline, after RPMI culture or RPMI + LPS treatment were measured by real-time RT-PCR. Results. (1) The whole coding frame region of the Cosmc gene was successfully amplified and directly sequenced. Four single nucleotide polymorphisms were detected in two IgAN patients. Two were missense mutations and the others were silent mutations. However, they are different from each other, and unrelated to expression levels; (2) the baseline Cosmc mRNA expression in IgAN patients was significantly lower than normal controls (CtCOSMC/GAPDH 1.29 ± 0.08 versus 1.20 ± 0.01, 31% of normal controls); (3) the Cosmc mRNA expression level of IgAN patients was remarkably increased after the RPMI culture (1.22 ± 0.12 versus 1.29 ± 0.08, 219% of the baseline level), while not in normal controls and (4) treatment with LPS (culture with RPMI + LPS) could strongly inhibit the expression of Cosmc mRNA (1.25 ± 0.01 versus 1.22 ± 0.12, 61% of the RPMI treatment group). Conclusion. No common Cosmc gene mutation was detected. Significantly increased Cosmc expression was observed in plasma-free culture, while LPS could significantly inhibit it, which suggested that it might not be genetic disorders but external suppression that causes the low Cosmc mRNA expression in IgAN. |
| doi_str_mv | 10.1093/ndt/gfm781 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69120591</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/ndt/gfm781</oup_id><sourcerecordid>20930682</sourcerecordid><originalsourceid>FETCH-LOGICAL-c477t-ff245c7ffd031213d1bc1595dff23d00f99898bf69a4f29664d53632d4c3d3043</originalsourceid><addsrcrecordid>eNqF0V1rFDEUBuAgit1Wb_wBEgS9EMbm5HNyWdZqCwUVFcWbkM0ku1NnJmMyQ7f_3tRdtuCFXgXOeTiB90XoGZA3QDQ7HZrpdB16VcMDtAAuSUVZLR6iRVlCRQTRR-g452tCiKZKPUZHUFNCSa0X6PP5dvJpsB3O8zgmn3MbB-zsnH3G08bjLt5gvz1sYvgzXcbcO7z2g8ftgC_XZ3jw4ybF0U6b2yfoUbBd9k_37wn6-u78y_Kiuvrw_nJ5dlU5rtRUhUC5cCqEhjCgwBpYORBaNGXBGkKC1rWuV0FqywPVUvJGMMlowx1rGOHsBL3a3R1T_DX7PJm-zc53nR18nLORGigRGv4LaQmKyJoW-OIveB3nu3SKgRqkBBAFvd4hl2LOyQczpra36dYAMXeFmFKI2RVS8PP9xXnV--ae7hso4OUe2OxsF5IdXJsPjpZsiOLs3sV5_PeH1c61efLbg7Tpp5GKKWEuvv8w3_gnUB-5MG_Zb0KxrnM</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>218166115</pqid></control><display><type>article</type><title>External suppression causes the low expression of the Cosmc gene in IgA nephropathy</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Oxford University Press Journals All Titles (1996-Current)</source><source>Alma/SFX Local Collection</source><creator>Qin, Wei ; Zhong, Xiang ; Fan, Jun Ming ; Zhang, Ying Juan ; Liu, Xian Rong ; Ma, Xing Yi</creator><creatorcontrib>Qin, Wei ; Zhong, Xiang ; Fan, Jun Ming ; Zhang, Ying Juan ; Liu, Xian Rong ; Ma, Xing Yi</creatorcontrib><description>Objective. IgA1 aberrant O-glycosylation is one of the main pathogeneses of IgA nephropathy (IgAN), and the core I β3-Gal-T-specific molecular chaperone (Cosmc) mRNA expression of IgAN patients was significantly decreased. This study tried to clarify whether the down-regulation was a result of genetic disorders or external suppressions. Method. Sixty-five IgAN patients, 23 non-IgAN glomerulonephritis patients and 21 normal controls were recruited. Genomic DNA was extracted and the Cosmc gene was PCR amplified and directly sequenced. Peripheral B lymphocytes of IgAN patients and normal controls were isolated, and cultured with RPMI-1640 alone or with lipopolysaccharide (LPS) for 72 h. The Cosmc mRNA expression levels at baseline, after RPMI culture or RPMI + LPS treatment were measured by real-time RT-PCR. Results. (1) The whole coding frame region of the Cosmc gene was successfully amplified and directly sequenced. Four single nucleotide polymorphisms were detected in two IgAN patients. Two were missense mutations and the others were silent mutations. However, they are different from each other, and unrelated to expression levels; (2) the baseline Cosmc mRNA expression in IgAN patients was significantly lower than normal controls (CtCOSMC/GAPDH 1.29 ± 0.08 versus 1.20 ± 0.01, 31% of normal controls); (3) the Cosmc mRNA expression level of IgAN patients was remarkably increased after the RPMI culture (1.22 ± 0.12 versus 1.29 ± 0.08, 219% of the baseline level), while not in normal controls and (4) treatment with LPS (culture with RPMI + LPS) could strongly inhibit the expression of Cosmc mRNA (1.25 ± 0.01 versus 1.22 ± 0.12, 61% of the RPMI treatment group). Conclusion. No common Cosmc gene mutation was detected. Significantly increased Cosmc expression was observed in plasma-free culture, while LPS could significantly inhibit it, which suggested that it might not be genetic disorders but external suppression that causes the low Cosmc mRNA expression in IgAN.</description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/ndt/gfm781</identifier><identifier>PMID: 18202089</identifier><identifier>CODEN: NDTREA</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; B-Lymphocytes - drug effects ; B-Lymphocytes - metabolism ; Base Sequence ; Biological and medical sciences ; Case-Control Studies ; Cosmc ; DNA Primers - genetics ; Down-Regulation - drug effects ; Emergency and intensive care: renal failure. Dialysis management ; Female ; Glomerulonephritis ; Glomerulonephritis, IGA - genetics ; Glomerulonephritis, IGA - metabolism ; Glycosylation ; Humans ; IgA nephropathy ; Immunoglobulin A - metabolism ; Intensive care medicine ; Lipopolysaccharides - pharmacology ; LPS ; Male ; Medical sciences ; Molecular Chaperones - genetics ; mRNA expression ; Mutation, Missense ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Polymorphism, Single Nucleotide ; real-time RT-PCR ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; RNA, Messenger - metabolism</subject><ispartof>Nephrology, dialysis, transplantation, 2008-05, Vol.23 (5), p.1608-1614</ispartof><rights>Oxford University Press © The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org 2008</rights><rights>2008 INIST-CNRS</rights><rights>The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c477t-ff245c7ffd031213d1bc1595dff23d00f99898bf69a4f29664d53632d4c3d3043</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1584,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20310743$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18202089$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qin, Wei</creatorcontrib><creatorcontrib>Zhong, Xiang</creatorcontrib><creatorcontrib>Fan, Jun Ming</creatorcontrib><creatorcontrib>Zhang, Ying Juan</creatorcontrib><creatorcontrib>Liu, Xian Rong</creatorcontrib><creatorcontrib>Ma, Xing Yi</creatorcontrib><title>External suppression causes the low expression of the Cosmc gene in IgA nephropathy</title><title>Nephrology, dialysis, transplantation</title><addtitle>Nephrol Dial Transplant</addtitle><addtitle>Nephrol Dial Transplant</addtitle><description>Objective. IgA1 aberrant O-glycosylation is one of the main pathogeneses of IgA nephropathy (IgAN), and the core I β3-Gal-T-specific molecular chaperone (Cosmc) mRNA expression of IgAN patients was significantly decreased. This study tried to clarify whether the down-regulation was a result of genetic disorders or external suppressions. Method. Sixty-five IgAN patients, 23 non-IgAN glomerulonephritis patients and 21 normal controls were recruited. Genomic DNA was extracted and the Cosmc gene was PCR amplified and directly sequenced. Peripheral B lymphocytes of IgAN patients and normal controls were isolated, and cultured with RPMI-1640 alone or with lipopolysaccharide (LPS) for 72 h. The Cosmc mRNA expression levels at baseline, after RPMI culture or RPMI + LPS treatment were measured by real-time RT-PCR. Results. (1) The whole coding frame region of the Cosmc gene was successfully amplified and directly sequenced. Four single nucleotide polymorphisms were detected in two IgAN patients. Two were missense mutations and the others were silent mutations. However, they are different from each other, and unrelated to expression levels; (2) the baseline Cosmc mRNA expression in IgAN patients was significantly lower than normal controls (CtCOSMC/GAPDH 1.29 ± 0.08 versus 1.20 ± 0.01, 31% of normal controls); (3) the Cosmc mRNA expression level of IgAN patients was remarkably increased after the RPMI culture (1.22 ± 0.12 versus 1.29 ± 0.08, 219% of the baseline level), while not in normal controls and (4) treatment with LPS (culture with RPMI + LPS) could strongly inhibit the expression of Cosmc mRNA (1.25 ± 0.01 versus 1.22 ± 0.12, 61% of the RPMI treatment group). Conclusion. No common Cosmc gene mutation was detected. Significantly increased Cosmc expression was observed in plasma-free culture, while LPS could significantly inhibit it, which suggested that it might not be genetic disorders but external suppression that causes the low Cosmc mRNA expression in IgAN.</description><subject>Adult</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>B-Lymphocytes - drug effects</subject><subject>B-Lymphocytes - metabolism</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Cosmc</subject><subject>DNA Primers - genetics</subject><subject>Down-Regulation - drug effects</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>Female</subject><subject>Glomerulonephritis</subject><subject>Glomerulonephritis, IGA - genetics</subject><subject>Glomerulonephritis, IGA - metabolism</subject><subject>Glycosylation</subject><subject>Humans</subject><subject>IgA nephropathy</subject><subject>Immunoglobulin A - metabolism</subject><subject>Intensive care medicine</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>LPS</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Molecular Chaperones - genetics</subject><subject>mRNA expression</subject><subject>Mutation, Missense</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Polymorphism, Single Nucleotide</subject><subject>real-time RT-PCR</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0V1rFDEUBuAgit1Wb_wBEgS9EMbm5HNyWdZqCwUVFcWbkM0ku1NnJmMyQ7f_3tRdtuCFXgXOeTiB90XoGZA3QDQ7HZrpdB16VcMDtAAuSUVZLR6iRVlCRQTRR-g452tCiKZKPUZHUFNCSa0X6PP5dvJpsB3O8zgmn3MbB-zsnH3G08bjLt5gvz1sYvgzXcbcO7z2g8ftgC_XZ3jw4ybF0U6b2yfoUbBd9k_37wn6-u78y_Kiuvrw_nJ5dlU5rtRUhUC5cCqEhjCgwBpYORBaNGXBGkKC1rWuV0FqywPVUvJGMMlowx1rGOHsBL3a3R1T_DX7PJm-zc53nR18nLORGigRGv4LaQmKyJoW-OIveB3nu3SKgRqkBBAFvd4hl2LOyQczpra36dYAMXeFmFKI2RVS8PP9xXnV--ae7hso4OUe2OxsF5IdXJsPjpZsiOLs3sV5_PeH1c61efLbg7Tpp5GKKWEuvv8w3_gnUB-5MG_Zb0KxrnM</recordid><startdate>20080501</startdate><enddate>20080501</enddate><creator>Qin, Wei</creator><creator>Zhong, Xiang</creator><creator>Fan, Jun Ming</creator><creator>Zhang, Ying Juan</creator><creator>Liu, Xian Rong</creator><creator>Ma, Xing Yi</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>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20080501</creationdate><title>External suppression causes the low expression of the Cosmc gene in IgA nephropathy</title><author>Qin, Wei ; Zhong, Xiang ; Fan, Jun Ming ; Zhang, Ying Juan ; Liu, Xian Rong ; Ma, Xing Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c477t-ff245c7ffd031213d1bc1595dff23d00f99898bf69a4f29664d53632d4c3d3043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>B-Lymphocytes - drug effects</topic><topic>B-Lymphocytes - metabolism</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Cosmc</topic><topic>DNA Primers - genetics</topic><topic>Down-Regulation - drug effects</topic><topic>Emergency and intensive care: renal failure. Dialysis management</topic><topic>Female</topic><topic>Glomerulonephritis</topic><topic>Glomerulonephritis, IGA - genetics</topic><topic>Glomerulonephritis, IGA - metabolism</topic><topic>Glycosylation</topic><topic>Humans</topic><topic>IgA nephropathy</topic><topic>Immunoglobulin A - metabolism</topic><topic>Intensive care medicine</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>LPS</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Molecular Chaperones - genetics</topic><topic>mRNA expression</topic><topic>Mutation, Missense</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Polymorphism, Single Nucleotide</topic><topic>real-time RT-PCR</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qin, Wei</creatorcontrib><creatorcontrib>Zhong, Xiang</creatorcontrib><creatorcontrib>Fan, Jun Ming</creatorcontrib><creatorcontrib>Zhang, Ying Juan</creatorcontrib><creatorcontrib>Liu, Xian Rong</creatorcontrib><creatorcontrib>Ma, Xing Yi</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qin, Wei</au><au>Zhong, Xiang</au><au>Fan, Jun Ming</au><au>Zhang, Ying Juan</au><au>Liu, Xian Rong</au><au>Ma, Xing Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>External suppression causes the low expression of the Cosmc gene in IgA nephropathy</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><stitle>Nephrol Dial Transplant</stitle><addtitle>Nephrol Dial Transplant</addtitle><date>2008-05-01</date><risdate>2008</risdate><volume>23</volume><issue>5</issue><spage>1608</spage><epage>1614</epage><pages>1608-1614</pages><issn>0931-0509</issn><eissn>1460-2385</eissn><coden>NDTREA</coden><abstract>Objective. IgA1 aberrant O-glycosylation is one of the main pathogeneses of IgA nephropathy (IgAN), and the core I β3-Gal-T-specific molecular chaperone (Cosmc) mRNA expression of IgAN patients was significantly decreased. This study tried to clarify whether the down-regulation was a result of genetic disorders or external suppressions. Method. Sixty-five IgAN patients, 23 non-IgAN glomerulonephritis patients and 21 normal controls were recruited. Genomic DNA was extracted and the Cosmc gene was PCR amplified and directly sequenced. Peripheral B lymphocytes of IgAN patients and normal controls were isolated, and cultured with RPMI-1640 alone or with lipopolysaccharide (LPS) for 72 h. The Cosmc mRNA expression levels at baseline, after RPMI culture or RPMI + LPS treatment were measured by real-time RT-PCR. Results. (1) The whole coding frame region of the Cosmc gene was successfully amplified and directly sequenced. Four single nucleotide polymorphisms were detected in two IgAN patients. Two were missense mutations and the others were silent mutations. However, they are different from each other, and unrelated to expression levels; (2) the baseline Cosmc mRNA expression in IgAN patients was significantly lower than normal controls (CtCOSMC/GAPDH 1.29 ± 0.08 versus 1.20 ± 0.01, 31% of normal controls); (3) the Cosmc mRNA expression level of IgAN patients was remarkably increased after the RPMI culture (1.22 ± 0.12 versus 1.29 ± 0.08, 219% of the baseline level), while not in normal controls and (4) treatment with LPS (culture with RPMI + LPS) could strongly inhibit the expression of Cosmc mRNA (1.25 ± 0.01 versus 1.22 ± 0.12, 61% of the RPMI treatment group). Conclusion. No common Cosmc gene mutation was detected. Significantly increased Cosmc expression was observed in plasma-free culture, while LPS could significantly inhibit it, which suggested that it might not be genetic disorders but external suppression that causes the low Cosmc mRNA expression in IgAN.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>18202089</pmid><doi>10.1093/ndt/gfm781</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy B-Lymphocytes - drug effects B-Lymphocytes - metabolism Base Sequence Biological and medical sciences Case-Control Studies Cosmc DNA Primers - genetics Down-Regulation - drug effects Emergency and intensive care: renal failure. Dialysis management Female Glomerulonephritis Glomerulonephritis, IGA - genetics Glomerulonephritis, IGA - metabolism Glycosylation Humans IgA nephropathy Immunoglobulin A - metabolism Intensive care medicine Lipopolysaccharides - pharmacology LPS Male Medical sciences Molecular Chaperones - genetics mRNA expression Mutation, Missense Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Polymorphism, Single Nucleotide real-time RT-PCR Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics RNA, Messenger - metabolism |
| title | External suppression causes the low expression of the Cosmc gene in IgA nephropathy |
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