Dysregulation of non-coding RNAs in autoimmune thyroid disease
Autoimmune thyroid disease (AITD) is a complex disorder with both genetic and environmental risk factors. A number of genetic factors such as HLA and CTLA-4 loci have been associated with risk of this disorder. In addition to these factors, recent studies have shown contribution of non-coding RNAs i...
Ausführliche Beschreibung
Autor*in: |
Taheri, Mohammad [verfasserIn] Eghtedarian, Reyhane [verfasserIn] Dinger, Marcel E. [verfasserIn] Ghafouri-Fard, Soudeh [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2020 |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: Experimental and molecular pathology - Orlando, Fla. : Academic Press, 1962, 117 |
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Übergeordnetes Werk: |
volume:117 |
DOI / URN: |
10.1016/j.yexmp.2020.104527 |
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Katalog-ID: |
ELV005121132 |
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520 | |a Autoimmune thyroid disease (AITD) is a complex disorder with both genetic and environmental risk factors. A number of genetic factors such as HLA and CTLA-4 loci have been associated with risk of this disorder. In addition to these factors, recent studies have shown contribution of non-coding RNAs in the pathogenesis of this condition. Several microRNAs (miRNAs) and a number of long noncoding RNAs (lncRNAs) such as IFNG-AS1, Heg, NR_038461, NR_038462, T204821 and NR_104125 have been dysregulated in peripheral blood of patients with AITD. These transcripts are mostly enriched in pathways that modulate humoral and cellular immune responses such as those associated with antigen presentation and differentiation of Th1, Th2 and Th17 cells. Functional studies verified the role of a number of lncRNAs and miRNAs in regulation of critical immune-related pathways in AITD. Thus, they participate in the pathophysiology of AITD. In the current review, we summarize the results of studies that assessed participation of non-coding RNAs in the pathophysiology of AITD. | ||
650 | 4 | |a Autoimmune thyroid disease | |
650 | 4 | |a AITD | |
650 | 4 | |a Hashimoto's thyroiditis | |
650 | 4 | |a Graves' disease | |
650 | 4 | |a miRNA | |
650 | 4 | |a lncRNA | |
700 | 1 | |a Eghtedarian, Reyhane |e verfasserin |4 aut | |
700 | 1 | |a Dinger, Marcel E. |e verfasserin |4 aut | |
700 | 1 | |a Ghafouri-Fard, Soudeh |e verfasserin |4 aut | |
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2020 |
allfields |
10.1016/j.yexmp.2020.104527 doi (DE-627)ELV005121132 (ELSEVIER)S0014-4800(20)30803-0 DE-627 ger DE-627 rda eng 610 DE-600 44.47 bkl Taheri, Mohammad verfasserin aut Dysregulation of non-coding RNAs in autoimmune thyroid disease 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Autoimmune thyroid disease (AITD) is a complex disorder with both genetic and environmental risk factors. A number of genetic factors such as HLA and CTLA-4 loci have been associated with risk of this disorder. In addition to these factors, recent studies have shown contribution of non-coding RNAs in the pathogenesis of this condition. Several microRNAs (miRNAs) and a number of long noncoding RNAs (lncRNAs) such as IFNG-AS1, Heg, NR_038461, NR_038462, T204821 and NR_104125 have been dysregulated in peripheral blood of patients with AITD. These transcripts are mostly enriched in pathways that modulate humoral and cellular immune responses such as those associated with antigen presentation and differentiation of Th1, Th2 and Th17 cells. Functional studies verified the role of a number of lncRNAs and miRNAs in regulation of critical immune-related pathways in AITD. Thus, they participate in the pathophysiology of AITD. In the current review, we summarize the results of studies that assessed participation of non-coding RNAs in the pathophysiology of AITD. Autoimmune thyroid disease AITD Hashimoto's thyroiditis Graves' disease miRNA lncRNA Eghtedarian, Reyhane verfasserin aut Dinger, Marcel E. verfasserin aut Ghafouri-Fard, Soudeh verfasserin aut Enthalten in Experimental and molecular pathology Orlando, Fla. : Academic Press, 1962 117 Online-Ressource (DE-627)266016693 (DE-600)1466769-1 (DE-576)106845918 1096-0945 nnns volume:117 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.47 Pathologie Medizin AR 117 |
spelling |
10.1016/j.yexmp.2020.104527 doi (DE-627)ELV005121132 (ELSEVIER)S0014-4800(20)30803-0 DE-627 ger DE-627 rda eng 610 DE-600 44.47 bkl Taheri, Mohammad verfasserin aut Dysregulation of non-coding RNAs in autoimmune thyroid disease 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Autoimmune thyroid disease (AITD) is a complex disorder with both genetic and environmental risk factors. A number of genetic factors such as HLA and CTLA-4 loci have been associated with risk of this disorder. In addition to these factors, recent studies have shown contribution of non-coding RNAs in the pathogenesis of this condition. Several microRNAs (miRNAs) and a number of long noncoding RNAs (lncRNAs) such as IFNG-AS1, Heg, NR_038461, NR_038462, T204821 and NR_104125 have been dysregulated in peripheral blood of patients with AITD. These transcripts are mostly enriched in pathways that modulate humoral and cellular immune responses such as those associated with antigen presentation and differentiation of Th1, Th2 and Th17 cells. Functional studies verified the role of a number of lncRNAs and miRNAs in regulation of critical immune-related pathways in AITD. Thus, they participate in the pathophysiology of AITD. In the current review, we summarize the results of studies that assessed participation of non-coding RNAs in the pathophysiology of AITD. Autoimmune thyroid disease AITD Hashimoto's thyroiditis Graves' disease miRNA lncRNA Eghtedarian, Reyhane verfasserin aut Dinger, Marcel E. verfasserin aut Ghafouri-Fard, Soudeh verfasserin aut Enthalten in Experimental and molecular pathology Orlando, Fla. : Academic Press, 1962 117 Online-Ressource (DE-627)266016693 (DE-600)1466769-1 (DE-576)106845918 1096-0945 nnns volume:117 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.47 Pathologie Medizin AR 117 |
allfields_unstemmed |
10.1016/j.yexmp.2020.104527 doi (DE-627)ELV005121132 (ELSEVIER)S0014-4800(20)30803-0 DE-627 ger DE-627 rda eng 610 DE-600 44.47 bkl Taheri, Mohammad verfasserin aut Dysregulation of non-coding RNAs in autoimmune thyroid disease 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Autoimmune thyroid disease (AITD) is a complex disorder with both genetic and environmental risk factors. A number of genetic factors such as HLA and CTLA-4 loci have been associated with risk of this disorder. In addition to these factors, recent studies have shown contribution of non-coding RNAs in the pathogenesis of this condition. Several microRNAs (miRNAs) and a number of long noncoding RNAs (lncRNAs) such as IFNG-AS1, Heg, NR_038461, NR_038462, T204821 and NR_104125 have been dysregulated in peripheral blood of patients with AITD. These transcripts are mostly enriched in pathways that modulate humoral and cellular immune responses such as those associated with antigen presentation and differentiation of Th1, Th2 and Th17 cells. Functional studies verified the role of a number of lncRNAs and miRNAs in regulation of critical immune-related pathways in AITD. Thus, they participate in the pathophysiology of AITD. In the current review, we summarize the results of studies that assessed participation of non-coding RNAs in the pathophysiology of AITD. Autoimmune thyroid disease AITD Hashimoto's thyroiditis Graves' disease miRNA lncRNA Eghtedarian, Reyhane verfasserin aut Dinger, Marcel E. verfasserin aut Ghafouri-Fard, Soudeh verfasserin aut Enthalten in Experimental and molecular pathology Orlando, Fla. : Academic Press, 1962 117 Online-Ressource (DE-627)266016693 (DE-600)1466769-1 (DE-576)106845918 1096-0945 nnns volume:117 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.47 Pathologie Medizin AR 117 |
allfieldsGer |
10.1016/j.yexmp.2020.104527 doi (DE-627)ELV005121132 (ELSEVIER)S0014-4800(20)30803-0 DE-627 ger DE-627 rda eng 610 DE-600 44.47 bkl Taheri, Mohammad verfasserin aut Dysregulation of non-coding RNAs in autoimmune thyroid disease 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Autoimmune thyroid disease (AITD) is a complex disorder with both genetic and environmental risk factors. A number of genetic factors such as HLA and CTLA-4 loci have been associated with risk of this disorder. In addition to these factors, recent studies have shown contribution of non-coding RNAs in the pathogenesis of this condition. Several microRNAs (miRNAs) and a number of long noncoding RNAs (lncRNAs) such as IFNG-AS1, Heg, NR_038461, NR_038462, T204821 and NR_104125 have been dysregulated in peripheral blood of patients with AITD. These transcripts are mostly enriched in pathways that modulate humoral and cellular immune responses such as those associated with antigen presentation and differentiation of Th1, Th2 and Th17 cells. Functional studies verified the role of a number of lncRNAs and miRNAs in regulation of critical immune-related pathways in AITD. Thus, they participate in the pathophysiology of AITD. In the current review, we summarize the results of studies that assessed participation of non-coding RNAs in the pathophysiology of AITD. Autoimmune thyroid disease AITD Hashimoto's thyroiditis Graves' disease miRNA lncRNA Eghtedarian, Reyhane verfasserin aut Dinger, Marcel E. verfasserin aut Ghafouri-Fard, Soudeh verfasserin aut Enthalten in Experimental and molecular pathology Orlando, Fla. : Academic Press, 1962 117 Online-Ressource (DE-627)266016693 (DE-600)1466769-1 (DE-576)106845918 1096-0945 nnns volume:117 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.47 Pathologie Medizin AR 117 |
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10.1016/j.yexmp.2020.104527 doi (DE-627)ELV005121132 (ELSEVIER)S0014-4800(20)30803-0 DE-627 ger DE-627 rda eng 610 DE-600 44.47 bkl Taheri, Mohammad verfasserin aut Dysregulation of non-coding RNAs in autoimmune thyroid disease 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Autoimmune thyroid disease (AITD) is a complex disorder with both genetic and environmental risk factors. A number of genetic factors such as HLA and CTLA-4 loci have been associated with risk of this disorder. In addition to these factors, recent studies have shown contribution of non-coding RNAs in the pathogenesis of this condition. Several microRNAs (miRNAs) and a number of long noncoding RNAs (lncRNAs) such as IFNG-AS1, Heg, NR_038461, NR_038462, T204821 and NR_104125 have been dysregulated in peripheral blood of patients with AITD. These transcripts are mostly enriched in pathways that modulate humoral and cellular immune responses such as those associated with antigen presentation and differentiation of Th1, Th2 and Th17 cells. Functional studies verified the role of a number of lncRNAs and miRNAs in regulation of critical immune-related pathways in AITD. Thus, they participate in the pathophysiology of AITD. In the current review, we summarize the results of studies that assessed participation of non-coding RNAs in the pathophysiology of AITD. Autoimmune thyroid disease AITD Hashimoto's thyroiditis Graves' disease miRNA lncRNA Eghtedarian, Reyhane verfasserin aut Dinger, Marcel E. verfasserin aut Ghafouri-Fard, Soudeh verfasserin aut Enthalten in Experimental and molecular pathology Orlando, Fla. : Academic Press, 1962 117 Online-Ressource (DE-627)266016693 (DE-600)1466769-1 (DE-576)106845918 1096-0945 nnns volume:117 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.47 Pathologie Medizin AR 117 |
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610 DE-600 44.47 bkl Dysregulation of non-coding RNAs in autoimmune thyroid disease Autoimmune thyroid disease AITD Hashimoto's thyroiditis Graves' disease miRNA lncRNA |
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ddc 610 bkl 44.47 misc Autoimmune thyroid disease misc AITD misc Hashimoto's thyroiditis misc Graves' disease misc miRNA misc lncRNA |
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Dysregulation of non-coding RNAs in autoimmune thyroid disease |
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Dysregulation of non-coding RNAs in autoimmune thyroid disease |
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Taheri, Mohammad |
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Experimental and molecular pathology |
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Taheri, Mohammad Eghtedarian, Reyhane Dinger, Marcel E. Ghafouri-Fard, Soudeh |
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10.1016/j.yexmp.2020.104527 |
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dysregulation of non-coding rnas in autoimmune thyroid disease |
title_auth |
Dysregulation of non-coding RNAs in autoimmune thyroid disease |
abstract |
Autoimmune thyroid disease (AITD) is a complex disorder with both genetic and environmental risk factors. A number of genetic factors such as HLA and CTLA-4 loci have been associated with risk of this disorder. In addition to these factors, recent studies have shown contribution of non-coding RNAs in the pathogenesis of this condition. Several microRNAs (miRNAs) and a number of long noncoding RNAs (lncRNAs) such as IFNG-AS1, Heg, NR_038461, NR_038462, T204821 and NR_104125 have been dysregulated in peripheral blood of patients with AITD. These transcripts are mostly enriched in pathways that modulate humoral and cellular immune responses such as those associated with antigen presentation and differentiation of Th1, Th2 and Th17 cells. Functional studies verified the role of a number of lncRNAs and miRNAs in regulation of critical immune-related pathways in AITD. Thus, they participate in the pathophysiology of AITD. In the current review, we summarize the results of studies that assessed participation of non-coding RNAs in the pathophysiology of AITD. |
abstractGer |
Autoimmune thyroid disease (AITD) is a complex disorder with both genetic and environmental risk factors. A number of genetic factors such as HLA and CTLA-4 loci have been associated with risk of this disorder. In addition to these factors, recent studies have shown contribution of non-coding RNAs in the pathogenesis of this condition. Several microRNAs (miRNAs) and a number of long noncoding RNAs (lncRNAs) such as IFNG-AS1, Heg, NR_038461, NR_038462, T204821 and NR_104125 have been dysregulated in peripheral blood of patients with AITD. These transcripts are mostly enriched in pathways that modulate humoral and cellular immune responses such as those associated with antigen presentation and differentiation of Th1, Th2 and Th17 cells. Functional studies verified the role of a number of lncRNAs and miRNAs in regulation of critical immune-related pathways in AITD. Thus, they participate in the pathophysiology of AITD. In the current review, we summarize the results of studies that assessed participation of non-coding RNAs in the pathophysiology of AITD. |
abstract_unstemmed |
Autoimmune thyroid disease (AITD) is a complex disorder with both genetic and environmental risk factors. A number of genetic factors such as HLA and CTLA-4 loci have been associated with risk of this disorder. In addition to these factors, recent studies have shown contribution of non-coding RNAs in the pathogenesis of this condition. Several microRNAs (miRNAs) and a number of long noncoding RNAs (lncRNAs) such as IFNG-AS1, Heg, NR_038461, NR_038462, T204821 and NR_104125 have been dysregulated in peripheral blood of patients with AITD. These transcripts are mostly enriched in pathways that modulate humoral and cellular immune responses such as those associated with antigen presentation and differentiation of Th1, Th2 and Th17 cells. Functional studies verified the role of a number of lncRNAs and miRNAs in regulation of critical immune-related pathways in AITD. Thus, they participate in the pathophysiology of AITD. In the current review, we summarize the results of studies that assessed participation of non-coding RNAs in the pathophysiology of AITD. |
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title_short |
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