Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension
Mutations in mitochondrial DNA, especially in mitochondrial tRNA (mt-tRNA) genes, are the important causes for maternally inherited hypertension. In this study, we reported the clinical, genetic, and molecular characterization of a Han Chinese family with hypertension. Most strikingly, this family e...
Ausführliche Beschreibung
Autor*in: |
Ping Zheng [verfasserIn] Shiliang Li [verfasserIn] Chun Liu [verfasserIn] Zhengbiao Zha [verfasserIn] Xiang Wei [verfasserIn] Yuan Yuan [verfasserIn] |
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Englisch |
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2018 |
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In: Clinical and Experimental Hypertension - Taylor & Francis Group, 2023, 40(2018), 6, Seite 595-600 |
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volume:40 ; year:2018 ; number:6 ; pages:595-600 |
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DOI / URN: |
10.1080/10641963.2017.1411497 |
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Katalog-ID: |
DOAJ099476886 |
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10.1080/10641963.2017.1411497 doi (DE-627)DOAJ099476886 (DE-599)DOAJ815133d2f7f24456bd740c6a1d15f121 DE-627 ger DE-627 rakwb eng RC666-701 Ping Zheng verfasserin aut Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mutations in mitochondrial DNA, especially in mitochondrial tRNA (mt-tRNA) genes, are the important causes for maternally inherited hypertension. In this study, we reported the clinical, genetic, and molecular characterization of a Han Chinese family with hypertension. Most strikingly, this family exhibited a high penetrance and expressivity of hypertension. Sequence analysis of the complete mt-tRNA genes showed the presence of tRNAMet A4435G and tRNAAla C5601T mutations. The A4435G had already been reported as a pathogenic mutation associated with hypertension; in addition, the C5601T mutation, which was located at the highly conserved nucleotide of T arm of tRNAAla, created a novel Watson–Crick base pairing and may result in failure of tRNA metabolism. Moreover, bioinformatics analysis indicated that the C5601T mutation altered the secondary structure of tRNAAla. Thus, the mitochondrial dysfunction, caused by the A4435G mutation, may be worsened by the C5601T mutation. Taken together, our data indicated that the co-occurrence of the A4435G and C5601T mutations may account for the high penetrance and expressivity of hypertension in this family. Therefore, our study provided novel insight into the pathophysiology of maternally inherited hypertension. hypertension mt-trna a4435g mutation c5601t mutation Diseases of the circulatory (Cardiovascular) system Shiliang Li verfasserin aut Chun Liu verfasserin aut Zhengbiao Zha verfasserin aut Xiang Wei verfasserin aut Yuan Yuan verfasserin aut In Clinical and Experimental Hypertension Taylor & Francis Group, 2023 40(2018), 6, Seite 595-600 (DE-627)323606504 (DE-600)2026245-0 15256006 nnns volume:40 year:2018 number:6 pages:595-600 https://doi.org/10.1080/10641963.2017.1411497 kostenfrei https://doaj.org/article/815133d2f7f24456bd740c6a1d15f121 kostenfrei http://dx.doi.org/10.1080/10641963.2017.1411497 kostenfrei https://doaj.org/toc/1064-1963 Journal toc kostenfrei https://doaj.org/toc/1525-6006 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_206 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4305 GBV_ILN_4338 AR 40 2018 6 595-600 |
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10.1080/10641963.2017.1411497 doi (DE-627)DOAJ099476886 (DE-599)DOAJ815133d2f7f24456bd740c6a1d15f121 DE-627 ger DE-627 rakwb eng RC666-701 Ping Zheng verfasserin aut Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mutations in mitochondrial DNA, especially in mitochondrial tRNA (mt-tRNA) genes, are the important causes for maternally inherited hypertension. In this study, we reported the clinical, genetic, and molecular characterization of a Han Chinese family with hypertension. Most strikingly, this family exhibited a high penetrance and expressivity of hypertension. Sequence analysis of the complete mt-tRNA genes showed the presence of tRNAMet A4435G and tRNAAla C5601T mutations. The A4435G had already been reported as a pathogenic mutation associated with hypertension; in addition, the C5601T mutation, which was located at the highly conserved nucleotide of T arm of tRNAAla, created a novel Watson–Crick base pairing and may result in failure of tRNA metabolism. Moreover, bioinformatics analysis indicated that the C5601T mutation altered the secondary structure of tRNAAla. Thus, the mitochondrial dysfunction, caused by the A4435G mutation, may be worsened by the C5601T mutation. Taken together, our data indicated that the co-occurrence of the A4435G and C5601T mutations may account for the high penetrance and expressivity of hypertension in this family. Therefore, our study provided novel insight into the pathophysiology of maternally inherited hypertension. hypertension mt-trna a4435g mutation c5601t mutation Diseases of the circulatory (Cardiovascular) system Shiliang Li verfasserin aut Chun Liu verfasserin aut Zhengbiao Zha verfasserin aut Xiang Wei verfasserin aut Yuan Yuan verfasserin aut In Clinical and Experimental Hypertension Taylor & Francis Group, 2023 40(2018), 6, Seite 595-600 (DE-627)323606504 (DE-600)2026245-0 15256006 nnns volume:40 year:2018 number:6 pages:595-600 https://doi.org/10.1080/10641963.2017.1411497 kostenfrei https://doaj.org/article/815133d2f7f24456bd740c6a1d15f121 kostenfrei http://dx.doi.org/10.1080/10641963.2017.1411497 kostenfrei https://doaj.org/toc/1064-1963 Journal toc kostenfrei https://doaj.org/toc/1525-6006 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_206 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4305 GBV_ILN_4338 AR 40 2018 6 595-600 |
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10.1080/10641963.2017.1411497 doi (DE-627)DOAJ099476886 (DE-599)DOAJ815133d2f7f24456bd740c6a1d15f121 DE-627 ger DE-627 rakwb eng RC666-701 Ping Zheng verfasserin aut Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mutations in mitochondrial DNA, especially in mitochondrial tRNA (mt-tRNA) genes, are the important causes for maternally inherited hypertension. In this study, we reported the clinical, genetic, and molecular characterization of a Han Chinese family with hypertension. Most strikingly, this family exhibited a high penetrance and expressivity of hypertension. Sequence analysis of the complete mt-tRNA genes showed the presence of tRNAMet A4435G and tRNAAla C5601T mutations. The A4435G had already been reported as a pathogenic mutation associated with hypertension; in addition, the C5601T mutation, which was located at the highly conserved nucleotide of T arm of tRNAAla, created a novel Watson–Crick base pairing and may result in failure of tRNA metabolism. Moreover, bioinformatics analysis indicated that the C5601T mutation altered the secondary structure of tRNAAla. Thus, the mitochondrial dysfunction, caused by the A4435G mutation, may be worsened by the C5601T mutation. Taken together, our data indicated that the co-occurrence of the A4435G and C5601T mutations may account for the high penetrance and expressivity of hypertension in this family. Therefore, our study provided novel insight into the pathophysiology of maternally inherited hypertension. hypertension mt-trna a4435g mutation c5601t mutation Diseases of the circulatory (Cardiovascular) system Shiliang Li verfasserin aut Chun Liu verfasserin aut Zhengbiao Zha verfasserin aut Xiang Wei verfasserin aut Yuan Yuan verfasserin aut In Clinical and Experimental Hypertension Taylor & Francis Group, 2023 40(2018), 6, Seite 595-600 (DE-627)323606504 (DE-600)2026245-0 15256006 nnns volume:40 year:2018 number:6 pages:595-600 https://doi.org/10.1080/10641963.2017.1411497 kostenfrei https://doaj.org/article/815133d2f7f24456bd740c6a1d15f121 kostenfrei http://dx.doi.org/10.1080/10641963.2017.1411497 kostenfrei https://doaj.org/toc/1064-1963 Journal toc kostenfrei https://doaj.org/toc/1525-6006 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_206 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4305 GBV_ILN_4338 AR 40 2018 6 595-600 |
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10.1080/10641963.2017.1411497 doi (DE-627)DOAJ099476886 (DE-599)DOAJ815133d2f7f24456bd740c6a1d15f121 DE-627 ger DE-627 rakwb eng RC666-701 Ping Zheng verfasserin aut Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mutations in mitochondrial DNA, especially in mitochondrial tRNA (mt-tRNA) genes, are the important causes for maternally inherited hypertension. In this study, we reported the clinical, genetic, and molecular characterization of a Han Chinese family with hypertension. Most strikingly, this family exhibited a high penetrance and expressivity of hypertension. Sequence analysis of the complete mt-tRNA genes showed the presence of tRNAMet A4435G and tRNAAla C5601T mutations. The A4435G had already been reported as a pathogenic mutation associated with hypertension; in addition, the C5601T mutation, which was located at the highly conserved nucleotide of T arm of tRNAAla, created a novel Watson–Crick base pairing and may result in failure of tRNA metabolism. Moreover, bioinformatics analysis indicated that the C5601T mutation altered the secondary structure of tRNAAla. Thus, the mitochondrial dysfunction, caused by the A4435G mutation, may be worsened by the C5601T mutation. Taken together, our data indicated that the co-occurrence of the A4435G and C5601T mutations may account for the high penetrance and expressivity of hypertension in this family. Therefore, our study provided novel insight into the pathophysiology of maternally inherited hypertension. hypertension mt-trna a4435g mutation c5601t mutation Diseases of the circulatory (Cardiovascular) system Shiliang Li verfasserin aut Chun Liu verfasserin aut Zhengbiao Zha verfasserin aut Xiang Wei verfasserin aut Yuan Yuan verfasserin aut In Clinical and Experimental Hypertension Taylor & Francis Group, 2023 40(2018), 6, Seite 595-600 (DE-627)323606504 (DE-600)2026245-0 15256006 nnns volume:40 year:2018 number:6 pages:595-600 https://doi.org/10.1080/10641963.2017.1411497 kostenfrei https://doaj.org/article/815133d2f7f24456bd740c6a1d15f121 kostenfrei http://dx.doi.org/10.1080/10641963.2017.1411497 kostenfrei https://doaj.org/toc/1064-1963 Journal toc kostenfrei https://doaj.org/toc/1525-6006 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_206 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4305 GBV_ILN_4338 AR 40 2018 6 595-600 |
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10.1080/10641963.2017.1411497 doi (DE-627)DOAJ099476886 (DE-599)DOAJ815133d2f7f24456bd740c6a1d15f121 DE-627 ger DE-627 rakwb eng RC666-701 Ping Zheng verfasserin aut Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mutations in mitochondrial DNA, especially in mitochondrial tRNA (mt-tRNA) genes, are the important causes for maternally inherited hypertension. In this study, we reported the clinical, genetic, and molecular characterization of a Han Chinese family with hypertension. Most strikingly, this family exhibited a high penetrance and expressivity of hypertension. Sequence analysis of the complete mt-tRNA genes showed the presence of tRNAMet A4435G and tRNAAla C5601T mutations. The A4435G had already been reported as a pathogenic mutation associated with hypertension; in addition, the C5601T mutation, which was located at the highly conserved nucleotide of T arm of tRNAAla, created a novel Watson–Crick base pairing and may result in failure of tRNA metabolism. Moreover, bioinformatics analysis indicated that the C5601T mutation altered the secondary structure of tRNAAla. Thus, the mitochondrial dysfunction, caused by the A4435G mutation, may be worsened by the C5601T mutation. Taken together, our data indicated that the co-occurrence of the A4435G and C5601T mutations may account for the high penetrance and expressivity of hypertension in this family. Therefore, our study provided novel insight into the pathophysiology of maternally inherited hypertension. hypertension mt-trna a4435g mutation c5601t mutation Diseases of the circulatory (Cardiovascular) system Shiliang Li verfasserin aut Chun Liu verfasserin aut Zhengbiao Zha verfasserin aut Xiang Wei verfasserin aut Yuan Yuan verfasserin aut In Clinical and Experimental Hypertension Taylor & Francis Group, 2023 40(2018), 6, Seite 595-600 (DE-627)323606504 (DE-600)2026245-0 15256006 nnns volume:40 year:2018 number:6 pages:595-600 https://doi.org/10.1080/10641963.2017.1411497 kostenfrei https://doaj.org/article/815133d2f7f24456bd740c6a1d15f121 kostenfrei http://dx.doi.org/10.1080/10641963.2017.1411497 kostenfrei https://doaj.org/toc/1064-1963 Journal toc kostenfrei https://doaj.org/toc/1525-6006 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_206 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4305 GBV_ILN_4338 AR 40 2018 6 595-600 |
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In this study, we reported the clinical, genetic, and molecular characterization of a Han Chinese family with hypertension. Most strikingly, this family exhibited a high penetrance and expressivity of hypertension. Sequence analysis of the complete mt-tRNA genes showed the presence of tRNAMet A4435G and tRNAAla C5601T mutations. The A4435G had already been reported as a pathogenic mutation associated with hypertension; in addition, the C5601T mutation, which was located at the highly conserved nucleotide of T arm of tRNAAla, created a novel Watson–Crick base pairing and may result in failure of tRNA metabolism. Moreover, bioinformatics analysis indicated that the C5601T mutation altered the secondary structure of tRNAAla. Thus, the mitochondrial dysfunction, caused by the A4435G mutation, may be worsened by the C5601T mutation. Taken together, our data indicated that the co-occurrence of the A4435G and C5601T mutations may account for the high penetrance and expressivity of hypertension in this family. 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Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension |
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Mutations in mitochondrial DNA, especially in mitochondrial tRNA (mt-tRNA) genes, are the important causes for maternally inherited hypertension. In this study, we reported the clinical, genetic, and molecular characterization of a Han Chinese family with hypertension. Most strikingly, this family exhibited a high penetrance and expressivity of hypertension. Sequence analysis of the complete mt-tRNA genes showed the presence of tRNAMet A4435G and tRNAAla C5601T mutations. The A4435G had already been reported as a pathogenic mutation associated with hypertension; in addition, the C5601T mutation, which was located at the highly conserved nucleotide of T arm of tRNAAla, created a novel Watson–Crick base pairing and may result in failure of tRNA metabolism. Moreover, bioinformatics analysis indicated that the C5601T mutation altered the secondary structure of tRNAAla. Thus, the mitochondrial dysfunction, caused by the A4435G mutation, may be worsened by the C5601T mutation. Taken together, our data indicated that the co-occurrence of the A4435G and C5601T mutations may account for the high penetrance and expressivity of hypertension in this family. Therefore, our study provided novel insight into the pathophysiology of maternally inherited hypertension. |
abstractGer |
Mutations in mitochondrial DNA, especially in mitochondrial tRNA (mt-tRNA) genes, are the important causes for maternally inherited hypertension. In this study, we reported the clinical, genetic, and molecular characterization of a Han Chinese family with hypertension. Most strikingly, this family exhibited a high penetrance and expressivity of hypertension. Sequence analysis of the complete mt-tRNA genes showed the presence of tRNAMet A4435G and tRNAAla C5601T mutations. The A4435G had already been reported as a pathogenic mutation associated with hypertension; in addition, the C5601T mutation, which was located at the highly conserved nucleotide of T arm of tRNAAla, created a novel Watson–Crick base pairing and may result in failure of tRNA metabolism. Moreover, bioinformatics analysis indicated that the C5601T mutation altered the secondary structure of tRNAAla. Thus, the mitochondrial dysfunction, caused by the A4435G mutation, may be worsened by the C5601T mutation. Taken together, our data indicated that the co-occurrence of the A4435G and C5601T mutations may account for the high penetrance and expressivity of hypertension in this family. Therefore, our study provided novel insight into the pathophysiology of maternally inherited hypertension. |
abstract_unstemmed |
Mutations in mitochondrial DNA, especially in mitochondrial tRNA (mt-tRNA) genes, are the important causes for maternally inherited hypertension. In this study, we reported the clinical, genetic, and molecular characterization of a Han Chinese family with hypertension. Most strikingly, this family exhibited a high penetrance and expressivity of hypertension. Sequence analysis of the complete mt-tRNA genes showed the presence of tRNAMet A4435G and tRNAAla C5601T mutations. The A4435G had already been reported as a pathogenic mutation associated with hypertension; in addition, the C5601T mutation, which was located at the highly conserved nucleotide of T arm of tRNAAla, created a novel Watson–Crick base pairing and may result in failure of tRNA metabolism. Moreover, bioinformatics analysis indicated that the C5601T mutation altered the secondary structure of tRNAAla. Thus, the mitochondrial dysfunction, caused by the A4435G mutation, may be worsened by the C5601T mutation. Taken together, our data indicated that the co-occurrence of the A4435G and C5601T mutations may account for the high penetrance and expressivity of hypertension in this family. Therefore, our study provided novel insight into the pathophysiology of maternally inherited hypertension. |
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score |
7.4011145 |