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

Gespeichert in:

Autor*in:	Ping Zheng [verfasserIn] Shiliang Li [verfasserIn] Chun Liu [verfasserIn] Zhengbiao Zha [verfasserIn] Xiang Wei [verfasserIn] Yuan Yuan [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	hypertension mt-trna a4435g mutation c5601t mutation

Übergeordnetes Werk:	In: Clinical and Experimental Hypertension - Taylor & Francis Group, 2023, 40(2018), 6, Seite 595-600
Übergeordnetes Werk:	volume:40 ; year:2018 ; number:6 ; pages:595-600

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1080/10641963.2017.1411497

Katalog-ID:	DOAJ099476886

Internformat


LEADER	01000naa a22002652 4500
001	DOAJ099476886
003	DE-627
005	20240414034836.0
007	cr uuu---uuuuu
008	240414s2018 xx \|\|\|\|\|o 00\| \|\|eng c
024	7		\|a 10.1080/10641963.2017.1411497 \|2 doi
035			\|a (DE-627)DOAJ099476886
035			\|a (DE-599)DOAJ815133d2f7f24456bd740c6a1d15f121
040			\|a DE-627 \|b ger \|c DE-627 \|e rakwb
041			\|a eng
050		0	\|a RC666-701
100	0		\|a Ping Zheng \|e verfasserin \|4 aut
245	1	0	\|a Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension
264		1	\|c 2018
336			\|a Text \|b txt \|2 rdacontent
337			\|a Computermedien \|b c \|2 rdamedia
338			\|a Online-Ressource \|b cr \|2 rdacarrier
520			\|a 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.
650		4	\|a hypertension
650		4	\|a mt-trna
650		4	\|a a4435g mutation
650		4	\|a c5601t mutation
653		0	\|a Diseases of the circulatory (Cardiovascular) system
700	0		\|a Shiliang Li \|e verfasserin \|4 aut
700	0		\|a Chun Liu \|e verfasserin \|4 aut
700	0		\|a Zhengbiao Zha \|e verfasserin \|4 aut
700	0		\|a Xiang Wei \|e verfasserin \|4 aut
700	0		\|a Yuan Yuan \|e verfasserin \|4 aut
773	0	8	\|i In \|t Clinical and Experimental Hypertension \|d Taylor & Francis Group, 2023 \|g 40(2018), 6, Seite 595-600 \|w (DE-627)323606504 \|w (DE-600)2026245-0 \|x 15256006 \|7 nnns
773	1	8	\|g volume:40 \|g year:2018 \|g number:6 \|g pages:595-600
856	4	0	\|u https://doi.org/10.1080/10641963.2017.1411497 \|z kostenfrei
856	4	0	\|u https://doaj.org/article/815133d2f7f24456bd740c6a1d15f121 \|z kostenfrei
856	4	0	\|u http://dx.doi.org/10.1080/10641963.2017.1411497 \|z kostenfrei
856	4	2	\|u https://doaj.org/toc/1064-1963 \|y Journal toc \|z kostenfrei
856	4	2	\|u https://doaj.org/toc/1525-6006 \|y Journal toc \|z kostenfrei
912			\|a GBV_USEFLAG_A
912			\|a SYSFLAG_A
912			\|a GBV_DOAJ
912			\|a GBV_ILN_206
912			\|a GBV_ILN_702
912			\|a GBV_ILN_2001
912			\|a GBV_ILN_2003
912			\|a GBV_ILN_2005
912			\|a GBV_ILN_2006
912			\|a GBV_ILN_2008
912			\|a GBV_ILN_2009
912			\|a GBV_ILN_2010
912			\|a GBV_ILN_2011
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_2015
912			\|a GBV_ILN_2020
912			\|a GBV_ILN_2021
912			\|a GBV_ILN_2025
912			\|a GBV_ILN_2031
912			\|a GBV_ILN_2038
912			\|a GBV_ILN_2044
912			\|a GBV_ILN_2048
912			\|a GBV_ILN_2050
912			\|a GBV_ILN_2055
912			\|a GBV_ILN_2056
912			\|a GBV_ILN_2057
912			\|a GBV_ILN_2061
912			\|a GBV_ILN_2111
912			\|a GBV_ILN_2113
912			\|a GBV_ILN_2190
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4338
951			\|a AR
952			\|d 40 \|j 2018 \|e 6 \|h 595-600

Indexfelder

author_variant	p z pz s l sl c l cl z z zz x w xw y y yy
matchkey_str	article:15256006:2018----::iohnratnaa50tuainamdlttelnclxrsinfraea45mttoia
hierarchy_sort_str	2018
callnumber-subject-code	RC
publishDate	2018
allfields	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
spelling	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
allfields_unstemmed	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
allfieldsGer	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
allfieldsSound	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
language	English
source	In Clinical and Experimental Hypertension 40(2018), 6, Seite 595-600 volume:40 year:2018 number:6 pages:595-600
sourceStr	In Clinical and Experimental Hypertension 40(2018), 6, Seite 595-600 volume:40 year:2018 number:6 pages:595-600
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	hypertension mt-trna a4435g mutation c5601t mutation Diseases of the circulatory (Cardiovascular) system
isfreeaccess_bool	true
container_title	Clinical and Experimental Hypertension
authorswithroles_txt_mv	Ping Zheng @@aut@@ Shiliang Li @@aut@@ Chun Liu @@aut@@ Zhengbiao Zha @@aut@@ Xiang Wei @@aut@@ Yuan Yuan @@aut@@
publishDateDaySort_date	2018-01-01T00:00:00Z
hierarchy_top_id	323606504
id	DOAJ099476886
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">DOAJ099476886</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240414034836.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">240414s2018 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1080/10641963.2017.1411497</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ099476886</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ815133d2f7f24456bd740c6a1d15f121</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC666-701</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Ping Zheng</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">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.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">hypertension</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">mt-trna</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">a4435g mutation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">c5601t mutation</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Diseases of the circulatory (Cardiovascular) system</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Shiliang Li</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Chun Liu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Zhengbiao Zha</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Xiang Wei</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yuan Yuan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Clinical and Experimental Hypertension</subfield><subfield code="d">Taylor & Francis Group, 2023</subfield><subfield code="g">40(2018), 6, Seite 595-600</subfield><subfield code="w">(DE-627)323606504</subfield><subfield code="w">(DE-600)2026245-0</subfield><subfield code="x">15256006</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:40</subfield><subfield code="g">year:2018</subfield><subfield code="g">number:6</subfield><subfield code="g">pages:595-600</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1080/10641963.2017.1411497</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/815133d2f7f24456bd740c6a1d15f121</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1080/10641963.2017.1411497</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1064-1963</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1525-6006</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_702</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2001</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2003</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2005</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2006</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2008</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2009</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2010</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2011</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2015</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2020</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2021</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2025</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2031</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2038</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2044</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2048</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2050</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2055</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2056</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2057</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2061</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2111</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2113</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2190</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">40</subfield><subfield code="j">2018</subfield><subfield code="e">6</subfield><subfield code="h">595-600</subfield></datafield></record></collection>
callnumber-first	R - Medicine
author	Ping Zheng
spellingShingle	Ping Zheng misc RC666-701 misc hypertension misc mt-trna misc a4435g mutation misc c5601t mutation misc Diseases of the circulatory (Cardiovascular) system Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension
authorStr	Ping Zheng
ppnlink_with_tag_str_mv	@@773@@(DE-627)323606504
format	electronic Article
delete_txt_mv	keep
author_role	aut aut aut aut aut aut
collection	DOAJ
remote_str	true
callnumber-label	RC666-701
illustrated	Not Illustrated
issn	15256006
topic_title	RC666-701 Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension hypertension mt-trna a4435g mutation c5601t mutation
topic	misc RC666-701 misc hypertension misc mt-trna misc a4435g mutation misc c5601t mutation misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc hypertension misc mt-trna misc a4435g mutation misc c5601t mutation misc Diseases of the circulatory (Cardiovascular) system
topic_browse	misc RC666-701 misc hypertension misc mt-trna misc a4435g mutation misc c5601t mutation misc Diseases of the circulatory (Cardiovascular) system
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
format_main_str_mv	Text Zeitschrift/Artikel
carriertype_str_mv	cr
hierarchy_parent_title	Clinical and Experimental Hypertension
hierarchy_parent_id	323606504
hierarchy_top_title	Clinical and Experimental Hypertension
isfreeaccess_txt	true
familylinks_str_mv	(DE-627)323606504 (DE-600)2026245-0
title	Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension
ctrlnum	(DE-627)DOAJ099476886 (DE-599)DOAJ815133d2f7f24456bd740c6a1d15f121
title_full	Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension
author_sort	Ping Zheng
journal	Clinical and Experimental Hypertension
journalStr	Clinical and Experimental Hypertension
callnumber-first-code	R
lang_code	eng
isOA_bool	true
recordtype	marc
publishDateSort	2018
contenttype_str_mv	txt
container_start_page	595
author_browse	Ping Zheng Shiliang Li Chun Liu Zhengbiao Zha Xiang Wei Yuan Yuan
container_volume	40
class	RC666-701
format_se	Elektronische Aufsätze
author-letter	Ping Zheng
doi_str_mv	10.1080/10641963.2017.1411497
author2-role	verfasserin
title_sort	mitochondrial trnaala c5601t mutation may modulate the clinical expression of trnamet a4435g mutation in a han chinese family with hypertension
callnumber	RC666-701
title_auth	Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension
abstract	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.
collection_details	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
container_issue	6
title_short	Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension
url	https://doi.org/10.1080/10641963.2017.1411497 https://doaj.org/article/815133d2f7f24456bd740c6a1d15f121 http://dx.doi.org/10.1080/10641963.2017.1411497 https://doaj.org/toc/1064-1963 https://doaj.org/toc/1525-6006
remote_bool	true
author2	Shiliang Li Chun Liu Zhengbiao Zha Xiang Wei Yuan Yuan
author2Str	Shiliang Li Chun Liu Zhengbiao Zha Xiang Wei Yuan Yuan
ppnlink	323606504
callnumber-subject	RC - Internal Medicine
mediatype_str_mv	c
isOA_txt	true
hochschulschrift_bool	false
doi_str	10.1080/10641963.2017.1411497
callnumber-a	RC666-701
up_date	2024-07-03T22:58:40.402Z
_version_	1803600548759339008
fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">DOAJ099476886</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240414034836.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">240414s2018 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1080/10641963.2017.1411497</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ099476886</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ815133d2f7f24456bd740c6a1d15f121</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC666-701</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Ping Zheng</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">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.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">hypertension</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">mt-trna</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">a4435g mutation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">c5601t mutation</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Diseases of the circulatory (Cardiovascular) system</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Shiliang Li</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Chun Liu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Zhengbiao Zha</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Xiang Wei</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yuan Yuan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Clinical and Experimental Hypertension</subfield><subfield code="d">Taylor & Francis Group, 2023</subfield><subfield code="g">40(2018), 6, Seite 595-600</subfield><subfield code="w">(DE-627)323606504</subfield><subfield code="w">(DE-600)2026245-0</subfield><subfield code="x">15256006</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:40</subfield><subfield code="g">year:2018</subfield><subfield code="g">number:6</subfield><subfield code="g">pages:595-600</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1080/10641963.2017.1411497</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/815133d2f7f24456bd740c6a1d15f121</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1080/10641963.2017.1411497</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1064-1963</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1525-6006</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_702</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2001</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2003</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2005</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2006</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2008</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2009</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2010</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2011</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2015</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2020</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2021</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2025</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2031</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2038</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2044</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2048</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2050</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2055</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2056</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2057</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2061</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2111</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2113</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2190</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">40</subfield><subfield code="j">2018</subfield><subfield code="e">6</subfield><subfield code="h">595-600</subfield></datafield></record></collection>
score	7.4011145

Nicht das Richtige dabei?

Schreiben Sie uns!

Mitochondrial tRNAAla C5601T mutation may modulate the clinical expression of tRNAMet A4435G mutation in a Han Chinese family with hypertension

Nicht das Richtige dabei?

Zugang & Verfügbarkeit

Vorhandene Bände

Nicht das Richtige dabei?