The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment

Mutations in mitochondrial DNA (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Ch...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Yu Ding [verfasserIn] Qi Liu [verfasserIn] Yao-Shu Teng [verfasserIn] Hui Zheng [verfasserIn] Jian-Hang Leng [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	mitochondrial trnathr g15930a nshl

Übergeordnetes Werk:	In: Mitochondrial DNA. Part B. Resources - Taylor & Francis Group, 2023, 4(2019), 1, Seite 1347-1349
Übergeordnetes Werk:	volume:4 ; year:2019 ; number:1 ; pages:1347-1349

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1080/23802359.2019.1597648

Katalog-ID:	DOAJ096895349

Internformat


LEADER	01000naa a22002652 4500
001	DOAJ096895349
003	DE-627
005	20240413163933.0
007	cr uuu---uuuuu
008	240413s2019 xx \|\|\|\|\|o 00\| \|\|eng c
024	7		\|a 10.1080/23802359.2019.1597648 \|2 doi
035			\|a (DE-627)DOAJ096895349
035			\|a (DE-599)DOAJb1ce2bf334b449a099759af42cb10d4a
040			\|a DE-627 \|b ger \|c DE-627 \|e rakwb
041			\|a eng
050		0	\|a QH426-470
100	0		\|a Yu Ding \|e verfasserin \|4 aut
245	1	4	\|a The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment
264		1	\|c 2019
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 (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Chinese family with maternally inherited NSHL. Clinical evaluation showed a variable age at onset of NSHL. Molecular analysis of the matrilineal relatives from this family showed the presence of a novel mt-tRNAThr G15930A mutation, together with a set of genetic polymorphisms belonging to East Asia haplogroup B4b1. Interestingly, the G15930A mutation, which is localized at the highly conserved nucleotide of the anticodon stem of tRNAThr, created a novel base-pairing. Bioinformatics analysis showed that the G15930A mutation altered the secondary structure of tRNAThr and may result a failure in tRNA metabolism. As a result, the G15930A mutation may cause the mitochondrial dysfunction that was responsible for NSHL. Taken together, our data indicated that the G15930A may be a novel mutation associated with NSHL. Thus, our finding provided novel insight into the pathophysiology of maternally inherited NSHL.
650		4	\|a mitochondrial
650		4	\|a trnathr
650		4	\|a g15930a
650		4	\|a nshl
653		0	\|a Genetics
700	0		\|a Qi Liu \|e verfasserin \|4 aut
700	0		\|a Yao-Shu Teng \|e verfasserin \|4 aut
700	0		\|a Hui Zheng \|e verfasserin \|4 aut
700	0		\|a Jian-Hang Leng \|e verfasserin \|4 aut
773	0	8	\|i In \|t Mitochondrial DNA. Part B. Resources \|d Taylor & Francis Group, 2023 \|g 4(2019), 1, Seite 1347-1349 \|w (DE-627)867996722 \|w (DE-600)2868557-X \|x 23802359 \|7 nnns
773	1	8	\|g volume:4 \|g year:2019 \|g number:1 \|g pages:1347-1349
856	4	0	\|u https://doi.org/10.1080/23802359.2019.1597648 \|z kostenfrei
856	4	0	\|u https://doaj.org/article/b1ce2bf334b449a099759af42cb10d4a \|z kostenfrei
856	4	0	\|u http://dx.doi.org/10.1080/23802359.2019.1597648 \|z kostenfrei
856	4	2	\|u https://doaj.org/toc/2380-2359 \|y Journal toc \|z kostenfrei
912			\|a GBV_USEFLAG_A
912			\|a SYSFLAG_A
912			\|a GBV_DOAJ
912			\|a GBV_ILN_20
912			\|a GBV_ILN_22
912			\|a GBV_ILN_23
912			\|a GBV_ILN_24
912			\|a GBV_ILN_31
912			\|a GBV_ILN_39
912			\|a GBV_ILN_40
912			\|a GBV_ILN_62
912			\|a GBV_ILN_63
912			\|a GBV_ILN_65
912			\|a GBV_ILN_69
912			\|a GBV_ILN_70
912			\|a GBV_ILN_73
912			\|a GBV_ILN_74
912			\|a GBV_ILN_95
912			\|a GBV_ILN_105
912			\|a GBV_ILN_110
912			\|a GBV_ILN_151
912			\|a GBV_ILN_161
912			\|a GBV_ILN_170
912			\|a GBV_ILN_213
912			\|a GBV_ILN_230
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
912			\|a GBV_ILN_602
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_4012
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
912			\|a GBV_ILN_4126
912			\|a GBV_ILN_4249
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4306
912			\|a GBV_ILN_4307
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4700
951			\|a AR
952			\|d 4 \|j 2019 \|e 1 \|h 1347-1349

Indexfelder

author_variant	y d yd q l ql y s t yst h z hz j h l jhl
matchkey_str	article:23802359:2019----::hmtcodilrahg53aabaoemttoascaew
hierarchy_sort_str	2019
callnumber-subject-code	QH
publishDate	2019
allfields	10.1080/23802359.2019.1597648 doi (DE-627)DOAJ096895349 (DE-599)DOAJb1ce2bf334b449a099759af42cb10d4a DE-627 ger DE-627 rakwb eng QH426-470 Yu Ding verfasserin aut The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mutations in mitochondrial DNA (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Chinese family with maternally inherited NSHL. Clinical evaluation showed a variable age at onset of NSHL. Molecular analysis of the matrilineal relatives from this family showed the presence of a novel mt-tRNAThr G15930A mutation, together with a set of genetic polymorphisms belonging to East Asia haplogroup B4b1. Interestingly, the G15930A mutation, which is localized at the highly conserved nucleotide of the anticodon stem of tRNAThr, created a novel base-pairing. Bioinformatics analysis showed that the G15930A mutation altered the secondary structure of tRNAThr and may result a failure in tRNA metabolism. As a result, the G15930A mutation may cause the mitochondrial dysfunction that was responsible for NSHL. Taken together, our data indicated that the G15930A may be a novel mutation associated with NSHL. Thus, our finding provided novel insight into the pathophysiology of maternally inherited NSHL. mitochondrial trnathr g15930a nshl Genetics Qi Liu verfasserin aut Yao-Shu Teng verfasserin aut Hui Zheng verfasserin aut Jian-Hang Leng verfasserin aut In Mitochondrial DNA. Part B. Resources Taylor & Francis Group, 2023 4(2019), 1, Seite 1347-1349 (DE-627)867996722 (DE-600)2868557-X 23802359 nnns volume:4 year:2019 number:1 pages:1347-1349 https://doi.org/10.1080/23802359.2019.1597648 kostenfrei https://doaj.org/article/b1ce2bf334b449a099759af42cb10d4a kostenfrei http://dx.doi.org/10.1080/23802359.2019.1597648 kostenfrei https://doaj.org/toc/2380-2359 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2019 1 1347-1349
spelling	10.1080/23802359.2019.1597648 doi (DE-627)DOAJ096895349 (DE-599)DOAJb1ce2bf334b449a099759af42cb10d4a DE-627 ger DE-627 rakwb eng QH426-470 Yu Ding verfasserin aut The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mutations in mitochondrial DNA (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Chinese family with maternally inherited NSHL. Clinical evaluation showed a variable age at onset of NSHL. Molecular analysis of the matrilineal relatives from this family showed the presence of a novel mt-tRNAThr G15930A mutation, together with a set of genetic polymorphisms belonging to East Asia haplogroup B4b1. Interestingly, the G15930A mutation, which is localized at the highly conserved nucleotide of the anticodon stem of tRNAThr, created a novel base-pairing. Bioinformatics analysis showed that the G15930A mutation altered the secondary structure of tRNAThr and may result a failure in tRNA metabolism. As a result, the G15930A mutation may cause the mitochondrial dysfunction that was responsible for NSHL. Taken together, our data indicated that the G15930A may be a novel mutation associated with NSHL. Thus, our finding provided novel insight into the pathophysiology of maternally inherited NSHL. mitochondrial trnathr g15930a nshl Genetics Qi Liu verfasserin aut Yao-Shu Teng verfasserin aut Hui Zheng verfasserin aut Jian-Hang Leng verfasserin aut In Mitochondrial DNA. Part B. Resources Taylor & Francis Group, 2023 4(2019), 1, Seite 1347-1349 (DE-627)867996722 (DE-600)2868557-X 23802359 nnns volume:4 year:2019 number:1 pages:1347-1349 https://doi.org/10.1080/23802359.2019.1597648 kostenfrei https://doaj.org/article/b1ce2bf334b449a099759af42cb10d4a kostenfrei http://dx.doi.org/10.1080/23802359.2019.1597648 kostenfrei https://doaj.org/toc/2380-2359 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2019 1 1347-1349
allfields_unstemmed	10.1080/23802359.2019.1597648 doi (DE-627)DOAJ096895349 (DE-599)DOAJb1ce2bf334b449a099759af42cb10d4a DE-627 ger DE-627 rakwb eng QH426-470 Yu Ding verfasserin aut The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mutations in mitochondrial DNA (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Chinese family with maternally inherited NSHL. Clinical evaluation showed a variable age at onset of NSHL. Molecular analysis of the matrilineal relatives from this family showed the presence of a novel mt-tRNAThr G15930A mutation, together with a set of genetic polymorphisms belonging to East Asia haplogroup B4b1. Interestingly, the G15930A mutation, which is localized at the highly conserved nucleotide of the anticodon stem of tRNAThr, created a novel base-pairing. Bioinformatics analysis showed that the G15930A mutation altered the secondary structure of tRNAThr and may result a failure in tRNA metabolism. As a result, the G15930A mutation may cause the mitochondrial dysfunction that was responsible for NSHL. Taken together, our data indicated that the G15930A may be a novel mutation associated with NSHL. Thus, our finding provided novel insight into the pathophysiology of maternally inherited NSHL. mitochondrial trnathr g15930a nshl Genetics Qi Liu verfasserin aut Yao-Shu Teng verfasserin aut Hui Zheng verfasserin aut Jian-Hang Leng verfasserin aut In Mitochondrial DNA. Part B. Resources Taylor & Francis Group, 2023 4(2019), 1, Seite 1347-1349 (DE-627)867996722 (DE-600)2868557-X 23802359 nnns volume:4 year:2019 number:1 pages:1347-1349 https://doi.org/10.1080/23802359.2019.1597648 kostenfrei https://doaj.org/article/b1ce2bf334b449a099759af42cb10d4a kostenfrei http://dx.doi.org/10.1080/23802359.2019.1597648 kostenfrei https://doaj.org/toc/2380-2359 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2019 1 1347-1349
allfieldsGer	10.1080/23802359.2019.1597648 doi (DE-627)DOAJ096895349 (DE-599)DOAJb1ce2bf334b449a099759af42cb10d4a DE-627 ger DE-627 rakwb eng QH426-470 Yu Ding verfasserin aut The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mutations in mitochondrial DNA (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Chinese family with maternally inherited NSHL. Clinical evaluation showed a variable age at onset of NSHL. Molecular analysis of the matrilineal relatives from this family showed the presence of a novel mt-tRNAThr G15930A mutation, together with a set of genetic polymorphisms belonging to East Asia haplogroup B4b1. Interestingly, the G15930A mutation, which is localized at the highly conserved nucleotide of the anticodon stem of tRNAThr, created a novel base-pairing. Bioinformatics analysis showed that the G15930A mutation altered the secondary structure of tRNAThr and may result a failure in tRNA metabolism. As a result, the G15930A mutation may cause the mitochondrial dysfunction that was responsible for NSHL. Taken together, our data indicated that the G15930A may be a novel mutation associated with NSHL. Thus, our finding provided novel insight into the pathophysiology of maternally inherited NSHL. mitochondrial trnathr g15930a nshl Genetics Qi Liu verfasserin aut Yao-Shu Teng verfasserin aut Hui Zheng verfasserin aut Jian-Hang Leng verfasserin aut In Mitochondrial DNA. Part B. Resources Taylor & Francis Group, 2023 4(2019), 1, Seite 1347-1349 (DE-627)867996722 (DE-600)2868557-X 23802359 nnns volume:4 year:2019 number:1 pages:1347-1349 https://doi.org/10.1080/23802359.2019.1597648 kostenfrei https://doaj.org/article/b1ce2bf334b449a099759af42cb10d4a kostenfrei http://dx.doi.org/10.1080/23802359.2019.1597648 kostenfrei https://doaj.org/toc/2380-2359 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2019 1 1347-1349
allfieldsSound	10.1080/23802359.2019.1597648 doi (DE-627)DOAJ096895349 (DE-599)DOAJb1ce2bf334b449a099759af42cb10d4a DE-627 ger DE-627 rakwb eng QH426-470 Yu Ding verfasserin aut The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mutations in mitochondrial DNA (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Chinese family with maternally inherited NSHL. Clinical evaluation showed a variable age at onset of NSHL. Molecular analysis of the matrilineal relatives from this family showed the presence of a novel mt-tRNAThr G15930A mutation, together with a set of genetic polymorphisms belonging to East Asia haplogroup B4b1. Interestingly, the G15930A mutation, which is localized at the highly conserved nucleotide of the anticodon stem of tRNAThr, created a novel base-pairing. Bioinformatics analysis showed that the G15930A mutation altered the secondary structure of tRNAThr and may result a failure in tRNA metabolism. As a result, the G15930A mutation may cause the mitochondrial dysfunction that was responsible for NSHL. Taken together, our data indicated that the G15930A may be a novel mutation associated with NSHL. Thus, our finding provided novel insight into the pathophysiology of maternally inherited NSHL. mitochondrial trnathr g15930a nshl Genetics Qi Liu verfasserin aut Yao-Shu Teng verfasserin aut Hui Zheng verfasserin aut Jian-Hang Leng verfasserin aut In Mitochondrial DNA. Part B. Resources Taylor & Francis Group, 2023 4(2019), 1, Seite 1347-1349 (DE-627)867996722 (DE-600)2868557-X 23802359 nnns volume:4 year:2019 number:1 pages:1347-1349 https://doi.org/10.1080/23802359.2019.1597648 kostenfrei https://doaj.org/article/b1ce2bf334b449a099759af42cb10d4a kostenfrei http://dx.doi.org/10.1080/23802359.2019.1597648 kostenfrei https://doaj.org/toc/2380-2359 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2019 1 1347-1349
language	English
source	In Mitochondrial DNA. Part B. Resources 4(2019), 1, Seite 1347-1349 volume:4 year:2019 number:1 pages:1347-1349
sourceStr	In Mitochondrial DNA. Part B. Resources 4(2019), 1, Seite 1347-1349 volume:4 year:2019 number:1 pages:1347-1349
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	mitochondrial trnathr g15930a nshl Genetics
isfreeaccess_bool	true
container_title	Mitochondrial DNA. Part B. Resources
authorswithroles_txt_mv	Yu Ding @@aut@@ Qi Liu @@aut@@ Yao-Shu Teng @@aut@@ Hui Zheng @@aut@@ Jian-Hang Leng @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	867996722
id	DOAJ096895349
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">DOAJ096895349</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240413163933.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">240413s2019 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1080/23802359.2019.1597648</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ096895349</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJb1ce2bf334b449a099759af42cb10d4a</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">QH426-470</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Yu Ding</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="4"><subfield code="a">The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2019</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 (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Chinese family with maternally inherited NSHL. Clinical evaluation showed a variable age at onset of NSHL. Molecular analysis of the matrilineal relatives from this family showed the presence of a novel mt-tRNAThr G15930A mutation, together with a set of genetic polymorphisms belonging to East Asia haplogroup B4b1. Interestingly, the G15930A mutation, which is localized at the highly conserved nucleotide of the anticodon stem of tRNAThr, created a novel base-pairing. Bioinformatics analysis showed that the G15930A mutation altered the secondary structure of tRNAThr and may result a failure in tRNA metabolism. As a result, the G15930A mutation may cause the mitochondrial dysfunction that was responsible for NSHL. Taken together, our data indicated that the G15930A may be a novel mutation associated with NSHL. Thus, our finding provided novel insight into the pathophysiology of maternally inherited NSHL.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">mitochondrial</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">trnathr</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">g15930a</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">nshl</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Genetics</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Qi Liu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yao-Shu Teng</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Hui Zheng</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jian-Hang Leng</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">Mitochondrial DNA. Part B. Resources</subfield><subfield code="d">Taylor & Francis Group, 2023</subfield><subfield code="g">4(2019), 1, Seite 1347-1349</subfield><subfield code="w">(DE-627)867996722</subfield><subfield code="w">(DE-600)2868557-X</subfield><subfield code="x">23802359</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:4</subfield><subfield code="g">year:2019</subfield><subfield code="g">number:1</subfield><subfield code="g">pages:1347-1349</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1080/23802359.2019.1597648</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/b1ce2bf334b449a099759af42cb10d4a</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1080/23802359.2019.1597648</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/2380-2359</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_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</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_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</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_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">4</subfield><subfield code="j">2019</subfield><subfield code="e">1</subfield><subfield code="h">1347-1349</subfield></datafield></record></collection>
callnumber-first	Q - Science
author	Yu Ding
spellingShingle	Yu Ding misc QH426-470 misc mitochondrial misc trnathr misc g15930a misc nshl misc Genetics The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment
authorStr	Yu Ding
ppnlink_with_tag_str_mv	@@773@@(DE-627)867996722
format	electronic Article
delete_txt_mv	keep
author_role	aut aut aut aut aut
collection	DOAJ
remote_str	true
callnumber-label	QH426-470
illustrated	Not Illustrated
issn	23802359
topic_title	QH426-470 The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment mitochondrial trnathr g15930a nshl
topic	misc QH426-470 misc mitochondrial misc trnathr misc g15930a misc nshl misc Genetics
topic_unstemmed	misc QH426-470 misc mitochondrial misc trnathr misc g15930a misc nshl misc Genetics
topic_browse	misc QH426-470 misc mitochondrial misc trnathr misc g15930a misc nshl misc Genetics
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
format_main_str_mv	Text Zeitschrift/Artikel
carriertype_str_mv	cr
hierarchy_parent_title	Mitochondrial DNA. Part B. Resources
hierarchy_parent_id	867996722
hierarchy_top_title	Mitochondrial DNA. Part B. Resources
isfreeaccess_txt	true
familylinks_str_mv	(DE-627)867996722 (DE-600)2868557-X
title	The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment
ctrlnum	(DE-627)DOAJ096895349 (DE-599)DOAJb1ce2bf334b449a099759af42cb10d4a
title_full	The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment
author_sort	Yu Ding
journal	Mitochondrial DNA. Part B. Resources
journalStr	Mitochondrial DNA. Part B. Resources
callnumber-first-code	Q
lang_code	eng
isOA_bool	true
recordtype	marc
publishDateSort	2019
contenttype_str_mv	txt
container_start_page	1347
author_browse	Yu Ding Qi Liu Yao-Shu Teng Hui Zheng Jian-Hang Leng
container_volume	4
class	QH426-470
format_se	Elektronische Aufsätze
author-letter	Yu Ding
doi_str_mv	10.1080/23802359.2019.1597648
author2-role	verfasserin
title_sort	mitochondrial trnathr g15930a may be a novel mutation associated with hearing impairment
callnumber	QH426-470
title_auth	The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment
abstract	Mutations in mitochondrial DNA (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Chinese family with maternally inherited NSHL. Clinical evaluation showed a variable age at onset of NSHL. Molecular analysis of the matrilineal relatives from this family showed the presence of a novel mt-tRNAThr G15930A mutation, together with a set of genetic polymorphisms belonging to East Asia haplogroup B4b1. Interestingly, the G15930A mutation, which is localized at the highly conserved nucleotide of the anticodon stem of tRNAThr, created a novel base-pairing. Bioinformatics analysis showed that the G15930A mutation altered the secondary structure of tRNAThr and may result a failure in tRNA metabolism. As a result, the G15930A mutation may cause the mitochondrial dysfunction that was responsible for NSHL. Taken together, our data indicated that the G15930A may be a novel mutation associated with NSHL. Thus, our finding provided novel insight into the pathophysiology of maternally inherited NSHL.
abstractGer	Mutations in mitochondrial DNA (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Chinese family with maternally inherited NSHL. Clinical evaluation showed a variable age at onset of NSHL. Molecular analysis of the matrilineal relatives from this family showed the presence of a novel mt-tRNAThr G15930A mutation, together with a set of genetic polymorphisms belonging to East Asia haplogroup B4b1. Interestingly, the G15930A mutation, which is localized at the highly conserved nucleotide of the anticodon stem of tRNAThr, created a novel base-pairing. Bioinformatics analysis showed that the G15930A mutation altered the secondary structure of tRNAThr and may result a failure in tRNA metabolism. As a result, the G15930A mutation may cause the mitochondrial dysfunction that was responsible for NSHL. Taken together, our data indicated that the G15930A may be a novel mutation associated with NSHL. Thus, our finding provided novel insight into the pathophysiology of maternally inherited NSHL.
abstract_unstemmed	Mutations in mitochondrial DNA (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Chinese family with maternally inherited NSHL. Clinical evaluation showed a variable age at onset of NSHL. Molecular analysis of the matrilineal relatives from this family showed the presence of a novel mt-tRNAThr G15930A mutation, together with a set of genetic polymorphisms belonging to East Asia haplogroup B4b1. Interestingly, the G15930A mutation, which is localized at the highly conserved nucleotide of the anticodon stem of tRNAThr, created a novel base-pairing. Bioinformatics analysis showed that the G15930A mutation altered the secondary structure of tRNAThr and may result a failure in tRNA metabolism. As a result, the G15930A mutation may cause the mitochondrial dysfunction that was responsible for NSHL. Taken together, our data indicated that the G15930A may be a novel mutation associated with NSHL. Thus, our finding provided novel insight into the pathophysiology of maternally inherited NSHL.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700
container_issue	1
title_short	The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment
url	https://doi.org/10.1080/23802359.2019.1597648 https://doaj.org/article/b1ce2bf334b449a099759af42cb10d4a http://dx.doi.org/10.1080/23802359.2019.1597648 https://doaj.org/toc/2380-2359
remote_bool	true
author2	Qi Liu Yao-Shu Teng Hui Zheng Jian-Hang Leng
author2Str	Qi Liu Yao-Shu Teng Hui Zheng Jian-Hang Leng
ppnlink	867996722
callnumber-subject	QH - Natural History and Biology
mediatype_str_mv	c
isOA_txt	true
hochschulschrift_bool	false
doi_str	10.1080/23802359.2019.1597648
callnumber-a	QH426-470
up_date	2024-07-03T22:50:36.571Z
_version_	1803600041419472896
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">DOAJ096895349</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240413163933.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">240413s2019 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1080/23802359.2019.1597648</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ096895349</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJb1ce2bf334b449a099759af42cb10d4a</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">QH426-470</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Yu Ding</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="4"><subfield code="a">The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2019</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 (mtDNA) were the important causes for non-syndromic hearing loss (NSHL). However, the molecular mechanism underlying mt-tRNA mutations and NSHL remained poorly understood. In this study, we reported here the clinical, genetic, and molecular characterization of a Han Chinese family with maternally inherited NSHL. Clinical evaluation showed a variable age at onset of NSHL. Molecular analysis of the matrilineal relatives from this family showed the presence of a novel mt-tRNAThr G15930A mutation, together with a set of genetic polymorphisms belonging to East Asia haplogroup B4b1. Interestingly, the G15930A mutation, which is localized at the highly conserved nucleotide of the anticodon stem of tRNAThr, created a novel base-pairing. Bioinformatics analysis showed that the G15930A mutation altered the secondary structure of tRNAThr and may result a failure in tRNA metabolism. As a result, the G15930A mutation may cause the mitochondrial dysfunction that was responsible for NSHL. Taken together, our data indicated that the G15930A may be a novel mutation associated with NSHL. Thus, our finding provided novel insight into the pathophysiology of maternally inherited NSHL.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">mitochondrial</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">trnathr</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">g15930a</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">nshl</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Genetics</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Qi Liu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yao-Shu Teng</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Hui Zheng</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jian-Hang Leng</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">Mitochondrial DNA. Part B. Resources</subfield><subfield code="d">Taylor & Francis Group, 2023</subfield><subfield code="g">4(2019), 1, Seite 1347-1349</subfield><subfield code="w">(DE-627)867996722</subfield><subfield code="w">(DE-600)2868557-X</subfield><subfield code="x">23802359</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:4</subfield><subfield code="g">year:2019</subfield><subfield code="g">number:1</subfield><subfield code="g">pages:1347-1349</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1080/23802359.2019.1597648</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/b1ce2bf334b449a099759af42cb10d4a</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1080/23802359.2019.1597648</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/2380-2359</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_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</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_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</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_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">4</subfield><subfield code="j">2019</subfield><subfield code="e">1</subfield><subfield code="h">1347-1349</subfield></datafield></record></collection>
score	7.399496

Nicht das Richtige dabei?

Schreiben Sie uns!

The mitochondrial tRNAThr G15930A may be a novel mutation associated with hearing impairment

Nicht das Richtige dabei?

Zugang & Verfügbarkeit

Vorhandene Bände

Nicht das Richtige dabei?