Respiration-deficient cells are caused by a single point mutation in the mitochondrial tRNA-Leu (UUR) gene in mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS).
about
Maternal inheritance of mouse mtDNA in interspecific hybrids: segregation of the leaked paternal mtDNA followed by the prevention of subsequent paternal leakageA mitochondrial DNA mutation at nucleotide pair 14459 of the NADH dehydrogenase subunit 6 gene associated with maternally inherited Leber hereditary optic neuropathy and dystoniaHow clonal are human mitochondria?Molecular biology of neurological diseases.New evidence of a mitochondrial genetic background paradox: impact of the J haplogroup on the A3243G mutation.Mitochondrial DNA haplogroups do not play a role in the variable phenotypic presentation of the A3243G mutation.Nonneutral mitochondrial DNA variation in humans and chimpanzeesDifferent cellular backgrounds confer a marked advantage to either mutant or wild-type mitochondrial genomes.The soluble epoxide hydrolase gene harbors sequence variation associated with susceptibility to and protection from incident ischemic stroke.Selective and continuous elimination of mitochondria microinjected into mouse eggs from spermatids, but not from liver cells, occurs throughout embryogenesisThe mitochondrial tRNA(Leu(UUR)) mutation in mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes (MELAS): genetic, biochemical, and morphological correlations in skeletal muscle.Impaired respiratory function in MELAS-induced pluripotent stem cells with high heteroplasmy levels.Unique features of animal mitochondrial translation systems. The non-universal genetic code, unusual features of the translational apparatus and their relevance to human mitochondrial diseasesMELAS: a new disease associated mitochondrial DNA mutation and evidence for further genetic heterogeneityMitochondrial biogenesis: a therapeutic target for neurodevelopmental disorders and neurodegenerative diseasesMELAS mutation in mtDNA binding site for transcription termination factor causes defects in protein synthesis and in respiration but no change in levels of upstream and downstream mature transcripts.Mouse models of mitochondrial DNA defects and their relevance for human disease.Codon-specific translational defect caused by a wobble modification deficiency in mutant tRNA from a human mitochondrial disease.Introduction of disease-related mitochondrial DNA deletions into HeLa cells lacking mitochondrial DNA results in mitochondrial dysfunction.Respiratory-deficient human fibroblasts exhibiting defective mitochondrial DNA replicationThe sequence of human mtDNA: the question of errors versus polymorphisms.
P2860
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P2860
Respiration-deficient cells are caused by a single point mutation in the mitochondrial tRNA-Leu (UUR) gene in mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS).
description
1991 nî lūn-bûn
@nan
1991 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
1991 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
1991年の論文
@ja
1991年論文
@yue
1991年論文
@zh-hant
1991年論文
@zh-hk
1991年論文
@zh-mo
1991年論文
@zh-tw
1991年论文
@wuu
name
Respiration-deficient cells ar ...... d strokelike episodes (MELAS).
@ast
Respiration-deficient cells ar ...... d strokelike episodes (MELAS).
@en
type
label
Respiration-deficient cells ar ...... d strokelike episodes (MELAS).
@ast
Respiration-deficient cells ar ...... d strokelike episodes (MELAS).
@en
prefLabel
Respiration-deficient cells ar ...... d strokelike episodes (MELAS).
@ast
Respiration-deficient cells ar ...... d strokelike episodes (MELAS).
@en
P2093
P2860
P1476
Respiration-deficient cells ar ...... d strokelike episodes (MELAS).
@en
P2093
Kobayashi Y
Shimoizumi H
Tominaga K
Yanagisawa M
P2860
P304
P407
P577
1991-09-01T00:00:00Z