Marked replicative advantage of human mtDNA carrying a point mutation that causes the MELAS encephalomyopathy.
about
Mitochondrial dysfunction in Pten haplo-insufficient mice with social deficits and repetitive behavior: interplay between Pten and p53A human mitochondrial GTP binding protein related to tRNA modification may modulate phenotypic expression of the deafness-associated mitochondrial 12S rRNA mutationMitochondrial DNA mutations in human diseaseCytoplasmic hybrid (cybrid) cell lines as a practical model for mitochondriopathiesUracil-DNA glycosylase-deficient yeast exhibit a mitochondrial mutator phenotype.Isolation and characterization of the putative nuclear modifier gene MTO1 involved in the pathogenesis of deafness-associated mitochondrial 12 S rRNA A1555G mutationHeterogeneous tissue distribution of a mitochondrial DNA polymorphism in heteroplasmic subjects without mitochondrial disordersThe mtDNA-encoded ND6 subunit of mitochondrial NADH dehydrogenase is essential for the assembly of the membrane arm and the respiratory function of the enzyme.Conflicting levels of selection in the accumulation of mitochondrial defects in Saccharomyces cerevisiae.Detection and characterization of CD133+ cancer stem cells in human solid tumours.A wide range of 3243A>G/tRNALeu(UUR) (MELAS) mutation loads may segregate in offspring through the female germline bottleneck.Control of mitochondrial integrity in ageing and diseaseThe road to rack and ruin: selecting deleterious mitochondrial DNA variantsTransmission of mitochondrial DNA diseases and ways to prevent them.Point mutation of the mitochondrial tRNA(Leu) gene (A 3243 G) in maternally inherited hypertrophic cardiomyopathy, diabetes mellitus, renal failure, and sensorineural deafnessMitochondria harbouring mutant mtDNA--a cuckoo in the nest?Human mitochondrial leucyl-tRNA synthetase corrects mitochondrial dysfunctions due to the tRNALeu(UUR) A3243G mutation, associated with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like symptoms and diabetesClonally expanded mtDNA point mutations are abundant in individual cells of human tissues.Frequent intracellular clonal expansions of somatic mtDNA mutations: significance and mechanisms.Different cellular backgrounds confer a marked advantage to either mutant or wild-type mitochondrial genomes.Mitochondrial encephalomyopathy and complex III deficiency associated with a stop-codon mutation in the cytochrome b gene.Human mitochondrial genetics.Analysis of mtDNA sequence variants in colorectal adenomatous polypsDeceleration of fusion-fission cycles improves mitochondrial quality control during aging.Mitochondrial genetics '98 is the bottleneck cracked?Potential therapeutic use of the ketogenic diet in autism spectrum disordersNon-random mtDNA segregation patterns indicate a metastable heteroplasmic segregation unit in m.3243A>G cybrid cells.Germline bottlenecks, biparental inheritance and selection on mitochondrial variants: a two-level selection modelReplicative advantage and tissue-specific segregation of RR mitochondrial DNA between C57BL/6 and RR heteroplasmic miceElectrophile and oxidant damage of mitochondrial DNA leading to rapid evolution of homoplasmic mutations.Mitochondrial nucleoids maintain genetic autonomy but allow for functional complementation.Pathomechanisms of work-related musculoskeletal disorders: conceptual issues.Muscle-specific mutations accumulate with aging in critical human mtDNA control sites for replication.A new mtDNA mutation showing accumulation with time and restriction to skeletal muscleHomopolymeric tract heteroplasmy in mtDNA from tissues and single oocytes: support for a genetic bottleneck.Intracellular mitochondrial triplasmy in a patient with two heteroplasmic base changesImpaired respiratory function in MELAS-induced pluripotent stem cells with high heteroplasmy levels.The biology of mitochondrial disease.Mitochondrial activity in gametes and transmission of viable mtDNAThe awakening of an advanced malignant cancer: an insult to the mitochondrial genome
P2860
Q21560776-0E393DBB-B9AE-45E0-8055-BC1EE6CFC82DQ24540271-0EB3CB46-FD32-49FE-84A1-EB78770435EEQ24676881-54BABFC3-6191-4266-8DEC-820871BB08A1Q26859496-86F1F76A-0845-45E4-956B-4504D994E900Q27940072-2DEA03BC-F21B-46EC-ACF1-1D461F6E84E5Q28217558-EEA723AD-D8FF-4977-B32A-26379214390EQ28364171-6A610848-C6C5-4F85-988F-1E0AD4BBD3FFQ28368398-5607E53D-8F5A-4510-826F-C3E4BDB0E3EEQ30308887-5C0C3344-9BFD-4508-A6F9-2F4CF6D910F4Q33378520-E9D5B4C0-D062-428F-944E-66E582532B98Q33578068-2AC6EBBF-F4FA-4639-A8D8-975CCF407101Q33655966-C229B570-0181-4DD5-A482-C92C1797A723Q33655994-C270B41C-16D7-4F10-83D0-998104037199Q33658696-A0C07D84-CB27-4F4C-99C4-D4422D1AE8C2Q33682328-4068C95C-3E5C-45E3-BF0B-135976E984C8Q33737272-3CC33270-FC38-400F-ABB9-7D55BD224A03Q33826223-FA70B0E9-E56E-4A66-9528-62058935D76DQ34025368-50D60699-CF91-4F59-9E94-E7C4DCD2BDB1Q34125463-2B39EE84-ED59-45A3-AF0A-6B9EB409F9B0Q34139746-7EAA29F4-1912-4448-8331-57922DBC44B4Q34144271-D8C88C79-3D2F-45E3-8B41-F88F48A1360DQ34187826-A21D2D48-C9C1-4A96-A2C7-4C21162FF873Q34221543-69A2ED3A-6655-43D8-8838-8D27D5D6428EQ34325475-BFC31440-8B74-4719-9163-25B3D531E824Q34385187-365C3FA7-3DEA-449F-AE5B-0F0DAE67CE3EQ34431317-5EB8B102-2004-4E51-80F8-0607AA6E76AFQ34525992-C0587A26-7F01-4B01-BBE6-5E3624BC060EQ34576588-58CD4D3B-BE27-48DD-B15F-7AC9DC06E7E2Q34609738-45B7AB01-7E8D-49B1-9D65-DDE7F21A2B98Q34762213-A9EB98ED-2264-4480-A5AD-821FF8CEE8ACQ34788426-7F37776D-CC74-481B-8861-4B761BF77C9FQ34824408-8AC86446-8794-467E-B89B-9655917BBF8FQ35051341-07814DDA-7A09-4235-946B-8DE6E328E6A2Q35238359-378F9C03-FF0E-420E-AF6A-AEA1C624CF0BQ35238386-FD41A5D8-82D1-4AFC-9B10-5012D4EF5935Q35250582-01F26B45-4162-46BB-BB44-EAA14BC8B33CQ35252601-E2AE217D-E942-4E4C-8534-0DE070130E61Q35266452-F1BF1CE7-059C-45F1-9C93-1461F10F7799Q35619766-317C39AE-87D9-4EEC-B5B4-6F376E61A9A9Q35718294-4033A2BB-8AA4-4C7D-9DB7-61341CAED26A
P2860
Marked replicative advantage of human mtDNA carrying a point mutation that causes the MELAS encephalomyopathy.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on December 1992
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Marked replicative advantage o ...... s the MELAS encephalomyopathy.
@en
Marked replicative advantage o ...... s the MELAS encephalomyopathy.
@nl
type
label
Marked replicative advantage o ...... s the MELAS encephalomyopathy.
@en
Marked replicative advantage o ...... s the MELAS encephalomyopathy.
@nl
prefLabel
Marked replicative advantage o ...... s the MELAS encephalomyopathy.
@en
Marked replicative advantage o ...... s the MELAS encephalomyopathy.
@nl
P2093
P2860
P356
P1476
Marked replicative advantage o ...... s the MELAS encephalomyopathy.
@en
P2093
P2860
P304
11164-11168
P356
10.1073/PNAS.89.23.11164
P407
P577
1992-12-01T00:00:00Z