Effects of Friedreich's ataxia GAA repeats on DNA replication in mammalian cells

scientific article published on 19 January 2012

Effects of Friedreich's ataxia GAA repeats on DNA replication in mammalian cells is …
instance of (P31):
scholarly articleQ13442814

External links are
P356DOI10.1093/NAR/GKS021
P932PMC publication ID3351192
P698PubMed publication ID22262734
P5875ResearchGate publication ID221764242

P2093author name stringMaria M Krasilnikova
Sergei M Mirkin
Gurangad S Chandok
Mayank P Patel
P2860cites workThe Epstein-Barr virus origin of plasmid replication, oriP, contains both the initiation and termination sites of DNA replicationQ45845623
Parental gender, age at birth and expansion length influence GAA repeat intergenerational instability in the X25 gene: pedigree studies and analysis of sperm from patients with Friedreich's ataxia.Q50857914
Hairpin formation in Friedreich's ataxia triplet repeat expansion.Q54534838
Sticky DNA: self-association properties of long GAA.TTC repeats in R.R.Y triplex structures from Friedreich's ataxia.Q55033015
DNA triplet repeats mediate heterochromatin-protein-1-sensitive variegated gene silencingQ59071144
Sea urchin zygote chromatin exhibit an unfolded nucleosomal array during the first S phaseQ71750651
Phenotypic variability in Friedreich ataxia: role of the associated GAA triplet repeat expansionQ73343750
Sticky DNA, a self-associated complex formed at long GAA*TTC repeats in intron 1 of the frataxin gene, inhibits transcriptionQ73842935
The GAA triplet-repeat sequence in Friedreich ataxia shows a high level of somatic instability in vivo, with a significant predilection for large contractionsQ74633178
GAA instability in Friedreich's Ataxia shares a common, DNA-directed and intraallelic mechanism with other trinucleotide diseasesQ74771975
Somatic instability of the expanded GAA triplet-repeat sequence in Friedreich ataxia progresses throughout lifeQ80325491
Replication from oriP of Epstein-Barr virus requires human ORC and is inhibited by gemininQ28213116
Frataxin is reduced in Friedreich ataxia patients and is associated with mitochondrial membranesQ28249379
Friedreich's ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansionQ28275699
Clinical and genetic abnormalities in patients with Friedreich's ataxiaQ28290611
Progressive GAA.TTC repeat expansion in human cell linesQ33513958
Development of histone deacetylase inhibitors as therapeutics for neurological diseaseQ33670661
Sperm DNA analysis in a Friedreich ataxia premutation carrier suggests both meiotic and mitotic expansion in the FRDA geneQ33681230
Bi-directional replication and random termination.Q33688903
Ribosomal DNA replication fork barrier and HOT1 recombination hot spot: shared sequences but independent activitiesQ33964531
Suicidal nucleotide sequences for DNA polymerization.Q34064436
Friedreich's ataxia induced pluripotent stem cells model intergenerational GAA⋅TTC triplet repeat instabilityQ34330367
The Friedreich ataxia GAA triplet repeat: premutation and normal alleles.Q34435679
Non-B DNA structure-induced genetic instability and evolutionQ34473652
A distinct first replication cycle of DNA introduced in mammalian cellsQ34723884
The molecular basis of Friedreich ataxia.Q35075287
Repeat-induced epigenetic changes in intron 1 of the frataxin gene and its consequences in Friedreich ataxiaQ35865338
Long intronic GAA*TTC repeats induce epigenetic changes and reporter gene silencing in a molecular model of Friedreich ataxiaQ36959663
DNA triplexes and Friedreich ataxiaQ37062600
Unwinding of the third strand of a DNA triple helix, a novel activity of the SV40 large T-antigen helicaseQ38362777
Replisome stalling and stabilization at CGG repeats, which are responsible for chromosomal fragilityQ39592950
Replication and expansion of trinucleotide repeats in yeastQ39700490
The SV40 large T-antigen helicase can unwind four stranded DNA structures linked by G-quartetsQ39718865
Plasmid maintenance of derivatives of oriP of Epstein-Barr virusQ39868910
Sequence-independent DNA binding and replication initiation by the human origin recognition complexQ39896073
Replication-mediated instability of the GAA triplet repeat mutation in Friedreich ataxiaQ40405624
Replication stalling at Friedreich's ataxia (GAA)n repeats in vivo.Q40633778
Replication initiates at multiple locations on an autonomously replicating plasmid in human cellsQ40677658
Length-dependent structure formation in Friedreich ataxia (GAA)n*(TTC)n repeats at neutral pH.Q40695802
Getting to the core of repeat expansions by cell reprogramming.Q41426270
Effects of Friedreich's ataxia (GAA)n*(TTC)n repeats on RNA synthesis and stabilityQ41871881
The relationship between trinucleotide (GAA) repeat length and clinical features in Friedreich ataxiaQ42176216
Replication-dependent instability at (CTG)•(CAG) repeat hairpins in human cellsQ42177075
Chromosome fragility at GAA tracts in yeast depends on repeat orientation and requires mismatch repairQ42556770
Large-scale expansions of Friedreich's ataxia GAA repeats in yeastQ43077169
The effect of parental gender on the GAA dynamic mutation in the FRDA geneQ43109067
Unexpected formation of parallel duplex in GAA and TTC trinucleotide repeats of Friedreich's ataxiaQ45302221
P275copyright licenseCreative Commons Attribution-NonCommercial 3.0 UnportedQ18810331
P6216copyright statuscopyrightedQ50423863
P433issue9
P407language of work or nameEnglishQ1860
P921main subjectFriedreich ataxiaQ913856
P304page(s)3964-3974
P577publication date2012-01-19
P1433published inNucleic Acids ResearchQ135122
P1476titleEffects of Friedreich's ataxia GAA repeats on DNA replication in mammalian cells
P478volume40

Reverse relations

cites work (P2860)
Q35137677Base excision repair of chemotherapeutically-induced alkylated DNA damage predominantly causes contractions of expanded GAA repeats associated with Friedreich's ataxia.
Q35239367CNV instability associated with DNA replication dynamics: evidence for replicative mechanisms in CNV mutagenesis
Q42113974Complexes between two GAA Repeats within DNA introduced into Cos-1 cells
Q57808238Detours to Replication: Functions of Specialized DNA Polymerases during Oncogene-induced Replication Stress
Q36663928Epigenetics in Friedreich's Ataxia: Challenges and Opportunities for Therapy
Q44271608Friedreich's ataxia-associated GAA repeats induce replication-fork reversal and unusual molecular junctions
Q28540063Generation and characterisation of Friedreich ataxia YG8R mouse fibroblast and neural stem cell models
Q40068916Genome-wide screen identifies pathways that govern GAA/TTC repeat fragility and expansions in dividing and nondividing yeast cells.
Q37149212Inhibition of DNA synthesis facilitates expansion of low-complexity repeats: is strand slippage stimulated by transient local depletion of specific dNTPs?
Q92479421Large-scale contractions of Friedreich's ataxia GAA repeats in yeast occur during DNA replication due to their triplex-forming ability
Q36642236Mature microsatellites: mechanisms underlying dinucleotide microsatellite mutational biases in human cells
Q90647964Mechanisms of genetic instability caused by (CGG)n repeats in an experimental mammalian system
Q93371579Mrc1 and Tof1 prevent fragility and instability at long CAG repeats by their fork stabilizing function
Q33817381MutLα heterodimers modify the molecular phenotype of Friedreich ataxia
Q89721926On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability
Q64935051R-loop formation during S phase is restricted by PrimPol-mediated repriming.
Q64251220Replication of G Quadruplex DNA
Q39028357Replication stalling and DNA microsatellite instability
Q37266016Stalled DNA Replication Forks at the Endogenous GAA Repeats Drive Repeat Expansion in Friedreich's Ataxia Cells
Q58051863Stratifying Heterogeneous Dimension of Neurodegenerative Diseases: Intervention for Stipulating Epigenetic Factors to Combat Oxidative Stress in Human Brain
Q38756391The Replication of Frataxin Gene Is Assured by Activation of Dormant Origins in the Presence of a GAA-Repeat Expansion.
Q36580985Trinucleotide repeat deletion via a unique hairpin bypass by DNA polymerase β and alternate flap cleavage by flap endonuclease 1.
Q36051360Triplex structures induce DNA double strand breaks via replication fork collapse in NER deficient cells.

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