Friedreich's ataxia-associated GAA repeats induce replication-fork reversal and unusual molecular junctions.
about
The balancing act of DNA repeat expansionsDNA bending facilitates the error-free DNA damage tolerance pathway and upholds genome integrity.Replication fork instability and the consequences of fork collisions from rereplicationPreventing replication fork collapse to maintain genome integrityDisruption of Higher Order DNA Structures in Friedreich's Ataxia (GAA)n Repeats by PNA or LNA TargetingVisualization of recombination-mediated damage bypass by template switching.Causes and consequences of replication stress.Trinucleotide expansion in disease: why is there a length threshold?Poly(ADP-ribosyl) glycohydrolase prevents the accumulation of unusual replication structures during unperturbed S phaseBase excision repair of chemotherapeutically-induced alkylated DNA damage predominantly causes contractions of expanded GAA repeats associated with Friedreich's ataxia.Involvement of a citrus meiotic recombination TTC-repeat motif in the formation of gross deletions generated by ionizing radiation and MULE activation.Regulation of recombination at yeast nuclear pores controls repair and triplet repeat stability.Repeat instability during DNA repair: Insights from model systemsHLTF's Ancient HIRAN Domain Binds 3' DNA Ends to Drive Replication Fork Reversal.The dual nature of mismatch repair as antimutator and mutator: for better or for worse.Replication fork reversal in eukaryotes: from dead end to dynamic response.The Replication of Frataxin Gene Is Assured by Activation of Dormant Origins in the Presence of a GAA-Repeat Expansion.Replication fork regression and its regulation.Relocalization of DNA lesions to the nuclear pore complex.Replication stalling and DNA microsatellite instability.Role of recombination and replication fork restart in repeat instability.Precarious maintenance of simple DNA repeats in eukaryotes.The role of break-induced replication in large-scale expansions of (CAG)n/(CTG)n repeats.Replication Fork Slowing and Reversal upon DNA Damage Require PCNA Polyubiquitination and ZRANB3 DNA Translocase Activity.RNA biology of disease-associated microsatellite repeat expansions.Stability of blocked replication forks in vivoCoupling transcriptional state to large-scale repeat expansions in yeast.Replication fork reversal triggers fork degradation in BRCA2-defective cells.Dynamic Architecture of Eukaryotic DNA Replication Forks In Vivo, Visualized by Electron Microscopy.The HIRAN domain of helicase-like transcription factor positions the DNA translocase motor to drive efficient DNA fork regression
P2860
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P2860
Friedreich's ataxia-associated GAA repeats induce replication-fork reversal and unusual molecular junctions.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年学术文章
@wuu
2013年学术文章
@zh-cn
2013年学术文章
@zh-hans
2013年学术文章
@zh-my
2013年学术文章
@zh-sg
2013年學術文章
@yue
2013年學術文章
@zh
2013年學術文章
@zh-hant
name
Friedreich's ataxia-associated ...... d unusual molecular junctions.
@en
Friedreich's ataxia-associated ...... d unusual molecular junctions.
@nl
type
label
Friedreich's ataxia-associated ...... d unusual molecular junctions.
@en
Friedreich's ataxia-associated ...... d unusual molecular junctions.
@nl
prefLabel
Friedreich's ataxia-associated ...... d unusual molecular junctions.
@en
Friedreich's ataxia-associated ...... d unusual molecular junctions.
@nl
P2093
P2860
P356
P1476
Friedreich's ataxia-associated ...... d unusual molecular junctions.
@en
P2093
Cindy Follonier
Judith Oehler
Massimo Lopes
Raquel Herrador
P2860
P2888
P304
P356
10.1038/NSMB.2520
P577
2013-03-03T00:00:00Z
P5875
P6179
1007161645