Chemotherapeutic deletion of CTG repeats in lymphoblast cells from DM1 patients. - Wikidata - awgldk - TriplyDB

Chemotherapeutic deletion of CTG repeats in lymphoblast cells from DM1 patients.

Chemotherapeutic deletion of CTG repeats in lymphoblast cells from DM1 patients.

http://www.wikidata.org/entity/Q40485534

about

New insights into repeat instability: role of RNA•DNA hybrids Length-dependent energetics of (CTG)n and (CAG)n trinucleotide repeats.Advances in mechanisms of genetic instability related to hereditary neurological diseases.The structural basis of actinomycin D-binding induces nucleotide flipping out, a sharp bend and a left-handed twist in CGG triplet repeats DNA instability in replicating Huntington's disease lymphoblasts Topoisomerase 1 and single-strand break repair modulate transcription-induced CAG repeat contraction in human cells.Base excision repair of chemotherapeutically-induced alkylated DNA damage predominantly causes contractions of expanded GAA repeats associated with Friedreich's ataxia.Instability of (CTG)n•(CAG)n trinucleotide repeats and DNA synthesis Altered replication in human cells promotes DMPK (CTG)(n) · (CAG)(n) repeat instability Repeat instability: mechanisms of dynamic mutations.Investigating the binding mode of an inhibitor of the MBNL1·RNA complex in myotonic dystrophy type 1 (DM1) leads to the unexpected discovery of a DNA-selective binder.Trinucleotide repeat deletion via a unique hairpin bypass by DNA polymerase β and alternate flap cleavage by flap endonuclease 1.FANCJ is essential to maintain microsatellite structure genome-wide during replication stress.Myotonic dystrophy mouse models: towards rational therapy development.Perspectives on gene therapy in myotonic dystrophy type 1.Novel computational study on π-stacking to understand mechanistic interactions of Tryptanthrin analogues with DNA.Length-dependent CTG·CAG triplet-repeat expansion in myotonic dystrophy patient-derived induced pluripotent stem cells.Replication-dependent instability at (CTG) x (CAG) repeat hairpins in human cells.(CAG)*(CTG) repeats associated with neurodegenerative diseases are stable in the Escherichia coli chromosome.Daunorubicin reduces MBNL1 sequestration caused by CUG-repeat expansion and rescues cardiac dysfunctions in a Drosophila model of myotonic dystrophy.Co(Chromomycin)₂ Complex Induces a Conformational Change of CCG Repeats from i-Motif to Base-Extruded DNA Duplex

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Chemotherapeutic deletion of CTG repeats in lymphoblast cells from DM1 patients.

http://www.wikidata.org/entity/Q40485534

description

2004 nî lūn-bûn

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2004年の論文

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

@zh-my

2004年学术文章

@zh-sg

2004年學術文章

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2004年學術文章

@zh

2004年學術文章

@zh-hant

name

Chemotherapeutic deletion of CTG repeats in lymphoblast cells from DM1 patients.

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type

label

Chemotherapeutic deletion of CTG repeats in lymphoblast cells from DM1 patients.

@en

prefLabel

Chemotherapeutic deletion of CTG repeats in lymphoblast cells from DM1 patients.

@en

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Nucleic Acids Research

P1476

Chemotherapeutic deletion of CTG repeats in lymphoblast cells from DM1 patients.

@en

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Elzbieta A Klysik

http://www.w3.org/2001/XMLSchema#string

Kuniko Tsuji

http://www.w3.org/2001/XMLSchema#string

Malgorzata J Pytlos

http://www.w3.org/2001/XMLSchema#string

Mehrdad Khajavi

http://www.w3.org/2001/XMLSchema#string

Richard R Sinden

http://www.w3.org/2001/XMLSchema#string

Tetsuo Ashizawa

http://www.w3.org/2001/XMLSchema#string

Vera I Hashem

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P2860

The GAA triplet-repeat expansion in Friedreich ataxia interferes with transcription and may be associated with an unusual DNA structure

Role of RAD52 epistasis group genes in homologous recombination and double-strand break repair

Transgenic mice carrying large human genomic sequences with expanded CTG repeat mimic closely the DM CTG repeat intergenerational and somatic instability.

The GAA*TTC triplet repeat expanded in Friedreich's ataxia impedes transcription elongation by T7 RNA polymerase in a length and supercoil dependent manner

Fourteen and counting: unraveling trinucleotide repeat diseases.

Replication inhibitors modulate instability of an expanded trinucleotide repeat at the myotonic dystrophy type 1 disease locus in human cells.

Insights from mouse models into the molecular basis of neurodegeneration.

On the deletion of inverted repeated DNA in Escherichia coli: effects of length, thermal stability, and cruciform formation in vivo.

Recombinational repair and restart of damaged replication forks.

Transgenic mouse models for myotonic dystrophy type 1 (DM1).

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6334-6346

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scholarly article

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10.1093/NAR/GKH976

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21

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32

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2004-12-01T00:00:00Z

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8152021

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15576360

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535684

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