Induced transcription through CAG repeats in human cells increases repeat contraction ∼15-fold in both confluent and proliferating cells. Repeats are stabilized against contraction by siRNA knockdown of MSH2, MSH3 or XPA, but not by knockdown of MSH6, XPC or FEN1. These results define a pathway for CAG·CTG repeat contraction that is initiated by transcription, depends on elements of mismatch and nucleotide-excision repair and does not require DNA replication
Despite substantial progress in understanding the mechanism by which expanded CTG/CAG trinucleotide ...
Despite substantial progress in understanding the mechanism by which expanded CTG/CAG trinucleotide ...
CAG/CTG repeat expansions cause over 13 neurological diseases that remain without a cure. Because lo...
Induced transcription through CAG repeats in human cells increases repeat contraction ∼15-fold in bo...
Induced transcription through CAG repeats in human cells increases repeat contraction ∼15-fold in bo...
Expansions of CAG repeat tracts in the germ line underlie several neurological diseases. In human pa...
Expanded trinucleotide repeats are responsible for a number of neurodegenerative diseases, such as H...
Expanded trinucleotide repeats are responsible for a number of neurodegenerative diseases, such as H...
Expanded trinucleotide repeats are responsible for a number of neurodegenerative diseases, such as H...
Expanded trinucleotide repeats are responsible for a number of neurodegenerative diseases, such as H...
Expanded trinucleotide repeats are responsible for a number of neurodegenerative diseases, such as H...
More than 12 neurogenetic disorders are caused by unstable expansions of (CTG)†(CAG) repeats. The ex...
Expansion of CAG•CTG tracts located in specific genes is responsible for 13 human neurodegenerative ...
Trinucleotide repeats (TNRs) undergo high frequency mutagenesis to cause at least 15 neurodegenerati...
Despite substantial progress in understanding the mechanism by which expanded CTG/CAG trinucleotide ...
Despite substantial progress in understanding the mechanism by which expanded CTG/CAG trinucleotide ...
Despite substantial progress in understanding the mechanism by which expanded CTG/CAG trinucleotide ...
CAG/CTG repeat expansions cause over 13 neurological diseases that remain without a cure. Because lo...
Induced transcription through CAG repeats in human cells increases repeat contraction ∼15-fold in bo...
Induced transcription through CAG repeats in human cells increases repeat contraction ∼15-fold in bo...
Expansions of CAG repeat tracts in the germ line underlie several neurological diseases. In human pa...
Expanded trinucleotide repeats are responsible for a number of neurodegenerative diseases, such as H...
Expanded trinucleotide repeats are responsible for a number of neurodegenerative diseases, such as H...
Expanded trinucleotide repeats are responsible for a number of neurodegenerative diseases, such as H...
Expanded trinucleotide repeats are responsible for a number of neurodegenerative diseases, such as H...
Expanded trinucleotide repeats are responsible for a number of neurodegenerative diseases, such as H...
More than 12 neurogenetic disorders are caused by unstable expansions of (CTG)†(CAG) repeats. The ex...
Expansion of CAG•CTG tracts located in specific genes is responsible for 13 human neurodegenerative ...
Trinucleotide repeats (TNRs) undergo high frequency mutagenesis to cause at least 15 neurodegenerati...
Despite substantial progress in understanding the mechanism by which expanded CTG/CAG trinucleotide ...
Despite substantial progress in understanding the mechanism by which expanded CTG/CAG trinucleotide ...
Despite substantial progress in understanding the mechanism by which expanded CTG/CAG trinucleotide ...
CAG/CTG repeat expansions cause over 13 neurological diseases that remain without a cure. Because lo...