Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Triplet nucleotide repeat-based siRNAs are highly toxic to cancer cells

ABSTRACT: Triplet nucleotide repeat-based siRNAs are highly toxic to cancer cells

PROVIDER: PRJNA413038 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6128990_1.fastq.gz	Fastqsanger.gz
	SRR6128990_2.fastq.gz	Fastqsanger.gz
	SRR6128991_1.fastq.gz	Fastqsanger.gz
	SRR6128991_2.fastq.gz	Fastqsanger.gz
	SRR6128992_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Triplet nucleotide repeat-based siRNAs are highly toxic to cancer cells

Project description:Triplet repeat siRNAs as found amplified in diseases such as Huntingtons disease can be used to kill cancer cells

2018-01-12 | GSE104552 | GEO

Friedreich’s Ataxia Induced Pluripotent Stem Cells Recapitulate GAA•TTC Triplet-Repeat Instability

Project description:The inherited neurodegenerative disease Friedreich’s ataxia (FRDA) is caused by hyperexpansion of GAA•TTC trinucleotide repeats within the first intron of the FXN gene, encoding the mitochondrial protein frataxin. Long GAA•TTC repeats causes heterochromatin-mediated silencing and loss of frataxin in affected individuals. We report the derivation of induced pluripotent stem cells (iPSCs) from FRDA patient fibroblasts through retroviral transduction of transcription factors. FXN gene repression is maintained in the iPSCs, as are the mRNA and miRNA global expression signatures reflecting the human disease. GAA•TTC repeats uniquely in FXN in the iPSCs exhibit repeat instability similar to patient families, where they expand and/or contract with discrete changes in length between generations. The mismatch repair enzyme Msh2, implicated in repeat instability in other triplet repeat diseases, is highly expressed in the iPSCs, occupies FXN intron 1, and shRNA silencing of Msh2 impedes repeat expansion, providing a possible molecular explanation for repeat expansion in FRDA.

2010-07-02 | GSE22651 | GEO

Friedreichâ??s Ataxia Induced Pluripotent Stem Cells Recapitulate GAAâ?¢TTC Triplet-Repeat Instability

Project description:The inherited neurodegenerative disease Friedreichâ??s ataxia (FRDA) is caused by hyperexpansion of GAAâ?¢TTC trinucleotide repeats within the first intron of the FXN gene, encoding the mitochondrial protein frataxin. Long GAAâ?¢TTC repeats causes heterochromatin-mediated silencing and loss of frataxin in affected individuals. We report the derivation of induced pluripotent stem cells (iPSCs) from FRDA patient fibroblasts through retroviral transduction of transcription factors. FXN gene repression is maintained in the iPSCs, as are the mRNA and miRNA global expression signatures reflecting the human disease. GAAâ?¢TTC repeats uniquely in FXN in the iPSCs exhibit repeat instability similar to patient families, where they expand and/or contract with discrete changes in length between generations. The mismatch repair enzyme Msh2, implicated in repeat instability in other triplet repeat diseases, is highly expressed in the iPSCs, occupies FXN intron 1, and shRNA silencing of Msh2 impedes repeat expansion, providing a possible molecular explanation for repeat expansion in FRDA. 65 samples from various number of tissue, primary cell lines undifferenatiated human embryonic stem cell lines, induces pluripotent stem cell lines have been run on Illumina HT12 v3 chips.

2010-07-30 | E-GEOD-22651 | biostudies-arrayexpress

RNA-dependent epigenetic silencing directs transcriptional down regulation caused by intronic repeat expansions

Project description:Transcriptional down regulation caused by intronic triplet repeat expansions underlies diseases such as Friedreich?s ataxia. This down regulation of gene expression is coupled with epigenetic changes but the underlying mechanisms are unknown. Here, we show that an intronic TTC/GAA triplet expansion within the IIL1 gene of Arabidopsis thaliana results in accumulation of 24-nt siRNAs and repressive histone marks at the IIL1 locus, which in turn causes its transcriptional down regulation and an associated phenotype. Knocking down DICER LIKE-3 (DCL3), which produces 24-nt siRNAs, suppressed transcriptional down regulation of IIL1 and the expansion-associated phenotype. Furthermore, knocking down additional components of the RNA-dependent DNA Methylation (RdDM) pathway, also suppressed both transcriptional down regulation of IIL1 and the repeat expansion associated phenotype. Thus our results show that triplet repeat expansions can lead to local siRNA biogenesis, which in turn down regulates transcription through an RdDM-dependent epigenetic modification.

2018-07-25 | GSE113923 | GEO

Effect of CWG-cPIP on CAG/CTG triplet repeat mouse brain

Project description:Effect of CWG-cPIP on CAG/CTG triplet repeat mouse brain

| PRJNA867693 | ENA

Transcription profiling of human lymphoblast cells from a Freidriechs Ataxia patient incubated with pyrrole-imidazole polyamides targeted to the GAA triplet repeat in the intron 1 reveals polyamides alleviate transcription inhibition associated with long repeat srepeats in Friedreicha??s ataxia

Project description:Lymphoblast cells from a patient with Freidriech's Ataxia were incubated with pyrrole-imidazole polyamides targeted to the GAA triplet repeat in the intron 1. The polyamides were shown in cell culture to increase levels of endogenous frataxin mRNA. A normal sibling derived lymphoblast cell line was used as a control. Experiment Overall Design: Normal (GM15851) and patient (GM15850) cell lines were incubated in the presence of match polyamide FA1 at 1uM, 2uM or mismatch polyamide FA2 at 2uM for 7days prior to RNA purification and microarray analysis.

2008-06-13 | E-GEOD-5040 | biostudies-arrayexpress

Gene expression analysis in liver collected from mice administered non-toxic, toxic, or severely toxic LNA sequences

2014-01-08 | GSE53230 | GEO

Gene expression analysis in liver collected from mice administered non-toxic, toxic, or severely toxic LNA sequences

Project description:Development of LNA gapmers, antisense oligonucleotides used for efficient inhibition of target RNA expression, is limited by non-target mediated hepatotoxicity issues. In the present study, we investigated hepatic transcription profiles of mice receiving non-toxic and toxic LNA gapmers after a single and repeat administration. To understand the mechanism of LNA gapmer-induced heptotoxicity in mice, we investigated the transcription profiles of liver RNA isolated from mice receiving non-toxic sequence (NTS-1), toxic sequence (TS-2), or severely toxic sequence (HTS-3) of LNA gapmers at 25 mg/kg (dose volume of 10 mL/kg) at 8, 16, or 72 hrs after a single administration (by subcutaneous injection ) using microarray analysis. We also investigated the transcription profiles of liver RNA isolated from mice receiving non-toxic sequence (NTS-1) or toxic sequence (TS-2) of LNA gapmers at 25 mg/kg (dose volume of 10 mL/kg) at 2 weeks after repeated administration (by subcutaneous injection ) using microarray analysis.

2014-01-08 | E-GEOD-53230 | biostudies-arrayexpress

22-nucleotide siRNAs mediate translational repression and trigger a silencing storm

Project description:Small interfering RNAs (siRNAs) are critical for proper development and immunity in eukaryotes1. Plants produce siRNAs with lengths of 21-, 22-, or 24- nucleotides (nt), wherein the 21- and 24-nt siRNAs mediate mRNA cleavage and DNA methylation2,3, respectively. However, the biological functions of 22-nt siRNAs remain elusive. Here we report the identification and characterization of a group of endogenous 22-nt siRNAs generated from the action of DICER-LIKE 2 (DCL2). When cytoplasmic RNA decay and DCL4 are deficient, the massive accumulation of 22-nt siRNAs causes pleiotropic growth disorders, including severe dwarfism, meristem defect, and pigmentation. Notably, two genes that encode nitrate reductases, NIA1 and NIA2, produce nearly half of the total of 22-nt siRNAs. Production of 22-nt siRNA triggers explosive self-amplification that leads to a small RNA storm, and induces dramatic translational repression both gene-specifically and globally. 22-nt siRNAs are also found to preferentially accumulate upon nitrogen deficiency, which acts to restrain plant growth and promote stress responses. Thus, our research uncovers the unique properties of 22-nt siRNAs, a previously unexplored class of plant siRNAs, and highlights the length of small RNA as a major functional determinant.

2020-04-13 | GSE148513 | GEO

22-nucleotide siRNAs mediate translational repression and trigger a silencing storm [es]

2020-04-13 | GSE148512 | GEO