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Next Generation Sequencing Facilitates Quantitative Analysis of wild type and Lmna R527C mutant mice spleen Transcriptomes with or without 4Gy irradiation.

ABSTRACT: To induced the atypical progeria symptoms of LMNA R527C mutant mice, mutant and wild type mice were irradiated at 6 weeks of age with doses of 4 Gy. And to examine the pathologic change of mutant mice, mice were sacrificed at day -1and day 7 post-irradiation and spleen was harvested for RNAseq.

ORGANISM(S): Mus musculus

PROVIDER: GSE190199 | GEO | 2021/12/07

REPOSITORIES: GEO

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Genome-wide maps of LADs distribution in control and Dam-WT/Dam-R527C LMNA stabilized Hela cells

Project description:To determine if LMNA R527C mutation affect the arrangement and function of LADs, we performed Lamin A DamID-seq in wild type and mutant LMNA-stablized Hela cells. Reads of Lamin A ChIP-seq in LADs were decreased in mutant cells compared with wild type. These data suggested that the binding affinity of Lamin A to LADs was reduced after R527C mutation

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Genome-wide maps of Lamin A-LADs binding affinity in control and LMNA R527C mutant MSCs

Project description:To determine if LMNA R527C mutation affect the arrangement and function of LADs, we performed Lamin A ChIP-seq in wild type and mutant MSCs. Reads of Lamin A ChIP-seq in LADs were decreased in mutant cells compared with wild type. These data suggested that the binding affinity of Lamin A to LADs was reduced after R527C mutation

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Genome-wide maps of chromatin openness in control and LMNA R527C mutant MSCs

Project description:We performed ATAC-seq to examine to chromatin of openness of coding genes in healthy control and LMNA R527C patient-derived MSCs. The reduction of LADs did not increase the accessibility of the promoters flanking coding genes. The genome wide analysis of ATAC-seq showed that openness of coding genes related chromatin was decreased in mutant MSCs.Thus, R527C mutant Lamin A led to dysfunction of LADs and dysregulation of gene transcription, probably, leading to slow down or arrest of cell proliferation and differentiation.

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High throughput sequencing of atypical progeria caused by LMNA R527C mutation

Project description:High throughput sequencing of atypical progeria caused by LMNA R527C mutation

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Genome-wide maps of chromatin openness in control and LMNA R527C mutant MSCs

Project description:Genome-wide maps of chromatin openness in control and LMNA R527C mutant MSCs

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Next Generation Sequencing Facilitates Quantitative Analysis of wild type and Lmna R527C mutant mice spleen Transcriptomes with or without 4Gy irradiation.

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of wild type and Lmna R527C mutant mice spleen Transcriptomes with or without 4Gy irradiation.

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Transcriptional profiling of liver samples from Lmna Gly609Gly knock-in mice

Project description:Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by a point mutation in the LMNA gene that activates a cryptic donor splice site and yields a truncated form of prelamin A called progerin. Small amounts of progerin are also produced during normal aging. Studies with mouse models of HGPS have allowed the recent development of the first therapeutic approaches for this disease. However, none of these earlier works have addressed the aberrant and pathogenic LMNA splicing observed in HGPS patients because of the lack of an appropriate mouse model. We report herein a genetically modified mouse strain that carries the HGPS mutation. These mice accumulate progerin, present histological and transcriptional alterations characteristic of progeroid models, and phenocopy the main clinical manifestations of human HGPS, including shortened life span and bone and cardiovascular aberrations. By using this animal model, we have developed an antisense morpholino–based therapy that prevents the pathogenic Lmna splicing, dramatically reducing the accumulation of progerin and its associated nuclear defects. Treatment of mutant mice with these morpholinos led to a marked amelioration of their progeroid phenotype and substantially extended their life span, supporting the effectiveness of antisense oligonucleotide–based therapies for treating human diseases of accelerated aging. 6 samples, three from LmnaG609G/G609G mice and three from control Lmna+/+ mice

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Next Generation Sequencing Facilitates Quantitative Analysis of healthy donor- and LMNA R527C mutant patient-derived MSCs Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of healthy donor- and LMNA R527C mutant patient-derived MSCs Transcriptomes

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Next Generation Sequencing Facilitates Quantitative Analysis of healthy donor- and LMNA R527C mutant patient-derived MSCs Transcriptomes

Project description:We reprogramed patient derived PBMCs into iPSCs, and differentiated the iPSCs into Mesenchymal stem cells. We performed whole genome wide RNA-seq of patient-derived MSCs and control MSCs. Up-regulated and down-regulated genes of LMNAR527C/R527C patient-derived MSCs were enriched and analyzed.

2021-12-07 | GSE190198 | GEO

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