Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Next Generation Sequencing Quantitative Analysis of Wild Type and Mki67-/- 4T1 mouse mammary carcinoma cell transcriptomes

ABSTRACT: Purpose: The goals of this study were to compare gene expression profiles of mouse 4T1 cells with intact or disrupted Mki67 gene. Methods: mRNA profiles of wild-type (WT) and two clones of Ki-67 knockout (Mki67−/−) mouse NIH/3T3 cells, all in duplicate, were generated by deep sequencing using Illumina Hiseq2500 in single-end read mode, 50bp. The sequence reads that passed quality filters were aligned to the mouse genome, quantified, and differential gene expression (DGE) analysis was performed using DEseq2. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (GRCm38.p6) and identified differentially expressed genes. This revealed widespread changes in gene expression, with 2558 genes significantly deregulated in independent clones of Mki67-/- cells (q < 0.05) Conclusions: Ki-67 knockout causes genome-scale transcriptome alterations

ORGANISM(S): Mus musculus

PROVIDER: GSE162358 | GEO | 2021/02/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Next Generation Sequencing Quantitative Analysis of the transcriptomes of Wild Type and Mki67-/- 4T1 tumors in mice

Project description:Purpose: The goals of this study were to compare gene expression profiles of mouse xenografted 4T1 tumors with intact or disrupted Mki67 gene. Methods: mRNA profiles of wild-type (WT) and Ki-67 knockout (Mki67−/−) mouse xenografted 4T1 tumors, in triplicate, were generated by deep sequencing using Illumina Hiseq2500 in paired-end read mode, 50bp. The sequence reads that passed quality filters were aligned to the mouse genome, quantified, and differential gene expression (DGE) analysis was performed using DEseq2. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (GRCm38.p6) and identified differentially expressed genes. This revealed widespread changes in gene expression Conclusions: Ki-67 knockout causes genome-scale transcriptome alterations

2021-02-18 | GSE162885 | GEO

Next Generation Sequencing Quantitative Analysis of the transcriptomes of Wild Type and Mki67-/- MDA-mb231 (human breast adenocarcinoma) cell line

Project description:Purpose: The goals of this study were to compare gene expression profiles of MDA-mb231 cell lines with intact or disrupted Mki67 gene. Methods: mRNA profiles of wild-type (WT) and three Ki-67 knockout (Mki67−/−) clones in the MDA-mb231 cell line, were generated by deep sequencing using DNBSEQ-G50 in paired-end read mode, 100bp. The sequence reads that passed quality filters were aligned to the mouse genome, quantified, and differential gene expression (DGE) analysis was performed using DEseq2. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (GRCh38) and identified differentially expressed genes. This revealed widespread changes in gene expression Conclusions: Ki-67 knockout causes genome-scale transcriptome alterations

2021-02-18 | GSE162879 | GEO

Next Generation Sequencing Quantitative Analysis of Wild Type and Mki67-/- 3T3 cell transcriptomes

Project description:Purpose: The goals of this study were to compare gene expression profiles of mouse NIH/3T3 cells with intact or disrupted Mki67 gene. Methods: mRNA profiles of wild-type (WT) and two clones of Ki-67 knockout (Mki67−/−) mouse NIH/3T3 cells, all in duplicate, were generated by deep sequencing using Illumina Hiseq2500 in single-end read mode, 50bp. The sequence reads that passed quality filters were aligned to the mouse genome, quantified, and differential gene expression (DGE) analysis was performed using DEseq2. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (GRCm38.p6) and identified differentially expressed genes. This revealed widespread changes in gene expression, with 2558 genes significantly deregulated in independent clones of Mki67-/- cells (q < 0.05) Conclusions: Our study represents the first detailed analysis of retinal transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.

2021-02-18 | GSE162352 | GEO

Next Generation Sequencing Quantitative Analysis of Wild Type and Mki67-/- 4T1 mouse mammary carcinoma cell histone modification

Project description:Ki-67 chromatin associated proteins that has been shown to broadly affect the transcription profiles of cells when knocked-out. To understand if those transcriptome changes are regulated by histone modifications we performed ChIP-seq analysis for three of the most recognized histone marks (H3K27me3, H3K4me3 and H3K27ac) as the regulators of gene expression, in wild-type (WT) and Ki-67 knockout (Mki67−/−) mouse 4T1 cells.

2021-02-18 | GSE163479 | GEO

Gene expression analysis of mouse intestinal cells that lack Cdk8

Project description:RNAseq is performed (50bp single end reads) on parental young adult mouse intestinal cells (YAMC) or two clones in which Cdk8 allele is ablated using CRISPR Examination of transcriptomic changes after knockout of Cdk8 using CRISPR. Two clones of Cdk8 knockouts are compared to parental YAMC cells

2015-07-31 | E-GEOD-71385 | biostudies-arrayexpress

Gene expression analysis of mouse intestinal cells that lack Cdk8

Project description:RNAseq is performed (50bp single end reads) on parental young adult mouse intestinal cells (YAMC) or two clones in which Cdk8 allele is ablated using CRISPR

2015-07-31 | GSE71385 | GEO

Ki-67 organises heterochromatin during cell proliferation

Project description:Antigen Ki-67 is a nuclear protein expressed in proliferating mammalian cells. It is widely used in cancer histopathology but its functions remain unclear. Here, we show that Ki-67 controls heterochromatin organisation. Altering Ki-67 expression levels did not significantly affect cell proliferation in vivo. Ki-67 mutant mice developed normally and cells lacking Ki-67 proliferated efficiently. Conversely, upregulation of Ki-67 expression in differentiated tissues did not inhibit cell cycle arrest. Ki-67 interactors included proteins involved in nucleolar processes and chromatin regulators. Ki-67 depletion disrupted nucleologenesis but did not inhibit pre-rRNA processing. In contrast, it altered gene expression. Ki-67 silencing also had wide-ranging effects on chromatin organisation, disrupting heterochromatin compaction and long-range genomic interactions. Trimethylation of histone H3K9 and H4K20 at heterochromatin was strongly reduced. Overexpression of human or Xenopus Ki-67 induced ectopic heterochromatin formation. Altogether, our results suggest that Ki-67 expression in proliferating cells spatially organises heterochromatin, thereby controlling gene expression.

2018-10-26 | PXD003551 | Pride

Next Generation Sequencing Quantitative Analysis of Wild Type, CDK8-/-, CDK19-/-, and CDK8-/-CDK19-/- mouse instestinal organoids transcriptomes

Project description:Purpose: The goals of this study were to compare gene expression profiles of mouse intestinal epithelium organoids with intact or disrupted CDK8 and CDK19 genes. Methods: mRNA profiles of all organoid genotypes, in biological triplicates, were generated by deep sequencing using the BGISEQ SE50 50 million single-end, 50bp reads per sample. The sequence reads that passed quality filters were aligned to the mouse genome, quantified, and differential gene expression (DGE) analysis was performed using DEseq2. Results: Using an optimized data analysis workflow, we mapped about 50 million sequence reads per sample to the mouse genome (GRCm38.p6) and identified differentially expressed genes. This mild changes in overall gene expression, preferentially enriched in tissue specif genes. The transcription profile showed an overlap between those present in a CFTR KO context. Conclusions: CDK8/19 knockout causes tissue specif expression alteration. Intestinal organoids presented a CFTR-like phenotype after removal of both genes

2022-10-23 | GSE186377 | GEO

Global transcriptome profiling of Oct4/Klf4/Sox2 (3Factor, 3F) + IL6 iPS clones derived from mouse embryonic fibroblasts.

Project description:We used heterokaryon cell fusion based reprogramming and identified the cytokine IL6 as a potential regulator of reprogramming to pluripotency. We generated iPS clones using the four reprogramming factors (4F) Oct4, Klf4, Sox2, and c-Myc. In addition, iPS clones were generated using only three factors (3F: Oct4, Klf4, amd Sox2) with the addition of the cytokine IL6 to reprogramming culture conditions. Global RNA-Seq of the 3F + IL6 derived iPS clones was done for comparison with 4F-derived iPS clones, mouse embryonic stem cells and mouse embryonic fibroblasts. This study includes 8 samples: 2 independently derived 3F + IL6 iPS clones, 2 independently derived 4F iPS clones, 2 biological replicates of mouse D3-GFP ES cells, and 2 biological replicates of mouse embryonic fibroblasts (MEFs). The latter 6 samples are provided as references for the 3F + IL6 iPS clones. Poly-A RNA was isolated and prepared for sequencing using the Illumina TruSeq RNA kit (v2) to generate 50bp reads. Reads were aligned to mm10.

2013-08-28 | E-GEOD-46104 | biostudies-arrayexpress

Ki-67 is necessary during DNA replication for forks protection and genome stability

Project description:Ki-67 molecular functions and properties have remained quite obscure for a long time, despite its importance as a major proliferation marker in clinic. Only recently it has been shown that Ki-67 has a major role in the formation of the mitotic chromosome periphery compartment, and it is a protein phosphatase 1 (PP1) binding protein. Understanding Ki-67 functions at different stages of the cell cycle has been so far hindered by the fact that the different phenotypes observed in cells upon Ki-67 depletion could be the outcome of secondary effects. Here, by using Auxin-inducible-degron (AID) system, we show that Ki-67 degradation at the G1/S boundary causes the disassembly of the replication machinery and leads to DNA damage. This triggers the interferon response and causes replication delay. Our results support the model whereby Ki-67 contributes to replication forks protection, and it is important for timely DNA replication and genome maintenance.

2024-04-13 | PXD037513 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data