Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1219294 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32235374_1.fastq.gz | Fastqsanger.gz | |||
| SRR32235374_2.fastq.gz | Fastqsanger.gz | |||
| SRR32235375_1.fastq.gz | Fastqsanger.gz | |||
| SRR32235375_2.fastq.gz | Fastqsanger.gz | |||
| SRR32235376_1.fastq.gz | Fastqsanger.gz |
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Project description:Poly(ADP-ribose) polymerase 1 (PARP1) is a highly conserved nuclear protein in multicellular organisms that modulates chromatin opening, and by doing so, it plays a significant role in gene expression regulation during development and differentiation. Despite its significance, all reported Parp1 total knockout mice strains are viable and fertile with no developmental anomalies. It was previously believed that functional redundancy with other PARP family members explain such a controversy. PARP2 is the main candidate to fulfill PARP1 functions in Parp1 knockout mice. Indeed, Parp1 Parp2 double knockout mice are arrested early in development and unable to proceed through gastrulation. However, while PARP2 has similar catalytic domain to PARP1, it lacks other domains that play important regulatory roles, thus making the lack of developmental problems in Parp1 mice total knockouts highly unlikely. To address this question, we checked the best investigated and publicly available Parp1 knockout mice strain. We found that Parp1 is still expressed in these mice, based on the presence of its mRNA transcript. Contrary to prior assumptions, we identified persistent mRNA expression in knockout mice, albeit at reduced levels. Detailed transcript analysis revealed an alternatively spliced PARP1 variant lacking exon two with introduced artificial cassette. Subsequent protein analysis confirmed the existence of a truncated PARP1 protein in knockout mice. We established embryonic stem cell lines from knockout mice and revealed the presence of pADPr. The decreased level of pADPr was detected in knockout ES cells with Western Blotting analysis, but immunofluorescence staining didn’t detect any difference in distribution or level of pADPr in nuclei of knockout ES cells compared to control ones. Moreover, in double Parp1 Parg mutant ES cells the accumulation of pADPr greatly exceeded its amount in normal and even in hypomorph Parg mutant ES cells, suggesting the presence of functionally active PARP1. Therefore, our findings challenge the conventional understanding of PARP1 depletion effects.
2024-07-15 | GSE248429 | GEO
Project description:BACKGROUND & AIMS: The immune system comprises an innate and an adaptive immune response to combat pathogenic agents. The human enteropathogen Salmonella enterica serovar Typhimurium invades the intestinal mucosa and triggers an early innate pro-inflammatory host gene response, which results in diarrheal disease. Several host factors are involved in the acute early response to Salmonella infection. Transcription factors and transcription co-regulators have an especially important function, because they are required for the expression and synthesis of pro-inflammatory cytokines, chemokines and adhesion molecules. A central transcription factor involved in inflammation is NF-κB, which requires the nuclear protein PARP1 as co-factor for the expression of some of its target genes. Here, we investigated the role of PARP1 during Salmonella infection using a mouse model for Salmonella-induced colitis. METHODS: To study enterocolitis by Salmonella Typhimurium, an established mouse model system, which relies on streptomycin-pretreatment prior to Salmonella infection, was employed. Histopathologic signs of inflammation and cecum colonization at various time-points after infection of wild type and PARP1 knockout mice were analyzed. PARP1 expression in the gut mucosa was studied by quantitative RT-PCR, Western blot and immunofluorescence. Gene expression profiles of infected and control infected mice in the wild type or PARP1 knockout background were obtained by whole mouse genome arrays and confirmed by quantitative RT-PCR. 2 genotypes (wildtype, PARP1 knockout), 2 treatments (Salmonella SB300 infection, Salmonella SB161 control infection), 2 time-points (6h, 10h). 2-3 replicates/condition.
2010-05-27 | E-GEOD-19174 | biostudies-arrayexpress
Project description:In this study, a Cre-loxP system was used to generate eIF3a conditional knockout mice. Tandem mass tag (TMT) labeling with LC-MS/MS analysis was used to identify differentially expressed proteins (DEPs) in fat, lungs, skin, and spleen tissue of the eIF3a knockout mice and controls. Bioinformatics analysis was then used to explore the functions and molecular signaling pathways of these protein landscapes.
2023-07-20 | PXD041416 | Pride
Project description:Poly(ADP-ribose) polymerases (PARPs) synthesize and bind branched polymers of ADP-ribose to acceptor proteins using NAD as a substrate, and participate to the control of gene transcription and DNA repair. PARP1, the most abundant isoform, regulates the expression of proinflammatory mediator - cytokines, chemokines and adhesion molecules, and inhibition of PARP1 enzymatic activity reduced or ameliorated autoimmune diseases in several experimental models, including colitis. However, the mechanism(s) underlying the protective effects of PARP1 inhibition in colitis and the cell types in which Parp1 deletion has the most significant impact are unknown. The objective of the current study was to determine the impact of Parp1 deletion on the innate immune response to mucosal injury. Genome-wide analysis of the colonic transcriptome was performed. Compared to WT, we demonstrated that Parp1-/-were protected from DSS-induced colitis and that this protection was associated with a dramatic transcriptional reprogramming in the colon. WT or Parp1-/- mice were treated with drinking water administered ad libitum without ot with 4% dextran sulfate (DSS) for seven days. Whole colon was collected for RNA extraction and hybridization on Affymetrix microarrays. Thee mice from each genotype/treatment groups were used in the analysis.
2016-01-08 | E-GEOD-76658 | biostudies-arrayexpress
Project description:In order to determine if there are any genetic differences among lungs of Nogo-A/B knockout mice which may explain their enhanced asthmatic-like responses, we have employed whole genome microarray expression profiling as a discovery platform to identify any genes that may be altered in the lung of Nogo-A/B knockout mice. RNA was isolated from three biological replicates of mouse lungs from naive WT and Nogo-A/B Knockout mice and run on agilent array. Two genes was significantly altered in Nogo-A/B Knockout lungs, SPLUNC1 and RTN4 (Nogo) which was significantly decreased and confirmed by real-time PCR. Gene expression in naïve mouse lungs of WT and Nogo-A/B knockout mice was measured in three individual biological replicates from each group.
2010-10-20 | E-GEOD-24218 | biostudies-arrayexpress
Project description:HLA-DR3, HLA-DR3.IL17A knockout and HLA-DR3.IFN-gamma knockout (KO) mice were challenged intraperitoneally with 10 microgram of staphylococcal enterotoxin B. 4 and 24 hours later mice were euthanized, lungs harvested, RNA extracted and processed for gene expression analysis using Clariom S arrays in comparison to respective naive mice After transcardial perfusion of mice with 10 ml of PBS, lungs were removed, Total RNA was extracted from perfused lungs at 4- and 24- hours after SEB challenge. Gene expression profiling was determined using mouse Clariom S arrays at ThermoFisher Corporation in comparison to respective naive mice.
2022-07-21 | GSE208651 | GEO
Project description:Transcriptionally active and inactive chromatin domains tend to segregate into separate sub-nuclear compartments to maintain stable expression patterns. However, we have uncovered here an inter-chromosomal network connecting active loci enriched in circadian genes to repressed lamina-associated domains (LADs). The interactome is regulated by PARP1 and its co-factor, CTCF, which not only mediate chromatin fiber interactions, but also promote the recruitment of circadian genes to the lamina. Synchronization of circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation. Furthermore, depletion of H3K9me2/3, inhibition of PARP activity by Olaparib or down-regulation of PARP1 or CTCF expression counteracts both recruitment to the envelope and circadian transcription. PARP1- and CTCF-regulated contacts between circadian loci and the repressive chromatin environment at the lamina thus mediate circadian transcriptional plasticity. ChIP-Seq for H3k9me2 in HCT116 colon cancer cells (2 replicates)
2015-08-27 | E-GEOD-58534 | biostudies-arrayexpress
Project description:We have shown that C57BL/6J CCR5 knockout mice develop 30.4% ± 8.6% fewer B16 F10 lung nodules compared to wild type mice after the intravenous injection of 100,000 B16 F10 cells. We sought to understand this phenomenon by comparing gene expression in the lungs of these mice at 6, 24, and 48 hours after tumor injection. There were 6 groups or conditions (CCR5 - 6 hours, WT - 6 hours, CCR5 - 24 hours, WT - 24 hours, CCR5 - 48 hours, WT - 48 hour); each group had 4 to 5 mice. All of the mice were injected with 100,000 B16 F10 melanoma cells by tail vein. At the designated time, the mice were anesthetized with Avertin and their lungs were perfused with PBS. After this, the lungs were harvested and snap frozen in liquid nitrogen. They were kept at minus 80 degrees C until processing. mRNA was extracted as described below and equivalent amounts of mRNA (by weight) was pooled by group.
2013-10-25 | E-GEOD-51422 | biostudies-arrayexpress