Aaages prior
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA354149 | ENA |
REPOSITORIES: ENA
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Project description:(i) Transcripts of DG75 iBZLF1 cells were analyzed comparing non-induced cells and cells induced with doxycycline (100 ng/ ml) for 6 h. Doxycycline induces the expression of the full length viral transcription factor BZLF1. (ii) For control purposes, the transcripts of DG75 cells equipped with a doxycycline-regulated truncated BZLF1 allele lacking its transactivation domain (DG75 iBZLF1 AD-truncated) were analyzed prior to and after induction with doxycycline for 6 h. (iii) For an additional control, the transcripts of parental, unmodified DG75 cells were analyzed prior to and after adding doxycycline for 6 h. All experiments were performed as triplicates. The analysis is based on Homo sapiens (human) genome assembly GRCh37 (hg19) from Genome Reference Consortium. Artificial ERCC Spike-in RNAs (Thermo Scientific) were added as external controls.
2021-02-07 | E-MTAB-8426 | biostudies-arrayexpress
Project description:Antibody response following Omicron infection is reported to be less robust than that to other variants. Here we investigated how prior vaccination and/or prior infection modulates that response. Disease severity, antibody responses and immune transcriptomes were characterized in four groups of Omicron-infected outpatients (n=83): unvaccinated/no prior infection, vaccinated/no prior infection, unvaccinated/prior infection and vaccinated/prior infection. The percentage of patients with asymptomatic or mild disease was highest in the vaccinated/no prior infection group (87%) and lowest in the unvaccinated/no prior infection group (47%). Significant anti-Omicron spike antibody levels and neutralizing activity were detected in the vaccinated group immediately after infection but were not present in the unvaccinated/no prior infection group. Within two weeks, antibody levels against Omicron, increased. Omicron neutralizing activity in the vaccinated group exceeded that of the prior infection group. No increase in neutralizing activity in the unvaccinated/no prior infection group was seen. The unvaccinated/prior infection group showed an intermediate response. We then investigated the early transcriptomic response following Omicron infection in these outpatient populations and compared it to that found in unvaccinated hospitalized patients with Alpha infection. Omicron infected patients showed a gradient of transcriptional response dependent upon whether or not they were previously vaccinated or infected. Vaccinated patients showed a significantly blunted interferon response as compared to both unvaccinated Omicron infected outpatients and unvaccinated Alpha infected hospitalized patients typified by the response of specific gene classes such as OAS and IFIT that control anti-viral responses and IFI27, a predictor of disease outcome.
2022-06-11 | GSE201530 | GEO
Project description:Prior vaccination exceeds prior infection in eliciting innate and humoral immune responses in Omicron infected outpatients
| PRJNA832132 | ENA
Project description:Primary objectives: The primary objective is to investigate circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
Primary endpoints: circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
| 2533916 | ecrin-mdr-crc
Project description:Serum microRNA expression prior to motion sickness stimulus
| PRJNA852603 | ENA
Project description:Id proteins have been shown to promote the differentiation of conventional αβ and γδT cells, and to suppress the expansion of invariant Natural Killer T (iNKT) cells and innate-like γδNKT within their respective cell lineages. However, it remains to be determined whether Id proteins regulate lineage specification in developing T cells that give rise to these distinct cell fates. Here we report that in the absence of Id2 and Id3 proteins, E2A prematurely activates genes critical for the iNKT cell lineage prior to TCR expression. Lack of Id proteins also promotes a biased TCR rearrangement in favor of iNKT cell fate prior to selection at the CD4+CD8+ double positive (DP) stage. Enhanced iNKT development in Id3-deficient mice lacking γδNKT cells suggests that Id3 regulates the lineage competition between these populations. RNA-Seq analysis establishes E2A as the transcriptional regulator of both iNKT and γδNKT development. In the absence of pre-TCR signaling, Id2/Id3 deletion gives rise to a large population of iNKT cells and a unique innate-like DP population, despite the block in conventional αβ T cell development. The transcriptional profile of these unique DP cells reflects enrichment of innate-like signature genes, including PLZF (Zbtb16) and Granzyme A (Gzma). Results from these genetic models and genome-wide analyses suggest that Id proteins suppress E2A-driven innate-like T cell programs prior to TCR selection to enforce predominance of conventional T cells.
2018-01-23 | GSE89847 | GEO
Project description:Prior Knowledge Transfer Across Transcriptional Datasets Using Compositional Statistics
| PRJNA297464 | ENA
Project description:The goal of this RNA-Sequencing experiment was to determine gene targets of Yap/Taz in the posterior palatal shelves prior to elevation at E14.5 in mouse.
2020-05-25 | GSE151121 | GEO
Project description:ChIP peaks were identified in both the human and viral genomes (genome assembly GRCh37 (hg19) and Epstein-Barr virus, Human Herpesvirus 4; GenBank accession KF717093.1).
2021-06-22 | E-MTAB-8421 | biostudies-arrayexpress
Project description:Differentiation of mouse embryonic stem cells (mESCs) is accompanied by global changes in replication timing. To elucidate this reorganization process and explore its potential impact on mouse development, we constructed genome-wide replication-timing profiles of 15 independent mouse cell types representing nine different stages of early mouse development, including all three germ layers. Overall, 45% of the genome exhibits significant changes in replication timing between cell types, indicating that replication-timing regulation is more extensive than previously estimated from neural differentiation. Intriguingly, analysis of early and late epiblast cell culture models suggest that the earliest changes in development include extensive lineage-independent early-to-late replication switches that are completed at a stage equivalent to the post-implantation epiblast, prior to germ layer specification and down-regulation of key pluripotency transcription factors (Oct4/Nanog/Sox2). These changes were stable in all subsequent lineages and involved a class of irreversibly silenced genes that were re-positioned closer to the nuclear periphery. Lineage-specific, late-to-early and early-to-late replication switches followed, which created cell-type specific replication profiles. Importantly, partially reprogrammed induced pluripotent stem cells (piPSCs) failed to restore ESC-specific replication timing and transcription programs particularly within regions of lineage-independent early-to-late replication changes, as well as the inactive X-chromosome. We conclude that lineage-independent, early-to-late replication-timing switches that occur in the post-implantation epiblast embody an epigenetic commitment to differentiation prior to germ layer specification.
2009-11-25 | GSE17983 | GEO