Ontology highlight
ABSTRACT:
PROVIDER: PRJNA397431 | ENA |
REPOSITORIES: ENA
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Project description:An early hallmark of Toxoplasma infection is the rapid control of the parasite population by a potent multifaceted innate immune response that engages resident and homing immune cells along with pro- and counter-inflammatory cytokines. In this context, IFN-γ activates a variety of Toxoplasma-targeting activities in immune and non-immune cells, but can also contribute to host immune pathology. Toxoplasma has evolved mechanisms to timely counteract the host IFN-γ defenses by interfering with the transcription of IFN-γ-stimulated genes. We now have identified TgIST as a critical molecular switch that is secreted by intracellular parasites and traffics to the host cell nucleus where it inhibits STAT1-dependent proinflammatory gene expression. We show that TgIST not only sequesters STAT1 on dedicated loci but also promotes shaping of a nonpermissive chromatin through its capacity to recruit the NuRD transcriptional repressor. We found that during mice acute infection, TgIST-deficient parasites are rapidly eliminated by the homing Gr1(+) inflammatory monocytes thus highlighting the protective role of TgIST against IFN-γ-mediated killing. By uncovering TgIST functions, this study brings novel evidence on how Toxoplasma has devised a molecular weapon of choice to take control over a ubiquitous immune gene expression mechanism in metazoans, as a way to promote long-term parasitism. HFF, 2fTGH (STAT1+/+) and U3A (STAT1-/-) human cells were left uninfected or infected for 24 hours with 76KGFP and 76KGFPÎ?TgIST Toxoplasma strains and stimulated with 100 U/ml IFN-γ for 6 hours before gene expression was measured. Three independent experiments were performed for each condition.
2016-07-18 | E-GEOD-81613 | biostudies-arrayexpress
Project description:How germ cells faithfully pass genetic material to the next generation despite undergoing several developmental transitions during maturation is poorly understood. Here we identify a novel factor in C. elegans, OEF-1, that is highly germline-specific, with early expression in the embryonic germ lineage and differential expression in larvae and adults depending on the gametogenesis program. OEF-1 is nuclear and associates with autosomal germline-expressed genes. Loss of OEF-1 triggers accelerated germ cell progression, leading to defects at multiple points during germline development. Thus OEF-1 may act to coordinate the timely progression of germ cells through proliferation, meiotic entry, and gametogenesis.
2017-11-22 | GSE107190 | GEO
Project description:Aging is associated with delayed skeletal muscle repair and regeneration. Loss of innervation occurs after degenerative muscle injury, however, the extent of denervation, whether the kinetics of reinnervation changes with aging, and the cellular consequences of neuromuscular junction (NMJ) disruption in adult and aged muscle have not been explored. Here we show after degenerative muscle injury progressive denervation and delayed reinnervation in aged compared to adult muscle. Using confocal microscopy and 3-D image rendering we found a relationship between innervation and myofiber size in aged regenerating muscle. Although timely inhibition of pro-inflammatory Ccr2 activity after degenerative muscle injury improved aged regenerated myofiber size, this was not associated with an increase in reinnervation. In contrast, single cell RNA sequencing (scRNASeq) analysis revealed denervation triggers an inflammatory response in target muscles regardless of age; however, pro-inflammatory signaling predominated in aged macrophages and fibroadipogenic progenitors (FAPs) compared to a pro-regenerative response in adult cells. Thus, denervation and delayed reinnervation of NMJs after injury is a feature of persistent pro-inflammatory signals associated with delayed repair and regeneration of aged muscle.
2022-06-05 | GSE205395 | GEO
Project description:It is currently unclear whether tissue changes surrounding multifocal epithelial tumors are a cause or consequence of cancer. Here, we provide evidence that loss of mesenchymal Notch/CSL signaling causes tissue alterations, including stromal atrophy and inflammation, which precede and are potent triggers for epithelial tumors. Mice carrying a mesenchymal-specific deletion of CSL/RBP-JK, a key Notch effector, exhibit spontaneous multifocal keratinocyte tumors that develop after dermal atrophy and inflammation. CSL-deficient dermal fibroblasts promote increased tumor cell proliferation through up-regulation of c-Jun and c-Fos expression and consequently higher levels of diffusible growth factors, inflammatory cytokines, and matrix remodeling enzymes. In human skin samples, stromal fields adjacent to cutaneous squamous cell carcinomas and multifocal premalignant actinic keratosis lesions exhibit decreased Notch/CSL signaling and associated molecular changes. Importantly, these changes in gene expression are also induced by UVA, a known environmental cause of cutaneous field cancerization and skin cancer. We used microarrays to detail the global changes in gene expression in dermal fibroblasts with in vivo and in vitro deletion of the RBP-Jk gene, compared to corresponding controls Global changes in gene expression in dermal fibroblasts with in vivo and in vitro deletion of the RBP-Jk gene were assessed, in parallel with the corresponding controls
2012-06-11 | E-GEOD-36359 | biostudies-arrayexpress
Project description:Project HERO is a 12-week study of the efficacy of Body Mind Training (BMT) for reducing fatigue in male cancer survivors. This 3-arm randomized clinical trial will examine inflammatory biology and selected gene-expression pathways that are hypothesized to contribute to the intervention’s effect.
| 2259149 | ecrin-mdr-crc
Project description:TNFα is a potent cytokine to mediate inflammatory response by activation of the master transcription factor NF-kB. Endothelial cells are important participants in inflammatory responses in animals. NF-kB is a major mediator to activate endothelial cells by inducing multiple pro-inflammatory genes in response to TNFα. NF-kB mediated gene transcription is known to accompany rapid changes in epigenetic states. However, the epigenetic landscape in response to the cytokine challenge TNFα in mouse endothelial cells has not been described. Our approach characterized the epigenetic profiles on a genome-wide scale and mapped putative active enhancers in primary mouse aortic endothelial cells.
2023-03-01 | E-MTAB-12212 | biostudies-arrayexpress
Project description:Arterialization requires the timely suppression of cell growth
| PRJNA666387 | ENA
Project description:Interventions: A group:Before using cetuximab;B group:After progression of disease:no
Primary outcome(s): KRAS gene sequence;NRAS gene sequence;BRAF gene sequence;PIK3CA gene sequence;EGFR gene sequence;EGFR gene copy numbers;EGFR expression;Her2 expression;c-Met expression;PTEN expression
Study Design: historical control
| 2671639 | ecrin-mdr-crc
Project description:During development and growth, dynamic signals need to be translated into spatially precise and temporally stable gene expression states, which define cell fate. In the context of the apical plant stem cell system, local accumulation of the small, highly mobile phytohormone auxin triggers organ initiation. Here we show that the WUSCHEL transcription factor locally protects stem cells from differentiation by controlling the auxin signaling and response pathways via regulation of Histone acetylation. Conversely, low levels of signaling are required for stem cell maintenance, demonstrating that WUSCHEL acts as a rheostat on the auxin pathway. Our results reveal an important mechanism that allows cells to differentially translate a potent and highly mobile developmental signal into appropriate cell behavior with high spatial precision and temporal robustness.
2019-11-11 | GSE122579 | GEO