Ontology highlight
ABSTRACT:
PROVIDER: PRJNA893818 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To dissect the molecular mechanisms of resistance mediated by Xa39,the transcriptome profiling of a rice line carrying Xa39 and its parents at the early stage of Xoo infection were investigated. A rice introgression line H471 carrying Xa39 exhibited a typical local hypersensitive response phenotype, accompanied by programmed cell death after inoculation with the Xoo Philippines’ race 9b.Our results indicated there might be cross-talk between the Xa39-mediated signal transduction cascades and the GA/BR signaling pathway, and the defense mechanism was related to diverse kinases, transcription factors, post-translational regulation, and R genes.
2015-12-30 | GSE62488 | GEO
Project description:Hybridization and introgression in marsh violets (Viola L.)
| PRJNA807904 | ENA
Project description:The tumor microenvironment (TME) is a unique niche governed by constant crosstalk within and across all intratumoral cellular compartments. In particular, intratumoral high potassium has shown its immune-suppression potency on T cells. However, as a pan-cancer characteristic related to local necrosis, the impact of this ionic disturbance on innate immunity is still unknown. Here, using both murine and human samples, we reveal that intratumoral high potassium leads to profound suppression of the anti-tumor capacity of tumor-associated macrophages (TAMs). We report the high-throughput profiling of the transcriptomes of murine primary BMDMs after tumor conditioned medium (TCM) stimulation.
2024-09-07 | GSE183634 | GEO
Project description:Background & Aims. As a T cell-mediated disease of the colonic epithelium, ulcerative colitis (UC) is likely to share pathogenic elements with other T cell-mediated inflammatory diseases. Recently we showed T cell-mediated rejection of kidney and heart transplants share large scale molecular changes. We hypothesized that UC would manifest a similar disturbance, and that these features would correlate with response to infliximab. Results. UC biopsies manifested coordinate transcript changes resembling rejecting transplants, with T cell, IFNG-induced, macrophage, and injury transcripts increasing while parenchymal transcripts decreased. The disturbance expressed as principal component 1 correlated with conventional assessments e.g. Mayo scores, serum albumin, and lymphoplasmacytic infiltrate. When assessed in published microarray studies, the disturbance predicted response to infliximab: patients with intense disturbance did not achieve clinical response, although quantitative improvement was usually seen even in non-responders. Similar changes were seen in CrohnM-bM-^@M-^Ys colitis (CDc). Conclusions. The molecular phenotype of UC manifests a large scale coordinate disturbance reflecting changes in inflammatory cells and parenchymal elements that correlates with conventional features and predicts response to infliximab. We studied 56 colon biopsies from patients with colitis, including 43 with UC, characterizing the clinical and histological features, and defined the mRNA phenotype with Affymetrix expression microarrays. We measured the expression of previously defined pathogenesis-based transcript sets representing effector T cells, macrophages, IFNG effects, and parenchymal injury response and dedifferentiation. We also studied 48 microarray files from human colon biopsies from the Gene Expression Omnibus database, classified by response to infliximab therapy to look for molecular changes that predict unresponsiveness.
2014-12-22 | E-GEOD-51785 | biostudies-arrayexpress
Project description:Background & Aims. As a T cell-mediated disease of the colonic epithelium, ulcerative colitis (UC) is likely to share pathogenic elements with other T cell-mediated inflammatory diseases. Recently we showed T cell-mediated rejection of kidney and heart transplants share large scale molecular changes. We hypothesized that UC would manifest a similar disturbance, and that these features would correlate with response to infliximab. Results. UC biopsies manifested coordinate transcript changes resembling rejecting transplants, with T cell, IFNG-induced, macrophage, and injury transcripts increasing while parenchymal transcripts decreased. The disturbance expressed as principal component 1 correlated with conventional assessments e.g. Mayo scores, serum albumin, and lymphoplasmacytic infiltrate. When assessed in published microarray studies, the disturbance predicted response to infliximab: patients with intense disturbance did not achieve clinical response, although quantitative improvement was usually seen even in non-responders. Similar changes were seen in Crohn’s colitis (CDc). Conclusions. The molecular phenotype of UC manifests a large scale coordinate disturbance reflecting changes in inflammatory cells and parenchymal elements that correlates with conventional features and predicts response to infliximab.
2014-12-22 | GSE51785 | GEO