Project description:We analyzed the transcriptional profile of small-intestinal lamina propria (SI-LP) CD4+ T cells isolated from germ-free and mice monocolonized with Bifidobacterium adolescentis, SFB, and Nexabiotic (a 23-strain, Th17-inducing, probiotic mix).
Project description:In chicken DT40 cells, there are six linker histone H1 variants and 12 of coding genes. We have previously reported of 11 out of 12 H1 knock out DT40 cells (Takami et al., Genes to Cell 1997 [PMID:9491804]) but complete H1 null DT40 cells could not established, so far. We identified one of the H1 variant, H1R was involved in genomic instabilities (Hashimoto et al., DNA repair (2007) [17613284]), so we re-introduced floxed H1R-eGFP and mer-cre-mer into 11 out of 12 H1 knock out DT40 cells. Then we targeted last enedogenous H1, we successfully established conditional H1 KO cells (K11). Next we treated with tamoxifen to loop out floxed H1R-eGFP, and cloning H1 completely null cells (K11-5, and K11-7). We analysis those gene expression pattern in wild-type, K11, and K11-5 cells Experiment Overall Design: Apoptosis is induced in H1 null cells, so we inhibit apoptosis with pan-caspase inhibitor, Z-VAD-FMK and extract RNAs.
Project description:In chicken DT40 cells, there are six linker histone H1 variants and 12 of coding genes. We have previously reported of 11 out of 12 H1 knock out DT40 cells (Takami et al., Genes to Cell 1997 [PMID:9491804]) but complete H1 null DT40 cells could not established, so far. We identified one of the H1 variant, H1R was involved in genomic instabilities (Hashimoto et al., DNA repair (2007) [17613284]), so we re-introduced floxed H1R-eGFP and mer-cre-mer into 11 out of 12 H1 knock out DT40 cells. Then we targeted last enedogenous H1, we successfully established conditional H1 KO cells (K11). Next we treated with tamoxifen to loop out floxed H1R-eGFP, and cloning H1 completely null cells (K11-5, and K11-7). We analysis those gene expression pattern in wild-type, K11, and K11-5 cells (Hashimoto et al., NAR (2010), PMID:20156997) Keywords: gene expression array-based, count
2008-05-01 | GSE8483 | GEO
Project description:Treatment of sham and ovariectomized mice with a probiotic mix
| PRJNA1187318 | ENA
Project description:Microbial diversity upon high-fat diet consumption with and without probiotic mix
Project description:To identify the putative genes involved in theacrine biosynthesis in tea plant, we carried out comparative transcriptome analysis of Kucha (K6 and K11) and conventional varieties (YH 9 and QX 1).
Project description:<p>Fecal microbiota transplantation (FMT) has emerged as a promising therapeutic strategy for Inflammatory Bowel Disease (UC), though its clinical success appears contingent upon donor microbiota engraftment degree. While microbial colonization dynamics remain poorly understood, our study identifies metabolism as a critical determinant of gut community assembly under UC nutrient-limiting intestinal conditions. Using an model, we demonstrate that microbial competence in influences engraftment outcomes. Building on this mechanistic insight, we engineered a novel probiotic-metabolite consortium (G-MIX) designed to synergistically enhance gut ecosystems. Through multi-step catalytic conversion G-MIX facilitates L-glutamate biosynthesis and ATP generation, thereby alleviating RNS-mediated barriers to donor microbiota colonization. In murine UC models, G-MIX supplementation during FMT significantly improved microbial engraftment fidelity, correlating with enhanced anti-inflammatory responses and attenuated colonic pathology. Network meta-analysis of clinical datasets further substantiated the prognostic value of donorin UC remission. Our findings utilisation as an ecological driver of microbiota engraftment and present a rationally designed microbial therapy that optimises FMT efficacy through targeted metabolic reprogramming.</p>