Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-19793
PROVIDER: PRJNA121817 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MyD88 is an adaptor protein in Toll-like receptor and interleukin 1 receptor mediated signaling pathways that plays an essential role in activation of immune responses following pathogen recognition. We investigate that role in the zebrafish embryo model by using a zebrafish mutant line that contains a premature stop condon in the gene encoding MyD88, leading to a truncated protein that lacks domains important for its normal function. We infected these MyD88 mutants and wildtype individuals with Mycobacterium marinum to compare the resulting immune response by transcriptome profiling on total RNA isolated from single embryos. Autophagy regulator dram1 was identified as one of the MyD88-dependent genes.
2014-06-01 | GSE49186 | GEO
Project description:MyD88 is an adaptor protein in Toll-like receptor and interleukin 1 receptor mediated signaling pathways that plays an essential role in activation of immune responses following pathogen recognition. We investigate that role in the zebrafish embryo model by using a zebrafish mutant line that contains a premature stop condon in the gene encoding MyD88, leading to a truncated protein that lacks domains important for its normal function. We infected these MyD88 mutants and wildtype individuals with S Mycobacterium marinum to compare the resulting immune response by transcriptome profiling on total RNA isolated from single embryos. Autophagy regulator dram1 was identified as one of the MyD88-dependent genes.
2014-06-01 | GSE49187 | GEO
Project description:MyD88 is an adaptor protein in Toll-like receptor and interleukin 1 receptor mediated signaling pathways that plays an essential role in activation of immune responses following pathogen recognition. We investigate that role in the zebrafish embryo model by using a zebrafish mutant line that contains a premature stop condon in the gene encoding MyD88, leading to a truncated protein that lacks domains important for its normal function. We infected these MyD88 mutants and wildtype individuals with Salmonella typhimurium and Edwardsiella tarda to compare the resulting immune response by transcriptome profiling on total RNA isolated from single embryos. The data derived from these microarray experiments confirms the vital role of MyD88 in pathogen recognition and provides many leads for further research.
2012-12-10 | GSE39274 | GEO
Project description:Inflammation has pleiotropic effects on carcinogenesis and tumor progression. Signaling through the adaptor protein MyD88 promotes carcinogenesis in several chemically induced cancer models. Interestingly, we observed a protective role for MyD88 in the development of AOM/DSS colitis-associated cancer. The inability of Myd88-/- mice to heal ulcers generated upon injury creates an inflammatory environment that increases the frequency of mutations and results in a dramatic increase in adenoma formation and cancer progression. Susceptibility to colitis development and enhanced polyp formation were also observed in Il18-/- mice upon AOM/DSS treatment, suggesting that the phenotype of MyD88 knockouts is in part due to their inability to signal through the IL-18 receptor. This study revealed a previously unknown level of complexity surrounding MyD88 activities downstream of different receptors that differentially impact tissue homeostasis and carcinogenesis.
2010-06-24 | GSE19793 | GEO
Project description:Gene expression profiling of total colon in AOM/DSS-treated Myd88 knockout and wild type
2015-09-08 | E-GEOD-19793 | ExpressionAtlas
Project description:Inflammation has pleiotropic effects on carcinogenesis and tumor progression. Signaling through the adaptor protein MyD88 promotes carcinogenesis in several chemically induced cancer models. Interestingly, we observed a protective role for MyD88 in the development of AOM/DSS colitis-associated cancer. The inability of Myd88-/- mice to heal ulcers generated upon injury creates an inflammatory environment that increases the frequency of mutations and results in a dramatic increase in adenoma formation and cancer progression. Susceptibility to colitis development and enhanced polyp formation were also observed in Il18-/- mice upon AOM/DSS treatment, suggesting that the phenotype of MyD88 knockouts is in part due to their inability to signal through the IL-18 receptor. This study revealed a previously unknown level of complexity surrounding MyD88 activities downstream of different receptors that differentially impact tissue homeostasis and carcinogenesis. The Myd88 knockout mice were backcrossed to obtain at least 98% congenicity to B6NCr background. As control groups, wild type mice of identical background were used. Ten biological repeats were performed for the treated wild type and Myd88 samples. Six biological repeats were performed for the untreated wild type and Myd88 samples.
2010-07-30 | E-GEOD-19793 | biostudies-arrayexpress
Project description:Progressive dysfunction and death of photoreceptors occurs in blinding diseases such as age-related macular degeneration and retinitis pigmentosa. The MyD88 protein is a central adaptor molecule for innate immune system Toll-like receptors (TLR) and interleukin-1 receptor (IL-1R), which are active in retinal disease and induce cytokine secretion from inflammatory cells. We recently demonstrated that inhibiting MyD88 in mouse models of retinal degeneration led to increased rod photoreceptor survival, which was associated with altered cytokine expression and increased neuroprotective microglia. However, additional molecular changes associated with MyD88 inhibitor-mediated neuroprotection are not known. Quantitative proteomics using iTRAQ LC-MS/MS is a high-throughput method ideal for providing new information about the molecular mechanisms contributing to photoreceptor protection. In this study, we used isobaric tags for relative and absolute quantification (iTRAQ) labeling followed by liquid chromatography–tandem mass spectrometry (LC-MS/MS) for quantitative proteomic analysis on the rd10 mouse model of retinal degeneration to identify protein pathways changed by MyD88 inhibition. A total of 42 proteins were differentially expressed in retinas from mice treated with MyD88 inhibitor compared with control. Notably, increased expression of multiple crystallins and chaperones that respond to cellular stress and have anti-apoptotic properties were identified in the MyD88 inhibited mice. Additional differentially expressed biological processes included pyrophosphatase activity and peptide biosynthesis. These data suggest that inhibiting MyD88 may enhance chaperone-mediated tissue protective pathways. Therefore, this study provides new insight into molecular events that contribute to photoreceptor protection from modulating inflammation.
2022-02-17 | PXD024501 | Pride
Project description:MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut II
| PRJNA1232145 | ENA
Project description:MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut I
| PRJNA1232146 | ENA