TWEAK/Fn14 signaling may regulate the expression of genes involved in epithelial repair and mucosal inflammation. Comparing the gene signatures in WT and TWEAK KO mice will inform the biology of TWEAK/Fn14 pathway in the GI tract.
Interleukin-13 damages intestinal mucosa via TWEAK and Fn14 in mice-a pathway associated with ulcerative colitis.
Specimen part, Treatment
View SamplesThe accumulation of intramyocellular lipid (IMCL) is recognized as an important determinant of insulin resistance, and is increased by a high-fat diet (HFD). However, the effects of HFD on IMCL and insulin sensitivity are highly variable.
Increased intramyocellular lipid/impaired insulin sensitivity is associated with altered lipid metabolic genes in muscle of high responders to a high-fat diet.
Sex, Specimen part, Time
View SamplesEndurance-trained athletes have high oxidative capacity, enhanced insulin sensitivity, and high intracellular lipid accumulation in muscle. These characteristics are likely due to altered gene expression levels in muscle.
Endurance Runners with Intramyocellular Lipid Accumulation and High Insulin Sensitivity Have Enhanced Expression of Genes Related to Lipid Metabolism in Muscle.
Sex, Specimen part
View SamplesHuR-deficient cells showed the decreased expression of genes involved in chemotaxis, cell proliferation and signal transduction.
Hu Antigen R Regulates Antiviral Innate Immune Responses through the Stabilization of mRNA for Polo-like Kinase 2.
Specimen part, Cell line
View SamplesTo identify the “time-lapse” TF networks during B lineage commitment, we established multipotent progenitors harboring a tamoxifen-inducible form of Id3, an in vitro system where virtually all cells became B cells within 6 days by simply withdrawing 4-OHT. In this study, transcriptome analysis at multiple time points was performed using the culture system. Overall design: Time-course transcriptomic profiles of multipotent iLS cells toward B committed cells were analyzed by deep sequencing, basically in triplicate, using Illumina Hiseq platform.
Three-step transcriptional priming that drives the commitment of multipotent progenitors toward B cells.
Specimen part, Cell line, Subject, Time
View SamplesIn lymphocyte lineages, mucosa-associated lymphoid tissue 1 (MALT1) mediates the nuclear factor-B activation signal that stimulates progression of malignant tumors. However, its expression is inactivated in oral carcinoma patients with worse prognosis. Unveiling genes under the control of MALT1 will provide valuable information for understanding of the mechanism of carcinoma progression.
Inhibition of TGF-β and EGF pathway gene expression and migration of oral carcinoma cells by mucosa-associated lymphoid tissue 1.
Specimen part, Cell line
View SamplesOral food intake maintains gastrointestinal cell turnover and impacts the morphology and function of intestinal epithelial cells. However, the underlying mechanism is not fully elucidated, especially in the large intestine. Therefore, we analyzed the colonic epithelial cell turnover in starved and re-fed mice.
Microbiota-derived lactate accelerates colon epithelial cell turnover in starvation-refed mice.
Sex, Age, Specimen part, Treatment
View SamplesGerminal centers (GCs) are clusters of activated B cells built on stromal cells known as follicular dendritic cells (FDCs). In the Peyers patches (PPs), GCs are chronically induced by bacteria and are the major sites for generation of gut IgA immune responses. Whether FDCs directly contribute to the IgA production in PP GCs is unknown.
The sensing of environmental stimuli by follicular dendritic cells promotes immunoglobulin A generation in the gut.
Specimen part
View SamplesAtopic dermatitis and psoriasis are driven by alternate type 2 and type 17 immune responses, but some proteins might be critical to both diseases. We show that a deficiency of the TNF superfamily molecule TWEAK (TNFSF12) in mice results in defective maintenance of atopic dermatitis-specific Th2 and psoriasis-specific Th17 cells in the skin, and impaired expression of disease-characteristic chemokines and cytokines, such as CCL17 and TSLP in atopic dermatitis, and CCL20 and IL-19 in psoriasis. The TWEAK receptor, Fn14, is upregulated in keratinocytes and dermal fibroblasts, and TWEAK induces these cytokines and chemokines alone and in synergy with the signature T helper cytokines of either disease, IL-13 and IL-17. Furthermore, subcutaneous injection of recombinant TWEAK into naïve mice induces cutaneous inflammation with histological and molecular signs of both diseases. TWEAK is therefore a critical contributor to skin inflammation and a possible therapeutic target in atopic dermatitis and psoriasis. Overall design: Eight- to 12-week old male mice were used. TWEAK-deficient animals were bred in house on the C57BL/6 background, and Fn14-deficient animals on a BALB/c. Atopic Dermatitis-like disease was induced by epicutaneous treatment with HDM extract (10 µg/mouse and treatment) and SEB (500 ng/mouse and treatment) given in 2 cycles on days 1 and 4, and 14 and 17, on the shaved and tape-stripped back skin over a 23 day period.
TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis.
Treatment, Subject
View SamplesBmi1 is a component of polycomb repressive complex 1 and its role in the inheritance of the stemness of adult somatic stem cells has been well characterized. Bmi1 maintains the self-renewal capacity of adult stem cells, at least partially, by repressing the Ink4a/Arf locus that encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf 14. Deletion of both Ink4a and Arf in Bmi1-deficient mice substantially restored the defective self-renewal capacity of HSCs and neural stem cells.
Poised lineage specification in multipotential hematopoietic stem and progenitor cells by the polycomb protein Bmi1.
Specimen part
View Samples