We measured gene expression of D. melanogaster female heads and abdomens after mating with males from six populations evolved under either enforced monogamy (no male-male competition, 3 populations) or sustained polygamy (intense male-male competition, 3 populations). Overall design: Three samples of virgin female heads and six samples of mated female heads (one each per male evolved population, of which there are three monogamous and three polygamous), for nine libraries. Also, three samples of virgin female abdomens and six samples of mated female abdomens (one each per male evolved population, of which there are three monogamous and three polygamous), for nine libraries. In total, eighteen libraries sequenced in 8 lanes.
Sexual conflict drives male manipulation of female postmating responses in <i>Drosophila melanogaster</i>.
Sex, Specimen part, Subject
View SamplesTWEAK/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 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 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 SamplesTumors consist of heterogeneous cell population, containing cancer cell subpopulations with anticancer drug-resistant property, called “persister” cells. To reveal the character of the persister cells, we analyzed gene expression profile of patient-derived gastric cells and residual cancer cells after treatment with 5-FU or SN38, an active metabolite of irinotecan. In our study, we identified ALDH1A3 as a marker and a cell proliferation factor of persister cells. To examine molecular pathways regulated by ALDH1A3, we analyzed gene expression profile of patient-derived gastric JSC15-3 in which ALDH1A3 was knocked down by using shRNAs.
ALDH1A3-mTOR axis as a therapeutic target for anticancer drug-tolerant persister cells in gastric cancer.
Specimen part, Cell line, Treatment
View SamplesIL-1R-associated kinases (IRAKs) participate in Toll-like receptor (TLR) signal transduction. MALP-2 is a TLR2 ligand, and stimulation of macrophages with MALP-2 activates expression of various genes including proinflammatory cytokines.
Sequential control of Toll-like receptor-dependent responses by IRAK1 and IRAK2.
No sample metadata fields
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 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 SamplesHOX genes encode a family of homeodomain-containing transcription factors involved in the determination of cell fate and identity during embryonic development. They also behave as oncogenes in some malignancies. In this study, we found high expression of the HOXD9 gene transcript in glioma cell lines and human glioma tissues by quantitative real-time PCR. Using immunocytochemistry, we observed HOXD9 protein expression in human brain tumor tissues, including astrocytomas and glioblastomas. To investigate the role of HOXD9 in gliomas, we silenced its expression in the glioma cell line U87 using HOXD9-specific siRNA, and observed decreased cell proliferation, cell cycle arrest, and induction of apoptosis. It was suggested that HOXD9 contributes to both cell proliferation and/or cell survival. The HOXD9 gene was highly expressed in a side population (SP) of SK-MG-1 cells that was previously identified as an enriched-cell fraction of glioma cancer stem-like cells. HOXD9 siRNA treatment of SK-MG-1 SP cells resulted in reduced cell proliferation. Finally, we cultured human glioma cancer stem cells (GCSCs) from patient specimens found with high expression of HOXD9 in GCSCs compared with normal astrocyte cells and neural stem/progenitor cells (NSPCs). Our results suggest that HOXD9 may be a novel marker of GCSCs and cell proliferation and/or survival factor in gliomas and glioma cancer stem-like cells, and a potential therapeutic target.
Functional analysis of HOXD9 in human gliomas and glioma cancer stem cells.
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 Samples