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Homo sapiens
6 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Idiopathic portal hypertension (IPH) is characterized by portal hypertension due to obstruction or stenosis of the intrahepatic peripheral portal branches. Researchers have suggested that IPH may be attributed to intrahepatic peripheral portal vein thrombosis, splenic factors, abnormal autoimmunity, and related factors, however, the etiology of IPH remains unclear.
Publication Title
Comprehensive Screening of Gene Function and Networks by DNA Microarray Analysis in Japanese Patients with Idiopathic Portal Hypertension.
Sample Metadata Fields
Specimen part, Disease stage
View Samples- Mus musculus
- 6 Downloadable Samples
Illumina HiSeq 2500
Description
Innate lymphoid cells (ILCs) are considered to be the innate counterparts of adaptive T lymphocytes and play important roles in host defense, tissue repair, metabolic homeostasis, and inflammatory diseases. ILCs are generally thought of as tissue-resident cells, but whether ILCs strictly behave in a tissue-resident manner or can move between sites during infection is unclear. We show here that IL-25- or helminthic infection-induced inflammatory ILC2s are not tissue-resident but circulating cells, which arise from resting ILC2s residing in intestinal lamina propria and then migrate to mesenteric lymph nodes, spleen, lung, and liver. IL-25 induces rapid proliferation of the intestinal ILC2s and a change in their sensitivity to S1P-mediated chemotaxis, leading to lymphatic entry, blood circulation, and accumulation in periphery sites, including the lung where they contribute to anti-helminth defense and tissue repair. Our finding of cytokine-driven expansion and migration of innate lymphocytes, a behavioral parallel to the antigen-driven priming, expansion, and migration of adaptive lymphocytes to effector sites in distant tissues, provides a significant advance in our overall understanding of ILCs and indicates that ILCs complement adaptive immunity by providing both local and distant site effector protection during infection. Overall design: We examined the transcriptomes of BM ILC2 progenitors, lung nILC2s, IL-33-activated lung nILC2s, intestinal ILC2s, IL-25-induced lung iILC2s, and MLN iILC2s by RNA-Seq.
Publication Title
S1P-dependent interorgan trafficking of group 2 innate lymphoid cells supports host defense.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
HuR-deficient cells showed the decreased expression of genes involved in chemotaxis, cell proliferation and signal transduction.
Publication Title
Hu Antigen R Regulates Antiviral Innate Immune Responses through the Stabilization of mRNA for Polo-like Kinase 2.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The spontaneous pulmonary metastasis model of human uterine sarcoma was established using GFP-expressed MES-SA cells. Several sublines with different metastatic potentials were generated by in vivo passaging.
Publication Title
Establishment and characterization of a novel orthotopic mouse model for human uterine sarcoma with different metastatic potentials.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 56 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
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.
Publication Title
Interleukin-13 damages intestinal mucosa via TWEAK and Fn14 in mice-a pathway associated with ulcerative colitis.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Transcriptional dominance of Pax7 in adult myogenesis is due to high-affinity recognition of homeodomain motifs.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This data set contains 3 replicates each for a Pax7 overexpression, Pax3 overexpression and an empty vector Control
Publication Title
Transcriptional dominance of Pax7 in adult myogenesis is due to high-affinity recognition of homeodomain motifs.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 17 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
iPSC-derived NSPCs, which were induced by two different protocols (Embryoid body or Neural rosette) followed by expansion in free-floating culture (neurospheres), had closely resembled profiles.
Publication Title
Pathological classification of human iPSC-derived neural stem/progenitor cells towards safety assessment of transplantation therapy for CNS diseases.
Sample Metadata Fields
Sex, Race
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GSE9244- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Homozygous disruption of Bteb2/Klf5, a homolog of Drosophila gap gene Krppel, led to increased expression of various differentiation marker genes, such as Fgf5, Cdx2, and Brachyury in mouse ES cells without compromising their ability to differentiate into all three germ layers. Upon removal of LIF, Klf5-deficient ES cells showed faster differentiation kinetics than wild-type ES cells. In contrast, overexpression of Klf5 in ES cells suppressed the transcription of differentiation marker genes, and maintained pluripotency in the absence of LIF. In order to search downstream genes of Klf5, we surveyed genes implicated in ES cell proliferation by microarray analysis
Publication Title
Krüppel-like factor 5 is essential for blastocyst development and the normal self-renewal of mouse ESCs.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 22 Downloadable Samples
- Illumina HiSeq 2500
Description
Atopic 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.
Publication Title
TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis.
Sample Metadata Fields
Treatment, Subject
View Samples