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GSE79827
Bos taurus
6 Downloadable Samples
Affymetrix Bovine Genome Array (bovine)
Description
While cold stress has been shown to seriously impact cattle industry, there are only a few reports investigating the effect of cold stress on cattle. Whether severe cold stress results in alterations in gene expression and affects molecular genetic mechanisms remains unknown.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 78 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
B cells were found to be directly associated with the onset and development of many smoking-induced diseases. However, the in vivo molecular response of B cells underlying the female cigarette smoking remains unknown.
Publication Title
Impact of female cigarette smoking on circulating B cells in vivo: the suppressed ICOSLG, TCF3, and VCAM1 gene functional network may inhibit normal cell function.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 11 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
To search for biomarkers to differentiate Adult-Onset Steroid Sensitive focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD).
Publication Title
Comparison of Glomerular Transcriptome Profiles of Adult-Onset Steroid Sensitive Focal Segmental Glomerulosclerosis and Minimal Change Disease.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Rattus norvegicus
- 9 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Liver fibrosis is a high-morbidity and high-mortality chronic disease throughout the world without any satisfying treatment Large-conductance Ca2+- and voltage-activated K+ (Slo1, BK) channels are widely expressed in human body and important for numerous physiological processes. Previous studies have shown that BK channels are expressed in HSCs of patients with liver fibrosis and they are involved in contraction/relaxation of the HSCs To investigate the molecular mechanism of antifibrotic effect of BK channel opener rottlerin using in vivo fibrosis models. transcriptomic analyses of differential expression genes in livers from rats of vehicle, CCl4 and CCl4 combined with rottlerin treatment were for discrimination. The RNA samples were extracted from three samples of each group for microarray profiling and performed in Affymetrix Rats Genome 230 2.0 arrays for gene expression profiling analysis, which contained 31 042 probe sets. The biotinylated cRNA targets were hybridized with the microarray. After hybridization, arrays were stained in the Fluidics Station 450 and scanned on the Affymetrix Scanner 3000. The microarray experiments were performed by following the protocol of Affymetrix Inc at Shanghai Biotechnology Corporation. Under the criteria fold change > 1.5 or < 0.67, we obtained 10672 differential expressed genes (DEGs) between CCl4 and CCl4 combined with rottlerin treatment group, and the data was applied to further analysis.
Publication Title
Activation of BK Channels Prevents Hepatic Stellate Cell Activation and Liver Fibrosis Through the Suppression of TGFβ1/SMAD3 and JAK/STAT3 Profibrotic Signaling Pathways.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The serine threonine kinase Stk40 has been shown to involve in mouse embryonic stem cell differentiation, pulmonary maturation and adipocyte differentiation. Here we report that targeted deletion of Stk40 leads to fetal liver hypoplasia and anemia in the mouse embryos. The reduction of erythrocytes in the fetal liver is accompanied by increased apoptosis and compromised erythroid maturation. Stk40-/- fetal liver cells have significantly reduced colony forming units (CFUs) capable of erythroid differentiation, including burst forming unit-erythroid (BFU-E), colony forming unit-erythroid (CFU-E), and CFU-granulocyte, erythrocyte, megakaryocyte and macrophage (CFU-GEMM), but not CFU-granulocyte/macrophages (CFU-GM). Purified Stk40-/- megakaryocyte-erythrocyte progenitors (MEPs) produced substantially fewer CFU-E colonies compared to control cells. Moreover, Stk40-/- fetal liver erythroblasts failed to form normal erythroblastic islands in association with wild type or Stk40-/- macrophages, indicating an intrinsic defect of Stk40-/- erythroblasts. Furthermore, the hematopoietic stem and progenitor cell pool is reduced in Stk40-/- fetal livers but still retains the multi-lineage reconstitution capacity. Finally, analysis of microarray data of E14.5 fetal liver cells suggests a potential role of aberrantly activated TNF- signaling in Stk40 depletion induced dyserythropoiesis with a concomitant increase in cleaved Caspase-3 and decrease in Gata1 proteins. Altogether, the identification of Stk40 as a regulator for fetal erythroid differentiation, maturation and survival provides new clues to the molecular regulation of erythropoiesis and related diseases.
Publication Title
Deletion of Stk40 impairs definitive erythropoiesis in the mouse fetal liver.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Collagen triple helix repeat containing 1 (CTHRC1) has been found to be up-regulated in many human solid tumors. In this study, we investigated the changes of gene expression by comparing CTHRC1-siRNA and Scramble-siRNA control in hepatocellular carcinoma cell line HCCLM3, which has high expression levels of CTHRC1.
Publication Title
No associated publication
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Mutations of SMAD family member 4 (Smad4) gene caused Hereditary Hemorrhagic Telangiectasia (HHT). It was believed that bleeding disorders were caused by arteriovenous malformation in this syndrome. Although several studies indicated dysfunction of platelets from HHT patient, the role(s) of smad4 in platelet function has not been examined. In this study, using megakaryocyte/platelet-specific Smad4-deficient mice, we investigated the physiological function of Smad4 in platelet activation and the underlying mechanism.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
Baicalein, a purified flavonoid compound with defined chemical structure extracted from the dry roots of Scutellaria radix that is a broadly used herb in China, has been proved to possess significant anti-hepatoma activity by inhibiting cell proliferation, invasion, metastasis and inducing apoptosis, autophagy via several cancer-related signaling molecules. In recent years, emerging studies have demonstrated that Chinese medicinal herbs can exert their anti-tumor effects through targeting lncRNAssuch as curcumin, camptothecin, resveratrolpaclitaxel. However, there is still no related report about the effects of baicalein on lncRNA expression profile when it exerts its inhibition on hepatoma tumor growth. To investigate whether the antitumor effect of baicalein is related to its modulation of lncRNA expression in hepatocellular carcinoma (HCC), we profiled the lncRNA expression in HCC cell line Bel-7402 treated with baicalein (0, 40, 80M) for 24 hours using lncRNA microarray and detected the changes by comparing the lncRNA expression profile of HCC cell line Bel-7402 treated with baicalein (40 and 80 M) and its DMSO control (0 M). These findings suggest that modulation of lncRNA expression may be an important mechanism underlying the anti-hepatoma effects of baicalein and lay the groundwork for further investigations.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 22 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Background: Signaling by receptor tyrosine kinases (RTK) is frequently dysregulated in gliomas. Inter-individual variability in the causes for dysregulated RTK signaling may have hampered the efficacy of targeted therapies. Using gene expression modules around key regulators in the RAS-RAF-MEK-MAPK cascade and in the phosphatidylinositol 3-kinase-AKT pathways, we developed a RMPA clustering scheme to distinguish gliomas with varying extents of RTK signaling.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Disease
View Samples- Arabidopsis thaliana
- 12 Downloadable Samples
- Arabidopsis Gene 1.0 ST Array (aragene10st)
Description
Upon illumination, etiolated seedlings experience a transition from heterotrophic to photoautotrophic growth. During this process, the tetrapyrrole biosynthesis pathway provides chlorophyll for photosynthesis. This pathway has to be tightly controlled to prevent the accumulation of photoreactive metabolites and to provide stoichiometric amounts of chlorophyll for its incorporation into photosynthetic protein complexes. Therefore, plants have evolved regulatory mechanisms to synchronize the biosynthesis of chlorophyll and chlorophyll-binding proteins. Two phytochrome-interacting factors (PIF1 and PIF3) and the DELLA proteins, which are controlled by the gibberellin pathway, are key regulators of this process. Here, we show that impairment of TARGET OF RAPAMYCIN (TOR) activity in Arabidopsis (Arabidopsis thaliana), either by mutation of the TOR complex component RAPTOR1B or by treatment with TOR inhibitors, leads to a significantly reduced accumulation of the photoreactive chlorophyll precursor protochlorophyllide in darkness but an increased greening rate of etiolated seedlings after exposure to light. Detailed profiling of metabolic, transcriptomic, and physiological parameters revealed that the TOR-repressed lines not only grow slower, they grow in a nutrient-saving mode, which allows them to resist longer periods of low nutrient availability. Our results also indicated that RAPTOR1B acts upstream of the gibberellin-DELLA pathway and its mutation complements the repressed greening phenotype of pif1 and pif3 after etiolation.
Publication Title
Inhibition of TOR Represses Nutrient Consumption, Which Improves Greening after Extended Periods of Etiolation.
Sample Metadata Fields
Specimen part, Treatment
View Samples