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GSE42697
Homo sapiens
10 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Despite advance in interferon-based treatment for chronic hepatitis C, difficult-to-treat patients remain in existence yet. To identify key genes involved in difficult-to-treat characteristics, gene expression patterns of miRNA and RNA were analyzed by profiling pretreatment liver tissues from five sustained virological responders (SVR), three relapsers (R) and four non-responders (NR). Expression levels of miRNA and mRNA were compared between SVR/R and NR groups by using microarray, respectively. Quantitative real-time reverse-transcriptase polymerase chain reaction and statistical analyses validated genes with significantly differential expression levels in 50 liver tissues: proliferation-, inflammation- and anti-apoptosis-related mRNA expression levels increased significantly in NR, compared to SVR/R. Of miRNA with significantly differential expression levels on microarray, several miRNA were correlated inversely with those significant mRNA. In vitro studies by using miRNA inhibitors and mimics verified the inverse correlation between the miRNA and mRNA. These findings enhance our understanding of the difficult-to-treat molecular mechanism and identification of target molecules for novel treatments.
Publication Title
Involvement of MAP3K8 and miR-17-5p in poor virologic response to interferon-based combination therapy for chronic hepatitis C.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Gene expression of Ethanol-treated hepatocytes from WT and transglutaminase 2 knockout mice
Publication Title
Role of transglutaminase 2 in liver injury via cross-linking and silencing of transcription factor Sp1.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
To identify the molecular targets of orosomucoid (Orm1) during liver regeneration, GeneChip analysis was performed at 48 h after partial hepatectomy (PH) in regenerating mouse liver treated with siControl or siOrm. A total of 180 differentially expressed genes in Orm1 konckdown mouse liver by comparing with siControl were identified with a fold change more than 2. Then, pathway analysis performed on the altered gene expression profiles using Ingenuity Pathways Analysis (IPA) program revealed that cell cycle, Toll-like receptor and TGF-beta receptor signaling pathways were under control of Orm1 in regenerating mouse livers.
Publication Title
Transcriptome Analysis Uncovers a Growth-Promoting Activity of Orosomucoid-1 on Hepatocytes.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
NPM1 was reported to regulate the SOD2 gene expression through regulation of NF-kB. However, the effect of NPM1 on the NF-kB-dependent transcriptome has not been exmained.
Publication Title
Efficient DNA binding of NF-κB requires the chaperone-like function of NPM1.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
To recruit phagocytes, apoptotic cells characteristically release ATP, which functions as a danger signal. Here, we found that the culture supernatant of apoptotic cells activated the macrophages to express anti-inflammatory genes such as NR4A and Thbs1. A high level of AMP accumulated in the apoptotic cell supernatant in a Pannexin1-dependent manner. A nucleotidase inhibitor and A2a adenosine receptor antagonist inhibited the apoptotic supernatant-induced gene expression, suggesting AMP was metabolized to adenosine by an ecto-5-nucleotidase expressed on macrophages, to activate the macrophage A2a adenosine receptor. Intraperitoneal injection of zymosan into AdoR A2a- or Panx1-deficient mice produced high, sustained levels of inflammatory mediators in the peritoneal lavage. These results indicated that AMP from apoptotic cells suppresses inflammation as a calm down signal.
Publication Title
Immunosuppression via adenosine receptor activation by adenosine monophosphate released from apoptotic cells.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
Ion Torrent Proton
Description
Analysis of murine cardiomyocyte cell line HL-1 treated with Ivermectin or Importazole. Results provide insight into the pathways regulated by the treatments. Overall design: RNA-seq of mouse HL-1 cardiomyocytes treated with vehicle (DMSO), Ivermectin, or Importazole for 24 hours, in triplicate, using Ion Proton System.
Publication Title
Antihypertrophic Effects of Small Molecules that Maintain Mitochondrial ATP Levels Under Hypoxia.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Arabidopsis thaliana
- 6 Downloadable Samples
- NextSeq 500
Description
Phytochromes are evolutionarily conserved photoreceptors in bacteria, fungi, and plants. The prototypical phytochrome comprises an N-terminal photosensory module and a C-terminal histidine kinase signaling-output module. However, the plant phytochrome has been postulated to transduce light signals by interacting with a group of nodal Phytochrome-Interacting transcription Factors (PIFs) and triggering their degradation via the N-terminal photosensory module, while its C-terminal output module, including a Histidine Kinase-Related Domain (HKRD), is thought not to participate directly in signaling. Here, we show that the C-terminal module of Arabidopsis phytochrome B (PHYB) is unexpectedly sufficient to mediate the degradation of PIF3 and to induce a distinct set of PIF-regulated photosynthetic genes. These signaling functions require the HKRD and particularly its dimerization. A D1040V mutation, which disrupts the dimerization of HKRD and the interaction between the C-terminal module and PIF3, abrogates the early light signaling functions of PHYB in nuclear accumulation, photobody biogenesis, and PIF3 degradation. In contrast, disruption of the interaction between PIF3 and PHYB's N-terminal photosensory module has little effect on PIF3 degradation. Together, this study provides novel insight into the central mechanism of early phytochrome signaling that the C-terminal signaling-output module of PHYB interacts with PIF3 in the nucleus to mediate PIF3 degradation by light. Overall design: Whole seedling mRNA profiles of 100h dark-grown phyB-9 mutant and BCY overexpression line were generated by deep sequencing, in triplicate, using Illumina NextSeq 500
Publication Title
Mechanism of early light signaling by the carboxy-terminal output module of Arabidopsis phytochrome B.
Sample Metadata Fields
Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Recurrent mutations in multiple components of the cohesin complex in myeloid neoplasms.
Sample Metadata Fields
Specimen part, Disease, Cell line
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We recently identified recurrent mutations of cohesin complex in myeloid neoplasms through whole-exome sequencing analysis. RAD21 is one of the main components of the cohesin complex.
Publication Title
Recurrent mutations in multiple components of the cohesin complex in myeloid neoplasms.
Sample Metadata Fields
Cell line
View Samples- Arabidopsis thaliana
- 18 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Plants grown under a canopy recognize changes in light quality and modify their growth patterns; this modification is known as shade avoidance syndrome. In leaves, leaf blade expansion is suppressed, whereas petiole elongation is promoted under the shade. However, the mechanisms that control these responses are largely unclear. Here, we demonstrated that both auxin and brassinosteroid (BR) are required for the normal leaf responses to shade. The microarray analysis of leaf blades and petioles treated with end-of-day far-red light (EODFR) revealed that almost half of the genes induced by the treatment in both parts were previously identified as auxin-responsive genes. Likewise, BR-responsive genes were overrepresented in the EODFR-induced genes. Hence, the auxin and BR responses were elevated by EODFR treatment in both leaf blades and petioles, although opposing growth responses were observed in these two parts. The analysis of the auxin-deficient doc1/big mutant and BR-deficient rot3/cyp90c1 mutant further indicates that auxin and BR were equally required for the normal petiole elongation response to the shade stimulus. In addition, the spotlight irradiation experiment revealed that phytochrome in leaf blades but not that in petioles regulated petiole elongation, which was probably mediated through regulation of the auxin/BR responses in petioles. On the basis of these findings, we conclude that auxin and BR cooperatively promote petiole elongation in response to the shade stimulus under the control of phytochrome in the leaf blade.
Publication Title
Involvement of auxin and brassinosteroid in the regulation of petiole elongation under the shade.
Sample Metadata Fields
Specimen part
View Samples