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SRP059754
Mus musculus
15 Downloadable Samples
Illumina HiSeq 2000
Description
Gan mice express Wnt1, Ptgs2, and Ptges, which develop inflammation-associated gastric tumors (Oshima et al, Gastroenterology 131: 1086, 2006). We examined the role of MyD88 in tumorigenesis by construction of Myd88-/- Gan mice and bone marrow transplantation into Gan mice from Myd88-/- mice. Overall design: Total RNA was prepared from wild-type normal glandular stomach (n=3: WT 1–WT 3), B6 C2mE mice (n=3: C2mE 1–C2mE 3), B6 Gan mice (n=3: Gan1–Gan3), B6 Gan MyD88-/- mice (n=3: Gan 1 (MyD88-/-)–Gan 3 (MyD88-/-)), and B6 bone marrow transplanted Gan mice from Myd88-/- mice (n=3: BMT-Gan 1 (from MyD88-/-)–BMT-Gan 3 (from MyD88-/-)). We used Illumina HiSeq 2000, and examined expression profiles.
Publication Title
NF-κB-induced NOX1 activation promotes gastric tumorigenesis through the expansion of SOX2-positive epithelial cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina HiSeq 2500
Description
Noxo1, a component of NADPH oxidase 1 (NOX1) complex, is upregulated in gastric cancer cells in a inflammation-dependent manner, and plays an important role in tumorigenesis (Oncogene, 33: 3820, 2014). To examine the mechanism of NOX1/ROS signaling in tumorigenesis, MKN45 gastric cancer cells were treated with apocynin, an inhibitor for NOX, and their gene expression was examined by RNA sequencing. Based on expression data, Sox2 was shown to be suppressed by apocynin, suggesting a role of Sox2 in a inflammation-associated gastric tumorigenesis. Overall design: Total mRNA expression profiles of Apocynin administrated MKN45 in 2 trials.
Publication Title
NF-κB-induced NOX1 activation promotes gastric tumorigenesis through the expansion of SOX2-positive epithelial cells.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 3 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The fields of drug discovery and regenerative medicine require large numbers of adult human primary hepatocytes. For this purpose, it is desirable to use hepatocyte-like cells (HLCs) differentiated from human pluripotent stem cells. To develop an efficient HLCs induction method, we constructed a red fluorescent reporter, CYP3A7R, in which DsRed is placed under the transcriptional regulation of CYP3A7 coding for a human fetus-type P450 enzyme. We created transgenic mice using mouse embryonic stem cells (mESCs) carrying a CYP3A7R transgene.
Publication Title
Real-time fluorometric evaluation of hepatoblast proliferation in vivo and in vitro using the expression of CYP3A7 coding for human fetus-specific P450.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Using microcell-mediated chromosome transfer (MMCT) into the mouse melanoma cell line, B16F10, we have previously found that human chromosome 5 carries a gene, or genes, that can negatively regulate TERT expression. To identify the gene responsible for the regulation of TERT transcription, we performed cDNA microarray analysis using parental B16F10 cells, telomerase negative B16F10 microcell hybrids with a human chromosome 5 (B16F10MH5), and its revertant clones (MH5R) with reactivated telomerase. Here we report the identification of PITX1, whose restoration leads to the downregulation of mouse tert (mtert) transcription, as a TERT suppressor gene. Additionally, both human TERT (hTERT) and mouse TERT (mtert) promoter activity can be suppressed by PITX1. We showed that three and one binding sites, respectively, within the hTERT and mtert promoters that express a unique conserved region are responsible for the transcriptional activation of TERT. Furthermore, we showed that PITX1 binds to the TERT promoter both in vitro and in vivo. Thus, PITX1 suppresses TERT transcription through direct binding to the TERT promoter, which ultimately regulates telomerase activity.
Publication Title
Identification of PITX1 as a TERT suppressor gene located on human chromosome 5.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
Apc(D716) mutant mice develop benign intestinal adenoma, while Apc(D716) and p53 R270H compound mutant mice develop invasive adenocarcinoma in the intestine. We examined expression profile of tumor-derived organoids using Apc(D716), Apc(D716) p53 Null, Apc(D716) p53 R270H mutant mice by RNA sequencing, and identified mutant p53-induced gene set. Overall design: Total RNA was extracted from Apc(D716) p53(+/+) tumor organoids, Apc(D716) p53(flox/flox) tumor organoids, and Apc(D716) p53(M/M) tumor organoids. For each genotype, two mice were used and organoids were prepared independently. p53(flox) allele is null mutation, whereas p53(M) allele carrys R270H mutation. We used Illumina HiSeq 2500, and examined expression profiles.
Publication Title
Intestinal cancer progression by mutant p53 through the acquisition of invasiveness associated with complex glandular formation.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
To investigate why dipeptides accumulate in immature CML cells, we examined upstream gene expression patterns. We isolated the most primitive long-term stem cells, short-term stem cells, and KLS- progenitor cells from healthy littermate control and CML-affected mice and performed gene expression profiling using next-generation RNA-sequencing. Overall design: Gene expression profiles of the most primitive long-term (LT) stem cells (CD150+CD48-CD135-KLS+ cells), short-term (ST) stem cells (CD150-CD48-CD135- KLS+ cells), and KLS- progenitor cells from healthy littermate control and CML-affected mice
Publication Title
Dipeptide species regulate p38MAPK-Smad3 signalling to maintain chronic myelogenous leukaemia stem cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Hair follicle (HF) regeneration begins when communication between quiescent epithelial stem cells (SCs) and underlying mesenchymal dermal papillae (DP) generates sufficient activating cues to overcome repressive BMP signals from surrounding niche cells. We uncovered a hitherto unrecognized DP transmitter, TGF2, which activates Smad2/3 transiently in HFSCs concomitant with entry into tissue regeneration.
Publication Title
Paracrine TGF-β signaling counterbalances BMP-mediated repression in hair follicle stem cell activation.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Werner syndrome (WS) is a premature aging disorder characterized by chromosomal instability and cancer predisposition. Mutations in WRN are responsible for the disease and cause telomere dysfunction, resulting in accelerated aging. In the present study, we describe the effects of long-term culture on WS iPSCs, which acquired and maintained infinite proliferative potential for self-renewal over 2 years. After long-term cultures, WS iPSCs exhibited stable undifferentiated states and differentiation capacity, and premature upregulation of senescence-associated genes in WS cells was completely suppressed in WS iPSCs despite WRN deficiency.
Publication Title
Reprogramming suppresses premature senescence phenotypes of Werner syndrome cells and maintains chromosomal stability over long-term culture.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2000
Description
We performed RNA-seq on purified squamous cell carcinoma stem cells (SCC-SCs) from primary mouse skin tumors transduced with TGF-beta reporter. Overall design: SCC-SCs were purified based on cell surface marker expression integrin alpha6 and CD44, after lineage negative selection, and separated by fluorescent TGF-beta reporter expression.
Publication Title
TGF-β promotes heterogeneity and drug resistance in squamous cell carcinoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Mesoangioblasts are stem/progenitor cells derived from a subset of pericytes expressing alkaline phosphatase. They have been shown to ameliorate muscular dystrophies (currently incurable diseases) in different animal models and are now undergoing clinical experimentation for Duchenne muscular dystrophy. We show here that patients affected by limb-girdle muscular dystrophy 2D (LGMD2D, characterized by -sarcoglycan deficit) have a reduction of this subset of pericytes and hence mesoangioblast could not be derived for cell therapy. Therefore, we reprogrammed LGMD2D fibroblasts and myoblasts to induced pluripotent stem cells (iPSCs) and developed a protocol for the derivation of mesoangioblast-like cells from them. These cells can be expanded and genetically corrected with a muscle-specific lentiviral vector expressing human -sarcoglycan. Upon transplantation into ad hoc generated -sarcoglycan-null immunodeficient mice, they generate myofibers expressing -sarcoglycan. This approach may be useful for muscular dystrophies that show a reduction of resident progenitors and provides evidence of pre-clinical safety and efficacy of disease-specific iPSCs.
Publication Title
Transplantation of genetically corrected human iPSC-derived progenitors in mice with limb-girdle muscular dystrophy.
Sample Metadata Fields
Sex, Specimen part
View Samples