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GSE33471
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- 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- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Mouse hair follicles undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by stem cells (SCs). Following hair regeneration, SCs within the bulge and its vicinity (upper ORS which becomes the bulge for the next cycle) briefly self-renew to replenish expended SCs and ensure long-term tissue regeneration.
Publication Title
An RNA interference screen uncovers a new molecule in stem cell self-renewal and long-term regeneration.
Sample Metadata Fields
Sex, Specimen part
View Samples- 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- Mus musculus
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
Genome-wide RNAi screens in mice identified Ctnnb1 and Mllt6 as physiological regulators of HrasG12V-dependent epidermal hyperplasia. To probe the consequences of Ctnnb1 and Mllt6 on HrasG12V-dependent oncogenic growth, we examined how their depletion impacts gene expression in the HrasoncoX2 epidermis. We performed RNA-seq analysis of FACS-purified embryonic epidermal cells, followed by network analysis of differentially regulated transcripts. Whether Ctnnb1 or Mllt6, knockdown markedly enhanced activity of genes restricting growth, and decreased expression of genes promoting epidermal proliferation. This contrasted with known transcriptional changes that typically follow epidermal expression of oncogenic Hras. Moreover, there was a significant overlap in genes whose expression was affected by Mllt6 and ß-catenin, further implying a level of shared function. Overall design: Transcriptional profiles of epidermal progenitors of embryonic day 18.5 animals of wild-type, HrasG12V, and HrasG12V depleted of Ctnnb1 or Mllt6 backgrounds.
Publication Title
RNAi screens in mice identify physiological regulators of oncogenic growth.
Sample Metadata Fields
Cell line, Subject
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
- 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
A frequently used experimental model of chronic pancreatitis (PC) recapitulating human disease is repeated injection of cerulein to mice. We found that two common substrains of C57BL/6 , C56BL/6J (Jackson) and C57BL/6NHsd (Harlan), exhibit different degree of CP with C57BL/6J beeing more susceptible to repetitive cerulein induced CP. The goal of this study was to identify genes associated with CP and also to identify genes differentially regulated between two substrains as candidates for the CP progression.
Publication Title
Differences in the degree of cerulein-induced chronic pancreatitis in C57BL/6 mouse substrains lead to new insights in identification of potential risk factors in the development of chronic pancreatitis.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
Gprc5b, a retinoic acid-inducible orphan G proteincoupled receptor, is a member of the group C metabotropic glutamate receptor family. Its function is unknown. However, recent evidence suggests that it binds Frizzled Wnt receptors and may activate noncanonical Wnt signaling pathways. Here we report the discovery of a brain-enriched C-terminal splice variant of Gprc5b, Gprc5b_v2, by cDNA microarray and RT-PCR analyses. The variant appeared to have been downregulated in the brains of learning/memory-deficient p97FE65 null mice. Despite the fact that the mice had been backcrossed with the C57Bl/6J strain for more than ten generations, Gprc5b and other genes surrounding the FE65 locus on mouse chromosome 7 were retained from the 129-derived ES cells used to generate the knockout line. The differential splicing is unlikely due to FE65 function, as originally suspected, as Gprc5b_v2 expression is also downregulated in the brains of 129/Sv substrains in comparison to C57Bl/6J mice. Further characterization revealed the expression of both Gprc5b_v2 and the previously described variant, Gprc5b_v1, in neurons. Interestingly, Gprc5b_v2 mRNA levels increase with neuronal maturation, paralleling the expression of synaptic proteins involved in the regulation of synaptic plasticity. Finally, we report evidence that both Gprc5b_v2 and Gprc5b_v1 regulate neurite outgrowth. These results are consistent with a putative function of Gprc5b in noncanonical Wnt signaling, which play roles in the regulation of neuronal morphology, and the formation and modulation of neuronal circuitry.
Publication Title
A flanking gene problem leads to the discovery of a Gprc5b splice variant predominantly expressed in C57Bl/6J mouse brain and in maturing neurons.
Sample Metadata Fields
No sample metadata fields
View Samples