Filters
Technology
Platform
GSE53503
Mus musculus
4 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
YY1 is indispensable for Lgr5+ intestinal stem cell renewal.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Crypts were isolated from either control or YY1f/f; Vil-Cre-ERT2 mice treated with tamoxifen for 4 days to induce knockout
Publication Title
YY1 is indispensable for Lgr5+ intestinal stem cell renewal.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Dynamic HoxB4-regulatory network during embryonic stem cell differentiation to hematopoietic cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Efficient in vitro generation of hematopoietic stem cells (HSCs) from embryonic stem cells (ESCs) holds great promise for cell-based therapies of hematological diseases. To date, HoxB4 remains to be the most effective transcription factor (TF) whose over-expression in ESCs confers long-term repopulating ability to ESC-derived HSCs. Despite its importance, the components and dynamics of the HoxB4 transcriptional regulatory network is poorly understood, hindering efforts to develop a more efficient protocol for in vitro derivation of HSCs. Towards this goal, we performed global gene expression profiling and chromatin immunoprecipitation coupled with deep sequencing (ChIP-Seq) at four stages of the HoxB4-mediated HSC development. Joint analyses of ChIP-Seq and gene expression profiles unveil a number of global features of the HoxB4 regulatory network.
Publication Title
Dynamic HoxB4-regulatory network during embryonic stem cell differentiation to hematopoietic cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
Illumina HiSeq 2500
Description
Nonsyndromic clefts of the palate and/or lip are common birth defects arising in about 1/700 live births worldwide. They are caused by multiple genetic and environmental factors, can only be corrected surgically and require complex post-operative care that imposes significant burdens on individuals and society. Our understanding of the molecular networks that control palatogenesis has advanced through studies on mouse genetic models of cleft palate. In particular, the transcription factor Pax9 regulates palatogenesis through the Bmp, Fgf and Shh pathways in mice. But there is still much to learn about Pax9's relationship with other signaling pathways in this process. Expression analyses and unbiased gene expression profiling studies offer a molecular explanation for the resolution of palatal defects by showing that Wnt and Eda/Edar-related genes are expressed in normal palatal tissues and that the Wnt and Eda/Edar signaling pathway is downstream of Pax9 in palatogenesis. Overall design: E13.5 mouse embryos palate were micro-dissceted, control and mutant samples were seperated and individually lyzed for the RNA extraction.
Publication Title
Small-molecule Wnt agonists correct cleft palates in <i>Pax9</i> mutant mice <i>in utero</i>.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 8 Downloadable Samples
- NextSeq 550
Description
In murine models, we find that irradiation of Paneth cells caused a gain of a stem cell-like transcriptome and induced activation of the Notch signaling pathway. This study documents plasticity by Paneth cells, a fully committed cell population to participate in epithelial replenishment following stem cell loss. Overall design: Single-cell dissociation was carried out as previously described (Li et al., 2016; Sato et al., 2011). Cell pellets were washed with cold PBS and re-suspended in FACS buffer. Cells were stained with DAPI, PerCP/Cy5.5-conjugated EpCAM, BUV395-conjugated CD45, and APC/fire 750-conjugated CD24. Cell suspensions were subjected to sorting by BD Biosciences Aria II Flow Cytometer. Single viable intestinal epithelial cells were gated by forward scatter, side scatter, and by negative staining for DAPI and CD45, and positive staining for EpCAM. Subpopulations were further gated based on CD24 and tdTomato (using R-phycoerythrin/PE channel). Paneth cells (tdT+CD24+) and derivative (tdT+CD24-) cells were FACS-sorted from irradiated (5 days after radiation) and non-irradiated 8-14 week old Lyz1CreER; R26R-tdT mice with one dose of tamoxifen adminstration (10mg/mouse), and subjected to total RNA extraction using Qiagen RNeasy Plus Micro kit.
Publication Title
Paneth Cell Multipotency Induced by Notch Activation following Injury.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 1 Downloadable Sample
- Illumina HiSeq 2500
Description
Nonsyndromic clefts of the palate and/or lip are common birth defects arising in about 1/700 live births worldwide. They are caused by multiple genetic and environmental factors, can only be corrected surgically and require complex post-operative care that imposes significant burdens on individuals and society. Our understanding of the molecular networks that control palatogenesis has advanced through studies on mouse genetic models of cleft palate. In particular, the transcription factor Pax9 regulates palatogenesis through the Bmp, Fgf and Shh pathways in mice. But there is still much to learn about Pax9''s relationship with other signaling pathways in this process. Here we show alterations of Wnt expression and decreased Wnt activity in Pax9-/- palatal shelves are a likely result of Pax9''s ability to directly bind and repress the promoters of Dkk1 and Dkk2, proteins that antagonize Wnt signaling. We exploited this relationship by delivering small-molecule Dkk inhibitors into the tail-veins of pregnant Pax9+/- females from E10.5 to E14.5. Such therapies restored Wnt signaling, promoted cell proliferation, bone formation and fusion of palatal shelves in Pax9-/- embryos. These data uncover a connection between the roles of Pax9 and Wnt genes in palatogenesis and offer a new approach for treating human cleft palates. Overall design: E14 embryos of Pax9-/- and control littermates with or without WAY-262611 treatment, mouse embryos palate were micro-dissected, control and mutant samples were separated and individually lysed for the RNA extraction.
Publication Title
Small-molecule Wnt agonists correct cleft palates in <i>Pax9</i> mutant mice <i>in utero</i>.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
In order to identify the effects of TFEB overexpression on the hela cells transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the hela TFEB stable clones
Publication Title
TFEB-driven endocytosis coordinates MTORC1 signaling and autophagy.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
During late gestation, structures called villi extend into the intestinal lumen to dramatically increase the surface area of the intestinal epithelium, preparing the gut for the neonatal diet. Incomplete development of the intestine is the most common gastrointestinal complication in neonates, but the causes are unclear. We provide evidence that Yin-Yang1 (Yy1) is critical for intestinal villus development. YY1 loss in the developing endoderm had no apparent consequences until late gestation, after which the intestine differentiated poorly and exhibited severely stunted villi. Transcriptome analysis revealed that YY1 is required for mitochondrial gene expression, and ultrastructural analysis confirmed compromised mitochondrial integrity in the mutant intestine. We found increased oxidative phosphorylation gene expression at the onset of villus elongation, suggesting that aerobic respiration may function as a regulator of villus growth. Mitochondrial inhibitors blocked villus growth in a fashion similar to Yy1 loss, thus further linking oxidative phosphorylation with late-gestation intestinal development. Interestingly, we find necrotizing enterocolitis patients also exhibit decreased expression of oxidative phosphorylation genes. Our study highlights the still unappreciated role of metabolic regulation during organogenesis, and suggests it may contribute to neonatal gastrointestinal disorders.
Publication Title
A YY1-dependent increase in aerobic metabolism is indispensable for intestinal organogenesis.
Sample Metadata Fields
Specimen part
View Samples- Bos taurus
- 36 Downloadable Samples
- Affymetrix Bovine Genome Array (bovine)
Description
BACKGROUND:
Publication Title
Milk yield responses to changes in milking frequency during early lactation are associated with coordinated and persistent changes in mammary gene expression.
Sample Metadata Fields
Specimen part, Time
View Samples