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GSE25812
Mus musculus
18 Downloadable Samples
Illumina MouseWG-6 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Mutations in the RNA granule component TDRD7 cause cataract and glaucoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Analysis of Tdrd7 deficiency in mouse lens epithelial-derived cell line at gene expression level. The hypothesis tested was that Tdrd7 is involved in post-transcriptional control of gene expression in the lens. Results provide evidence for differential regulation of genes involved in lens homeostasis and cataract formation in the absence of Tdrd7.
Publication Title
Mutations in the RNA granule component TDRD7 cause cataract and glaucoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Analysis of Tdrd7 deficiency in mouse lens epithelial-derived cell line at gene expression level. The hypothesis tested was that Tdrd7 is involved in post-transcriptional control of gene expression in the lens. Results provide evidence for differential regulation of genes involved in lens homeostasis and cataract formation in the absence of Tdrd7.
Publication Title
Mutations in the RNA granule component TDRD7 cause cataract and glaucoma.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Analysis of Tdrd7 deficiency in mouse lens epithelial-derived cell line at gene expression level. The hypothesis tested was that Tdrd7 is involved in post-transcriptional control of gene expression in the lens. Results provide evidence for differential regulation of genes involved in lens homeostasis and cataract formation in the absence of Tdrd7.
Publication Title
Mutations in the RNA granule component TDRD7 cause cataract and glaucoma.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Estrogens and progesterone control mammary gland development and breast carcinogenesis via their cognate receptors expressed in a subset of cells of the luminal layer of the mammary epithelium. The extracellular matrix (ECM) including the basement membrane (BM) is important in breast physiology and tumorigenesis but how epithelial hormone receptor signaling and ECM are linked mechanistically is unclear. We identify the secreted protease Adamts18 as critical intermediary. Luminal estrogen and progesterone receptor signaling via upregulation of Wnt4 expression and ensuing canonical Wnt signaling activation in basal cells control Adamts18 expression there. The protease has an epithelial-intrinsic role in stem cell activation. We identify multiple binding partners in the interstitial ECM and BM and show that ADAMTS18 cleaves fibronectin in vitro. Its deletion results in increased fibronectin, collagen I and IV, and laminin deposition in pubertal glands. Adamts18 interacts genetically with Col18a1, which encodes a proteoglycan that is BM-specific, in stem cell regulation. Adamts18 inactivation impairs Hippo signaling and reduces Fgfr2 expression and signaling, which are vital for stem cell function. Our findings link epithelial hormone signaling to BM remodeling by Adamts18, and define the BM as an essential stem cell niche component.
Publication Title
The secreted protease Adamts18 links hormone action to activation of the mammary stem cell niche.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 24 Downloadable Samples
Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Response of A549 cells treated with Aspergillus fumigatus wild type germinating conidia (WT_GC) or PrtT protease deficient mutant conidia (PrtT-GC) or inert acrylic 2-4 micron beads (Beads) for 8h
Publication Title
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Response of A549 cells treated with Aspergillus fumigatus wild type culture filtrate (WT-CF) or PrtT protease deficient mutant culture filtrate (PrtT-CF) for 8h
Publication Title
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Response of A549 cells treated with Aspergillus fumigatus germinating conidia (WT-GC) or culture filtrate (WT-CF) for 8h
Publication Title
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Cell migration is central to many biological processes including embryonic development, wound healing, and cancer progression. Cell migration is sensitive to environmental stiffness, and many cell types exhibit a stiffness optimum at which migration is maximal. Here we present a cell migration simulator that predicts a stiffness optimum that can be shifted by altering the number of active molecular motors and clutches. This prediction is verified experimentally by comparing cell traction and F-actin retrograde flow for two cell types with differing amounts of active motors and clutches: embryonic chick forebrain neurons (ECFNs; optimum ~1 kPa) and U251 glioma cells (optimum ~100 kPa). In addition, the model predicts, and experiments confirm, that the stiffness optimum of U251 glioma cell migration, morphology, and F-actin retrograde flow rate can be shifted to lower stiffness by simultaneous drug inhibition of myosin II motors and integrin-mediated adhesions.
Publication Title
Shifting the optimal stiffness for cell migration.
Sample Metadata Fields
Sex, Cell line
View Samples