Equine lameller tissues were collected to compare normal vs laminitis generated differences in transcriptom level.
Gene expression in the lamellar dermis-epidermis during the developmental phase of carbohydrate overload-induced laminitis in the horse.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
YAP promotes proliferation, chemoresistance, and angiogenesis in human cholangiocarcinoma through TEAD transcription factors.
Treatment
View SamplesThe YAP pathway in regulating organ size by integrating external signals to control the expression of genes involved in cell proliferation. YAP is known to be involved in tumorigenesis in several tissues, yet its role in cholangiocarcinoma is not established
YAP promotes proliferation, chemoresistance, and angiogenesis in human cholangiocarcinoma through TEAD transcription factors.
Cell line
View SamplesThe YAP pathway in regulating organ size by integrating external signals to control the expression of genes involved in cell proliferation. YAP is known to be involved in tumorigenesis in several tissues, yet its role in cholangiocarcinoma is not established
YAP promotes proliferation, chemoresistance, and angiogenesis in human cholangiocarcinoma through TEAD transcription factors.
No sample metadata fields
View SamplesThe YAP pathway in regulating organ size by integrating external signals to control the expression of genes involved in cell proliferation. YAP is known to be involved in tumorigenesis in several tissues, yet its role in cholangiocarcinoma is not established
YAP promotes proliferation, chemoresistance, and angiogenesis in human cholangiocarcinoma through TEAD transcription factors.
Treatment
View SamplesThis dataset was created to study M-CSF dependent in vitro differentiation of human monocytes to macrophages as a model process to demonstrate that independent component analysis (ICA) is a useful tool to support and extend knowledge-based strategies and to identify complex regulatory networks or novel regulatory candidate genes.
Analyzing M-CSF dependent monocyte/macrophage differentiation: expression modes and meta-modes derived from an independent component analysis.
Specimen part
View SamplesThe DNA methyl transferase inhibitor decitabine regulates gene expression in cancer cells.
Decitabine Enhances Lymphocyte Migration and Function and Synergizes with CTLA-4 Blockade in a Murine Ovarian Cancer Model.
Specimen part, Cell line
View SamplesEndothelial cells (ECs) express two members of the cadherin family, VE- and N-cadherin. While VE-cadherin induces EC homotypic adhesion, N-cadherin function in ECs remains largely unknown. EC-specific inactivation of either VE- or N-cadherin leads to early foetal lethality suggesting that these cadherins play a non-redundant role in vascular development.
Overlapping and divergent signaling pathways of N-cadherin and VE-cadherin in endothelial cells.
Specimen part, Cell line
View SamplesTranscriptomic analysis of H3.3 KO/Kd mouse embryonic fibroblasts (MEFs) Overall design: We isolated total RNA from control shRNA treated or shH3.3A treated H3.3B KO MEFs and carried out Ribozero RNA-seq analysis. RNA-seq analysis was carried out on pooled datasets from biological duplicate experiments.
Histone H3.3 regulates mitotic progression in mouse embryonic fibroblasts.
Specimen part, Cell line, Subject
View SamplesIn order to identify genes regulated by VE-cadherin expression, we compared a mouse VE-cadherin null cell line (VEC null) with the same line reconstituted with VE-cadherin wild type cDNA (VEC positive). The morphological and functional properties of these cell lines were described previously [Lampugnani,M.G. et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J. Cell Biol. 161, 793-804 (2003)]. By Affymetrix gene expression analysis we found several genes up-regulated by VE-cadherin, among which claudin-5 reached remarkably high levels. The up-regulation of these genes required not only VE-cadherin expression but also cell confluence suggesting that VE-cadherin clustering at junctions was needed.
Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5.
No sample metadata fields
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