Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA257703 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Studying the effects of the TEN1-ICD on transcriptional regulation
2025-01-24 | E-GEOD-61704 | ExpressionAtlas
Project description:Transcriptional profiling of long-term stimulated primary murine intestinal fibroblasts with interleukin-36.
2018-06-04 | E-MTAB-6476 | ExpressionAtlas
Project description:Comparing the effects of MITF on transcriptional regulation to the TEN1-ICD
2025-01-24 | E-GEOD-61705 | ExpressionAtlas
Project description:Transcriptional regulation in denervated murine GA muscle
| PRJNA265198 | ENA
Project description:Deep proteomic evaluation of primary and cell line motoneuron disease models delineates major differences in neuronal characteristics
2022-01-14 | E-PROT-12 | ExpressionAtlas
Project description:Quantitative analysis of wild type and cd36-/- murine peritoneal macrophage transcriptomes
2020-04-29 | E-GEOD-139439 | ExpressionAtlas
Project description:Effects of Diras2-knockdown in murine hippocampal primary cells
| PRJNA276905 | ENA
Project description:Type I and II Interferon-Stimulated Genes in Murine Primary Bone Marrow Macrophages
2015-09-28 | E-GEOD-35825 | ExpressionAtlas
Project description:Signaling through the AKT and ERK pathways controls cell proliferation. However, the integrated regulation of this multistep process, involving signal processing, cell growth and cell-cycle progression, is poorly understood. Here we study different murine hematopoietic cell types, in which AKT and ERK signaling is triggered by erythropoietin (Epo). Although these cell types share the molecular network topology for pro-proliferative Epo signaling, they exhibit distinct proliferative responses. Iterating quantitative experiments and mathematical modeling, we identify two molecular sources for cell-type-specific proliferation. First, cell-type-specific protein abundance patterns cause differential signal flow along the AKT and ERK pathways. Second, downstream regulators of both pathways have differential effects on proliferation, suggesting that protein synthesis is rate-limiting for faster-cycling cells while slower cell-cycles are controlled at the G1-S progression. The integrated mathematical model of Epo-driven proliferation explains cell-type-specific effects of targeted AKT and ERK inhibitors and faithfully predicts based on the protein abundance anti-proliferative effects of inhibitors in primary human erythroid progenitor cells. Our findings suggest that the effectiveness of targeted cancer therapy might become predictable from protein abundance patterns.
2017-03-31 | MSV000080844 | MassIVE
Project description:Regulation of gene expression in macrophage immune response
2020-04-22 | E-ENAD-41 | ExpressionAtlas