E-GEOD-18787
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA116693PRJNA121259
PROVIDER: E-GEOD-18787 | ExpressionAtlas | 2015-12-07
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Gene regulation in osmpk6 mutant cells expressing OsMKK4DD
| PRJNA121259 | ENA
Project description:Estradiol Treated Breast Cancer Cells Expressing Mutant Estrogen Receptors
| PRJNA87123 | ENA
Project description:<p>Although multi-agent combination chemotherapy is curative in a significant fraction of childhood acute lymphoblastic leukemia (ALL) patients, 20% of cases relapse and most die due to chemo-refractory disease. Here we used whole-exome and whole-genome sequencing to analyze the mutational landscape and pattern of clonal evolution at relapse in pediatric ALL cases. These analyses showed that ALL relapses originate from a common ancestral precursor clone of the diagnosis and relapsed populations and frequently harbor mutations implicated in chemotherapy resistance. RAS-MAPK pathway activating mutations in NRAS, KRAS and PTPN11 were present in 24/55 (44%) cases in our series. Notably, while some cases showed emergence of RAS mutant clones at relapse, in others, RAS mutant clones present at diagnosis were replaced by RAS wild type populations. Mechanistically, functional dissection of mouse and human wild type Kras and mutant Kras (Kras G12D) isogenic leukemia cells demonstrated induction of methotrexate resistance, but also improved response to vincristine, in mutant Kras- expressing lymphoblasts. These results identify chemotherapy driven selection as a central mechanism of leukemia clonal evolution and pave the road for the development of tailored personalized therapies for the treatment of relapsed ALL. </p>
| phs001072 | dbGaP
Project description:Murine Ba/F3 Cells: Ba/F3 cells expressing wild type JAK2 (WT cells) vs. Ba/F3 cells expressing JAK2 V617F mutant (VF cells)
| PRJNA149807 | ENA
Project description:Expression data from Treg cells expressing mutant FoxP3
| PRJNA352831 | ENA
Project description:The transcriptional factor FOXO1 is considered to play roles in the regulation of energy metabolism in various tissues. To determine the metabolic changes occurring due to the activation of FOXO1, we analyzed the metabolic profile of C2C12 myoblasts expressing FOXO1-estrogen receptor fusion protein using CE-TOFMS. In the FOXO1-activated cells, the metabolite levels during glycolysis were higher. In addition, the gene expression of pyruvate dehydrogenase kinase, an enzyme that inhibits glucose utilization, increased. In the FOXO1-activated cells, the metabolite levels of numerous amino acids decreased, with increased gene expression of branched chain amino acid metabolism enzymes. Our results suggest that FOXO1 suppresses glucose utilization and promotes the use of proteins/amino acids as energy sources in muscle cells, potentially during starvation.
2019-04-22 | ST001178 | MetabolomicsWorkbench
Project description:We study the gene regulation function of serine 473 phosphorylation of KAP1 (pS473-KAP1) in MDA-MB-231 cells. Wild type KAP1, S473A-KAP1 (phospho-acceptor site mutant) and S473D-KAP1 (phospho-mimetic mutant) are re-expressed in KAP1 knockdown cells. We analyze the gene expression profile in these three cells and find that many mitochondrial complex genes are up-regulated in S473D-KAP1 re-expressing cells. This study provides information about pS473-KAP1-regulated gene expression.
2016-11-08 | GSE63344 | GEO
Project description:Three quarters of all breast cancer cases express the estrogen receptor (ER, ESR1 gene), which promotes tumor growth and constitutes a direct target for endocrine therapies. ESR1 mutations have been implicated in therapy resistance in metastatic breast cancers, in particular to aromatase inhibitors. ESR1 mutations promote constitutive ER activity and affect other signaling pathways, allowing cancer cells to proliferate by employing mechanisms within and outwith direct regulation by the ER. Although subjected to extensive genetic and transcriptomic analyses, understanding of protein alterations remains poorly investigated. Towards this, we employed an integrated mass spectrometry (MS) based proteomic approach to profile the protein and phosphoprotein differences in breast cancer cell lines expressing the frequent Y537N and Y537S ER mutations. Global proteome analysis revealed enrichment of mitotic and immune signaling pathways in ER mutant cells, while phosphoprotein analysis evidenced enriched activity of proliferation associated kinases, in particular CDKs and MTOR. Integration of protein expression and phosphorylation data revealed pathway-dependent discrepancies (motility vs proliferation) that were observed at varying degrees across mutant and wt ER cells. Additionally, protein expression and phosphorylation patterns, while under different regulation, still recapitulated the estrogen-independent phenotype of ER mutant cells.
2024-03-26 | PXD032285 | Pride
Project description:Three quarters of all breast cancer cases express the estrogen receptor (ER, ESR1 gene), which promotes tumor growth and constitutes a direct target for endocrine therapies. ESR1 mutations have been implicated in therapy resistance in metastatic breast cancers, in particular to aromatase inhibitors. ESR1 mutations promote constitutive ER activity and affect other signaling pathways, allowing cancer cells to proliferate by employing mechanisms within and outwith direct regulation by the ER. Although subjected to extensive genetic and transcriptomic analyses, understanding of protein alterations remains poorly investigated. Towards this, we employed an integrated mass spectrometry (MS) based proteomic approach to profile the protein and phosphoprotein differences in breast cancer cell lines expressing the frequent Y537N and Y537S ER mutations. Global proteome analysis revealed enrichment of mitotic and immune signaling pathways in ER mutant cells, while phosphoprotein analysis evidenced enriched activity of proliferation associated kinases, in particular CDKs and MTOR. Integration of protein expression and phosphorylation data revealed pathway-dependent discrepancies (motility vs proliferation) that were observed at varying degrees across mutant and wt ER cells. Additionally, protein expression and phosphorylation patterns, while under different regulation, still recapitulated the estrogen-independent phenotype of ER mutant cells.
2024-03-26 | PXD032369 | Pride