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Differentiation of mammary epithelial cells with/without exposure to RANKL.
- Description
Summary from the GEO: "In order to investigate the mechanisms underlying defective alveologenesis caused by RANK over-expression in mice, global gene expression profiles from primary acinar cultures of mammary epithelial cells were analyzed." Overall design from the GEO: " Mammary epithelial cells from gestation day 16.5 WT and MMTV-RANK females were obtained. Cultures were established in the presence...
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Breast NeoplasmsEpithelial CellsRANK LigandReceptor Activator of Nuclear Factor-kappa B
- Access Rights
- Free to All
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Synthetic introns enable mutation-dependent targeting of cancer cells
- Authors
- North, KhrystynaBenbarche, SalimaAbdel-Wahab, Omar IbrahimBradley, Robert K.
- Description
Summary from GEO: "Many cancers carry recurrent change-of-function mutations in RNA splicing factor genes, which induce sequence-specific changes in RNA splicing. Here, we describe a method to harness this change in RNA splicing activity to drive splicing factor mutation-dependent gene expression in cancers and selectively eliminate these tumors. We engineered synthetic introns which were efficiently...
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Breast NeoplasmsEpithelial CellsGenetic TherapyIntrons/geneticsLeukemiaRNA Splicing Factors
- Access Rights
- Free to All
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LY6E is a pan-coronavirus restriction factor in the respiratory tract
- Authors
- Mar, KatrinaWells, Alexandra I.Caballero Van Dyke, Marley C.Lopez, Alexandra H.6 more author(s)...
- Description
Summary from GEO: "LY6E is an antiviral restriction factor that inhibits coronavirus spike-mediated fusion, but the cell types in vivo that require LY6E for protection from respiratory coronavirus infection are unknown. Here, we used a panel of seven conditional Ly6e knockout mice to define which Ly6e-expressing cells confer control of airway infection by murine coronavirus and SARS-CoV-2. Loss...
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Antiviral AgentsAntiviral Restriction FactorsEpithelial CellsRespiratory Tract InfectionsSARS-CoV-2Sequence Analysis, RNA
- Access Rights
- Free to All
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SETD2 Loss Creates A Permissive Epigenetic Landscape that Promotes Kidney Cancer Metastasis and Engenders Therapeutic Vulnerabilities
- Authors
- Xie, YuchenSahin, MerveCheng, Emily H.
- Description
Summary from GEO: "SETD2, a H3K36 trimethyltransferase, is frequently mutated in human cancers with the highest prevalence (13%) in clear cell renal cell carcinoma (ccRCC). Genomic profiling of primary ccRCC tumors reveals a positive correlation between SETD2 mutations and metastasis. However, whether and how SETD2-loss promotes metastasis remains unclear. Here, we detected SETD2 mutations in 24...
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Carcinoma, Renal CellEpigenesis, GeneticEpithelial CellsGenomicsHistone Chaperones
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [ATAC-seq]
- Authors
- Alonso-Curbelo, DirenaLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. For example, in the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and, ultimately, pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled...
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CarcinogenesisChromatin Immunoprecipitation SequencingEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [Set2]
- Authors
- Alonso-Curbelo, DirenaLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. In the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and ultimately pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled functional...
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CarcinogenesisChromatin Immunoprecipitation SequencingDoxycyclineEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [Set1]
- Authors
- Alonso-Curbelo, DirenaLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. In the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and ultimately pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled functional...
- Subject
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Chromatin Immunoprecipitation SequencingEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [scATAC-Seq]
- Authors
- Alonso-Curbelo, DirenaLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. For example, in the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and, ultimately, pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled...
- Subject
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CarcinogenesisChromatin Immunoprecipitation SequencingEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [ATACSeq_shBrd4]
- Authors
- Alonso-Curbelo, DirenaKoche, Richard PatrickLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. In the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and ultimately pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled functional...
- Subject
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CarcinogenesisChromatin Immunoprecipitation SequencingEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [ATACSeq_rIL33]
- Authors
- Alonso-Curbelo, DirenaKoche, Richard PatrickLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. In the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and ultimately pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled functional...
- Subject
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CarcinogenesisChromatin Immunoprecipitation SequencingEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All