This SuperSeries is composed of the SubSeries listed below.
Parsing the Interferon Transcriptional Network and Its Disease Associations.
Sex, Age, Specimen part, Treatment, Time
View SamplesWe analyze the expression profile of ISGs in the context of IFNAR1-KO primary murine B cells and macrophages. These analses were used to define ISG gene sets that are under tonic control. Furthermore, these analyses enabled the definition of ISGs that are dependent on Tyk2 signaling.
Parsing the Interferon Transcriptional Network and Its Disease Associations.
Sex, Age
View SamplesWe report cell specific responses to IFNg in 11 different peripheral immunocyte populations in the mouse. These cells represent the core ImmGen immunocyte lineage panel. Profiles from these were used to analyze cell specific responses to IFNg. In general a core set of ISG transcripts are induced in all cells. Smaller sets of ISGs were induced in a cell specific manner. In particular, splenic granulocytes and dendritic cells show restriced indcution of sets of ISGs.
Parsing the Interferon Transcriptional Network and Its Disease Associations.
Sex, Age
View SamplesB cells respond robustly to IFNa. Here we analyze gene expression profiles of primary murine splenic B cells treated with 10 fold serially diluted IFNa in vitro. We explore sensitivity to ISGs to IFNa as they relate to dose. Generally ISGs do not cluster significantly in a dose dependent manner. However there are notable spreads in sensitivity to IFNa.
Parsing the Interferon Transcriptional Network and Its Disease Associations.
Sex, Age
View SamplesWe seeked to determine in vivo effects of IFNg and IFNa response in peritoneal cavity macrophages. These cells were part of ImmGen Interferon cytokine study and immunocytes were sorted according to Immgen's standard lineage panel. Profiles from peritoneal cavity macrophages were used to analyze cell specific responses to IFNg.
Parsing the Interferon Transcriptional Network and Its Disease Associations.
Sex, Age, Specimen part, Treatment
View SamplesWe describe finely resolved kinetics of the transcriptional response to IFNa in B cells in vivo. Temporal changes in expression of the most robustly induced ISGs were analyzed across 23 (15min - 15hrs) timepoints. Most ISGs reach peak induction at approximately 2hrs and generally in a synchronus manner. These analses provide insight into the regulatory network structure of IFN responses.
Parsing the Interferon Transcriptional Network and Its Disease Associations.
Sex, Age
View SamplesWe report cell specific responses to IFNa in 11 different peripheral immunocyte populations in the mouse. These cells represent the core ImmGen immunocyte lineage panel. Profiles from these were used to analyze cell specific responses to IFNa. In general a core set of ISG transcripts are induced in all cells. Smaller sets of ISGs were induced in a cell specific manner. In particular, splenic granulocytes and dendritic cells show restriced indcution of sets of ISGs.
Parsing the Interferon Transcriptional Network and Its Disease Associations.
Sex, Age
View SamplesUnlike other terminally differentiated cell types, vascular SMCs display remarkable phenotypic plasticity. The adult, differentiated state is traditionally defined by expression of well-characterized SMC contractile genes. Extracellular cues, however, can induce contractile SMCs to remodel toward a synthetic state characterized by a spectrum of proliferative, migratory, and inflammatory phenotypes.
Integrative genomics identifies DSCR1 (RCAN1) as a novel NFAT-dependent mediator of phenotypic modulation in vascular smooth muscle cells.
Specimen part
View SamplesmicroRNA-126 is a microRNA predominately expressed by endothelial cells and controls angiogenesis. Unexpectedly, we found that mice deficient in miR-126 have a major impairment in their innate response to pathogen-associated nucleic acids, as well as HIV, which results in more widespread cell infection. Further examination revealed that this was due to miR-126 control of plasmacytoid DC (pDC) homeostasis and function, and that miR-126 regulates expression of TLR7, TLR9, NFkB1 and other innate response genes, as well as VEGF-receptor 2 (VEGFR2). Deletion of VEGFR2 on DCs resulted in reduced interferon production, supporting a role for VEGFR2 in miR-126 regulation of pDCs. These studies identify the miR-126/VEGFR2 axis as an important regulator of the innate response that operates through multiscale control of pDCs.
The miR-126-VEGFR2 axis controls the innate response to pathogen-associated nucleic acids.
Age, Specimen part
View SamplesPurpose: The goal of this study is to analyze the transcriptional pathways regulated by Fbxo22 and Keap1 in mouse lung adeno carcinoma cells. Methods: mouse lung adeno carcinoma cells either Keap1 wild type (KP) or mutant (KPK), have been transfected for 3 days with siRNA targeting Fbxo22. Knock down efficiency has been evaluated by western blot (using specific antibody for Fbxo22) and qPCR (using specific oligos for Fbxo22) . Results: The transcriptomic analysis helps us to support our finding that loss of either Keap1 or Fbxo22 induces metastases Overall design: All 12 samples generated by deep sequencing in triplicate
Nrf2 Activation Promotes Lung Cancer Metastasis by Inhibiting the Degradation of Bach1.
Specimen part, Subject
View Samples