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Gene expression analysis of murine peritoneal macrophages deficient for SAMHD1 and IFNAR

ABSTRACT: To investigate the contribution of type-1 IFN signalling to the upregulation of IFN- stimulated genes in SAMHD1-deficient cells, we performed global gene expression analysis of SAMHD1-deficient IFNAR-/- macrophages.

ORGANISM(S): Mus musculus

PROVIDER: GSE45358 | GEO | 2013/07/01

SECONDARY ACCESSION(S): PRJNA193592

REPOSITORIES: GEO

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Gene expression analysis of murine peritoneal macrophages deficient for SAMHD1 and IFNAR

Project description:To investigate the contribution of type-1 IFN signalling to the upregulation of IFN- stimulated genes in SAMHD1-deficient cells, we performed global gene expression analysis of SAMHD1-deficient IFNAR-/- macrophages. Peritoneal macrophages from ten SAMHD1-deficient IFNAR-/- and six SAMHD1-deficient controls were FACS sorted. RNA was subjected to next generation mRNA sequencing.

2013-07-01 | E-GEOD-45358 | biostudies-arrayexpress

Gene expression analysis of murine SAMHD1 deficient peritoneal macrophages

2012-12-01 | GSE37236 | GEO

Gene expression analysis of murine SAMHD1 deficient peritoneal macrophages

Project description:To elucidate responses of myeloid cells to SAMHD1 deficiency in the absence of exogenous viral infection, we performed global gene expression analysis of SAMHD1 deficient macrophages. Peritoneal macrophages from nine mutants and nine controls were FACS sorted. Cells from three animals were pooled to yield three poolls per group. RNA from these pools was subjected to next generation mRNA sequencing

2012-12-01 | E-GEOD-37236 | biostudies-arrayexpress

Gene expression analysis of murine SAMHD1 deficient peritoneal macrophages (S1056 to S1075)

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Gene expression analysis of murine SAMHD1 deficient peritoneal macrophages (S1056 to S1075)

Project description:To elucidate responses of myeloid cells to SAMHD1 deficiency in the absence of exogenous viral infection, we performed global gene expression analysis of SAMHD1 deficient macrophages. Peritoneal macrophages from 10 mutants and 10 controls were FACS sorted. Isolated RNA was subjected to next generation mRNA sequencing.

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Analysis of transcriptional differences between ZIKV-infected Ifnar-/- and Ifnar+/- placentas

Project description:Purpose: While type I interferons (IFN) are important for control of viral replication, we see that, upon infection of Ifnar-/- females were crossed to Ifnar+/- males with ZIKV, only Ifnar+/- fetuses are resorbed or develop severe growth restriction. To identify how IFN may be altering placenta development, we performed RNAsequencing on infected and uninfected Ifnar-/- and Ifnar+/- placentas. Methods: Ifnar-/- females were crossed to Ifnar+/- males and infected intravaginally with Cambodian ZIKV at E5.5. Placentas were harvested from infected and uninfected pregnant dams at E10.5. Results/ Conclusions: Comparison of ZIKV-infected Ifnar-/- and Ifnar+/- shows an elevated interferon stimulated gene (ISG) signature in Ifnar+/- placentas but does not reveal any underlying developmental defects that may be causing defects in placenta development.

2017-12-31 | GSE98423 | GEO

Adipose tissue RNAseq in T-cell-specific IFNAR-deficient mice.

Project description:We sequenced whole adipose tissue from control and LCMV infected mice 6dpi, in control vs T cell-specific IFNAR knockoutmice to understand the transcriptional changes in adipose tissue upon loss of type I IFN-T cell singaling axis, and how it contributes to cachexia.

2019-05-31 | GSE118819 | GEO

Gene expression changes in different clones of SAMHD1 knock-out (KO) cells

Project description:To investigate the signalling pathways affected by SAMHD1 depletion, whole transciptome profiling was performed in WT and in different clones of SAMHD1-KO breast cancer cell line (T47D cells)

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Adipose tissue RNAseq in T-cell-specific IFNAR-deficient mice.

Project description:Adipose tissue RNAseq in T-cell-specific IFNAR-deficient mice.

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WT and IFN-I receptor deficient mouse macropahge expression profiling under virus infection or under IFNb stimulation

Project description:To investigate the role of lncRNAs in viral infection and their relationship with the IFN-I system, we profiled lncRNA expression in wild type (WT) and IFN-I receptor deficient (Ifnar-/-) cells infected with or without vesicular stomatitis virus (VSV).

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