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The function of ERRalpha in viral infection

ABSTRACT: To explore the function of ERRalpha in viral infection, we compared the cDNA expression profile of ERRalpha knockdown 293T cells and control 293T cells. The cells infected with VSV for 12 h or left uninfected were collected and RNA was extracted by Trizol.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69661 | GEO | 2015/06/09

SECONDARY ACCESSION(S): PRJNA286119

REPOSITORIES: GEO

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The function of ERRalpha in viral infection

Project description:To explore the function of ERRalpha in viral infection, we compared the cDNA expression profile of ERRalpha knockdown 293T cells and control 293T cells. The cells infected with VSV for 12 h or left uninfected were collected and RNA was extracted by Trizol. Viral infection induced gene expression in ERRalpha knockdown 293T cells or control 293T cells were measured at 0 and 12 hours.

2015-06-09 | E-GEOD-69661 | biostudies-arrayexpress

ERRalpha mediates metabolic adaptations that drive lapatinib resistance in breast cancer (ERRalpha binding profiles in breast cancer cells by ChIP-seq)

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ERRalpha mediates metabolic adaptations that drive lapatinib resistance in breast cancer (gene expression profiles)

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ERRalpha mediates metabolic adaptations that drive lapatinib resistance in breast cancer (ERRalpha binding profiles in breast cancer cells by ChIP-seq)

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ERRalpha mediates metabolic adaptations that drive lapatinib resistance in breast cancer (gene expression profiles)

Project description:Ablation of ERRalpha significantly delays ERBB2-induced mammary tumorigenesis and ERRalpha regulates genes of the ERBB2 amplicon. To further investigate the relationship between ERRalpha activity and RTK signaling, we depleted ERRalpha in SKBr3 cells upon serum starvation, EGF treatment or heregulin treatment. Inhibition of ERBB2 signaling using the RTK inhibitor lapatinib impacts on ERRalpha stability. Since we have shown that the development of lapatinib-resistance restaures the expression of ERRalpha in breast cancer cells, we performed depletion of ERRalpha in SKBr3 cells that have developped resistance to lapatinib treatment in order to identify a potential reprogramming of ERRa transcriptional activity associated to lapatinib resistance, For the study of growth factor effec on ERRalpha activity, total RNA was obtained from human SKBr3 breast cancer cells cultured in DMEM deprived of FBS (starved) for 24 hours and treated with PBS, EGF (100uM) or Heregulin (100uM) for an additional 24h. Cells were transfected with siRNA against ERRalpha or with siControl for 60 hours prior to harvesting. For the effect of ERRalpha in lapatinib resistance cells, parental SKBr3 cells (pSKBr3) and Lapatinib-resistant cells (LRSKBr3, maintained in 2uM lapatinib) were transfected with siControl (siC) or siERRalpha for 60 hours prior to harvesting and RNA extraction

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Project description:PGC-1 transcription factor was customized to limit its interations to ERRalpha. This mutant (2x9) was used to dissect the transcription activation patterns that are attributable to the PGC1-ERR interaction and PGC-1 actions that are independent of ERR. Inactive mutant with the deleted LLXXL motifs (L2L3) and wt PGC-1 were used as negative and positive controls respectively. BGAL-expressing construct was used to control for non-specific effects of adenoviral infection. Keywords: ERRalpha, PGC-1alpha, nuclear receptor, orphan nuclear receptor, coactivator, transcription factors

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Transcription profiling of mouse hearts from mutants lacking estrogen-related receptor alpha (ERRalpha), a nuclear receptor

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Expression data from uninfected and VSV-infected Drosophila cells at 4 hours post-infection

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