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Gene expression profile changes in HDAC6 knockdown HT1080 cells cells after TLR3 stimulation

ABSTRACT: TLR3 stimulation by extracellular dsRNA (e.g. polyIC) induces expression of numerous genes. The knockdown of HDAC6 prior to TLR3 stimulation leads to an ablation of expression of IRF-3-dependent genes. Total RNA extracted from HT1080 cells expressing control-shRNA or HDAC6-shRNA, after 6 h of treatment with dsRNA (polyIC), compared to untreated controls

ORGANISM(S): Homo sapiens

SUBMITTER: Ganes Sen

PROVIDER: E-GEOD-43218 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Inhibition of viral pathogenesis and promotion of the septic shock response to bacterial infection by IRF-3 are regulated by the acetylation and phosphorylation of its coactivators.

Chattopadhyay Saurabh S Fensterl Volker V Zhang Ying Y Veleeparambil Manoj M Wetzel Jaime L JL Sen Ganes C GC

mBio 20130326 2

Interferon (IFN) is required for protecting mice from viral pathogenesis; reciprocally, it mediates the deleterious septic shock response to bacterial infection. The critical transcription factor for IFN induction, in both cases, is IRF-3, which is activated by TLR3 or RIG-I signaling in response to virus infection and TLR4 signaling in response to bacterial infection. Here, we report that IRF-3's transcriptional activity required its coactivators, β-catenin and CBP, to be modified by HDAC6-medi ...[more]

PMID: 23532979

Similar Datasets

Gene expression profile changes in HDAC6 knockdown HT1080 cells cells after TLR3 stimulation

Project description:TLR3 stimulation by extracellular dsRNA (e.g. polyIC) induces expression of numerous genes. The knockdown of HDAC6 prior to TLR3 stimulation leads to an ablation of expression of IRF-3-dependent genes.

2013-12-31 | GSE43218 | GEO

Gene expression profile changes in PKC-inhibitor-pretreated HT1080 cells cells after TLR3 stimulation

Project description:TLR3 stimulation by extracellular dsRNA (e.g. polyIC) induces expression of numerous genes. The inhibition of PKC by Go6976 prior to TLR3 stimulation leads to an ablation of expression of IRF-3-dependent genes. Total RNA extracted from HT1080 cells with or without 1 h pretreatment with 5 uM Go6976, after 6 h of treatment with dsRNA (polyIC), compared to untreated controls

2013-04-03 | E-GEOD-43217 | biostudies-arrayexpress

Gene expression profile changes in PKC-inhibitor-pretreated HT1080 cells cells after TLR3 stimulation

2013-04-03 | GSE43217 | GEO

Assessment of the impact of the TLR3 L412F variant in terms of TLR3-sensitive transcript induction

Project description:we assessed the impact of TLR3 L412F at endogenous cellular levels upon double stranded RNA (dsRNA) stimulation, by performing RNA-sequencing in primary fibroblasts from individuals homozygous for the ancestral allele (n =2) or homozygous for TLR3 L412F (n = 4) upon extracellular Poly(I:C) stimulation that activates the TLR3 pathway. The average response of TLR3 L412F homozygotes was significantly decreased (mean Δ log2 fold-change = 0.93; Wilcoxon p <10-16) compared to that of cells with the ancestral allele, approaching that of TLR3-deficient cells, used as negative control.

2023-01-13 | GSE216304 | GEO

Homo sapiens

Project description:Gene expression profile changes in HDAC6 knockdown HT1080 cells cells after TLR3 stimulation

| PRJNA184997 | ENA

Complete TLR3 deficiency

Project description:The objective of this study is to study the Toll-like receptor 3 (TLR3)-dependent gene expression in human fibroblast cells and peripheral blood mononuclear cells (PBMCs) Fibroblast cells and PBMCs from donors with autosomal recessive (AR) complete TLR3 deficiency and autosomal dominant (AD) partial TLR3 deficiency were collected for microarray analysis to measure the transcriptional responsiveness of TLR3 in fibroblast and PBMCs. A total of 3 healthy controls, 1 AD TLR3-deficient patient, 1 AR TLR3-deficient patient, 1 AR UNC-93B-deficient patient, 1 MyD88 deficient patien were used in this study. The fibroblast cells were cultured in DMEM medium supplemented with 10% fetal calf serum (FCS). The PBMCs were cultured in RPMI medium complemented with 10% FCS. Different kinetics (2 hours and 8 hours) of poly(I:C) (25ug/ml, purchased from Amersham) stimulations were performed, aiming to define TLR3-inducible genes in these human cells. A stimulation of IL-1β (20ng/ml, purchased from R&D system Inc.) was used as a positive activation control with same kinetics of stimulations. A total of one million cells per stimulation were used for fibroblasts, and around 1.5 million cells per stimulation for PBMCs.

2011-11-02 | E-GEOD-30951 | biostudies-arrayexpress

Hdac6 is a stem-cell specific modulator of Tip60-p400 function (gene expression)

Project description:To identify the functional role of Hdac6 in embryonic stem cells, we examined gene expression changes in mouse ES cells upon Tip60, Hdac6 and double knockdown. Two biological replicates each for control (GFP), Tip60, Hdac6 and double KD in E14 mouse ESCs. Lentiviral-based shRNA was used and gene expression changes were determined 3 days after KD. The global gene expression profiles of Tip60, Hdac6 and double KD were compared to control KD cells.

2013-11-20 | E-GEOD-42208 | biostudies-arrayexpress

TLR3, TLR7, and TLR9 stimulation in murine dorsal root ganglion neurons

Project description:TLR3, TLR7, and TLR9 stimulation induces many mouse inflammatory and autoimmune cytokines or immune receptors

2011-03-02 | GSE27579 | GEO

TLR3, TLR7, and TLR9 stimulation in murine dorsal root ganglion neurons

Project description:TLR3, TLR7, and TLR9 stimulation induces many mouse inflammatory and autoimmune cytokines or immune receptors DRGN were cultures 5 days prior to a 16 hour stimulation - Three separate studies were analyzed for inflammatory response

2011-03-02 | E-GEOD-27579 | biostudies-arrayexpress

Hdac6 regulates Tip60-p400 function in stem cells (sequencing)

Project description:The Tip60 (also known as Kat5) lysine acetyltransferase functions broadly as a transcriptional co-activator that acetylates histones. In contrast, Tip60 functions in embryonic stem cells (ESCs) both to silence genes that promote differentiation and to activate genes required for proliferation. The mechanism by which Tip60 functions as a repressor is unknown. Here we show that the class II histone deacetylase Hdac6 co-purifies with Tip60-p400 complex from ESCs and is necessary for complete silencing of most differentiation genes targeted by Tip60. In contrast to differentiated cells, where Hdac6 is mainly cytoplasmic and does not interact with Tip60, Hdac6 is largely nuclear in ESCs and neural stem cells (NSCs) and interacts with Tip60-p400 in both cell types. Hdac6 is enriched at promoters bound by Tip60-p400 in ESCs, but while Tip60 binds on both sides of transcription start sites (TSSs), Hdac6 binding overlaps with only the downstream Tip60 peak. Surprisingly, Hdac6 does not deacetylate histones at these sites, but rather is required for Tip60 binding. These data suggest that nuclear exclusion of Hdac6 during differentiation plays a major role in modulation of Tip60-p400 function. We determined the genome-wide localization of Tip60 and Hdac6 in mouse ES cells, and examined genomic binding profiles of Tip60 and Hdac6 upon indicated knockdown by ChIP-seq. We examined genomic binding profiles of p400 upon indicated knockdown by ChIP-seq.

2013-11-20 | E-GEOD-42209 | biostudies-arrayexpress

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