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Treatment of heat shocked HeLa cells with siRNA (siHSF1#1)

ABSTRACT: Although HSF1 is known to play an important role in regulating the cellular response to proteotoxic stressors, little is known about the structure and function of the HSF1 signaling network under both stressed and unstressed conditions. In this study, we used a combination of chromatin immunoprecipitation (ChIP) microarray analysis and time course gene expression microarray analysis with and without siRNA-mediated inhibition of HSF1 comprehensively identify genes directly and indirectly regulated by HSF1 and examine the structure of the extended HSF1 signaling network. Correlation between promoter binding and gene expression was not significant for all genes bound by HSF1 suggesting that HSF1 binding per se is not sufficient for expression. However, the correlation with promoter binding was significant for genes identified as HSF1-regulated following siRNA knockdown allowing the identification of direct transcriptional targets of HSF1. Among promoters bound by HSF1 following heat shock, a gene ontology (GO) analysis showed significant enrichment only in categories related to protein folding. In contrast, analysis of the extended HSF1 signaling network showed enrichment in a variety of categories related to protein folding, anti-apoptosis, RNA splicing, ubiquitination and others, highlighting a complex transcriptional program directly and indirectly regulated by HSF1. Keywords: Time Course, Heat Shock, siRNA

ORGANISM(S): Homo sapiens

PROVIDER: GSE3697 | GEO | 2006/02/05

SECONDARY ACCESSION(S): PRJNA93845

REPOSITORIES: GEO

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Transcription profiling of human heat shocked HeLa cell line with siRNA knockdown of HSF1

Project description:Although HSF1 is known to play an important role in regulating the cellular response to proteotoxic stressors, little is known about the structure and function of the HSF1 signaling network under both stressed and unstressed conditions. In this study, we used a combination of chromatin immunoprecipitation (ChIP) microarray analysis and time course gene expression microarray analysis with and without siRNA-mediated inhibition of HSF1 comprehensively identify genes directly and indirectly regulated by HSF1 and examine the structure of the extended HSF1 signaling network. Correlation between promoter binding and gene expression was not significant for all genes bound by HSF1 suggesting that HSF1 binding per se is not sufficient for expression. However, the correlation with promoter binding was significant for genes identified as HSF1-regulated following siRNA knockdown allowing the identification of direct transcriptional targets of HSF1. Among promoters bound by HSF1 following heat shock, a gene ontology (GO) analysis showed significant enrichment only in categories related to protein folding. In contrast, analysis of the extended HSF1 signaling network showed enrichment in a variety of categories related to protein folding, anti-apoptosis, RNA splicing, ubiquitination and others, highlighting a complex transcriptional program directly and indirectly regulated by HSF1.,SUBMITTER_CITATION: Genome-wide analysis of human HSF1 signaling reveals a transcriptional program linked to cellular adaptation and survival Authors: Todd J. Page, Devanjan Sikder, Longlong Yang, Linda Pluta, Russell D. Wolfinger, Thomas Kodadek, and Russell S. Thomas Journal: Molecular Biosystems 2:627-639

2007-06-22 | E-GEOD-3697 | biostudies-arrayexpress

Sivery2016 - A mammalian heat shock response model

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2022-01-25 | MODEL2201210001 | BioModels

Effect of 4-Hydroxynonenal on gene expression. Comparison of HSF1-siRNA silenced vs control cells

Project description:4-Hydroxynonenal (HNE), a cytotoxic and diffusible electrophile generated by the spontaneous decomposition of oxidized lipids, has a suspected role in neurodegenerative and inflammatory disease processes. In addition to promoting cell death, elevated levels of HNE lead to the engagement of cytoprotective signaling pathways, including the heat shock, antioxidant, DNA damage, and ER stress responses. Activation of the heat shock response, mediated by the transcription factor heat shock factor 1 (HSF1), is critical for maintaining cellular viability in the presence of HNE. Accordingly, silencing HSF1 expression using siRNA enhances the toxicity of HNE. Microarray analysis of samples from control and HSF1-silenced cells was performed to investigate which associated changes in gene could be responsible for the decrease in cellular viability. Four different experimental conditions were investigated. Samples were prepared and analyzed in triplicate. Samples 1-3 received NEG control siRNA and DMSO (vehicle) for 6 h. Samples 4-6 received NEG control siRNA and 50 uM HNE for 6 h. Samples 7-9 received HSF1 siRNA and DMSO (vehicle) for 6 h. Samples 10-12 received HSF1 siRNA and 50 uM HNE for 6 h.

2010-09-15 | E-GEOD-12762 | biostudies-arrayexpress

HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers [ChIP-Seq]

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2012-08-07 | E-GEOD-38901 | biostudies-arrayexpress

HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers [gene expression]

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HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers [ChIP-Seq]

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Genetic and Epigenetic Determinants Establish a Continuum of Hsf1 Occupancy and Activity Across the Yeast Genome

Project description:We performed ChIP-seq of Hsf1 under non heat shock, 5-minute heat shock and 120 minute heat shock conditions. We used the conditional chemical genetics approach known as “anchor away” (AA) to rapidly inactivate Hsf1. We coupled Hsf1-AA to and nascent RNA seq (NAC)-seq to define the genes whose expression depends on Hsf1 during heat shock.

2018-07-26 | GSE117653 | GEO

HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers [gene expression]

2012-08-06 | E-GEOD-38232 | biostudies-arrayexpress

HSF1 Activation Can Restrict HIV Replication

Project description:Host protein folding stress responses can play important roles in RNA virus replication and evolution. Intriguingly, prior work revealed a complicated interplay between the cytosolic proteostasis stress response, controlled by its master regulator heat shock factor 1 (HSF1) and human immunodeficiency virus-1 (HIV-1). We sought to isolate HSF1 transcription factor activity from proteostasis stress and elucidate the function of HSF1 in HIV-1 lifecycle in absence of cellular stress. We used chemical genetic, stress-independent control of HSF1 activity to establish whether and how HSF1 influences HIV-1 replication. Stress-independent HSF1 induction decreased both the total quantity and infectivity of HIV-1 virions. Moreover, HIV-1 was unable to escape HSF1-mediated restriction over the course of several serial passages. These results promote continued consideration of the heat shock response as a potential target for antiviral drugs.

2022-01-30 | GSE137591 | GEO

Effect of 4-Hydroxynonenal on gene expression. Comparison of HSF1-siRNA silenced vs control cells

2008-10-01 | GSE12762 | GEO

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