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Expression data from mouse B16-F10 cells treated with heat shock (HS), Lipofectamine 2000 (LA), and benzyl alcohol (BA)

ABSTRACT: Three types of stimuli -- heat shock, Lipofectamine 2000 and benzyl alcohol -- induce activity of some stress genes (hsp) in mouse B16-F10 cells. Besides hsp genes induction, each stimulus causes gene expression changes of different sets of genes. We used microarrays to analyze global gene expression changes in mouse B16-F10 cells treated with elevated temperature (heat shock, HS), with Lipofectamine 2000 (LA) or with 40mM benzyl alcohol (BA).

ORGANISM(S): Mus musculus

PROVIDER: GSE29743 | GEO | 2011/06/04

SECONDARY ACCESSION(S): PRJNA141173

REPOSITORIES: GEO

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Expression data from mouse B16-F10 cells treated with heat shock (HS), Lipofectamine 2000 (LA), and benzyl alcohol (BA)

Project description:Three types of stimuli -- heat shock, Lipofectamine 2000 and benzyl alcohol -- induce activity of some stress genes (hsp) in mouse B16-F10 cells. Besides hsp genes induction, each stimulus causes gene expression changes of different sets of genes. We used microarrays to analyze global gene expression changes in mouse B16-F10 cells treated with elevated temperature (heat shock, HS), with Lipofectamine 2000 (LA) or with 40mM benzyl alcohol (BA). In order to study how lipofection may affect cellular homeostasis, we used Affymetrix microarrays to analyze the whole transcriptome of mouse B16-F10 cells treated with Lipofectamine 2000. To find out which genes are affected, we compared the cells treated with Lipofectamine (LA1, LA2, LA3), the cells treated with 40mM benzyl alcohol (BA1, BA2, BA3), heat-shocked cells (HS1, HS2, HS3) and control, untreated cells (C1-5). RNA was extracted from cells 30 min after treatment.

2011-06-04 | E-GEOD-29743 | biostudies-arrayexpress

Mus musculus

Project description:Expression data from mouse B16-F10 cells treated with heat shock (HS), Lipofectamine 2000 (LA), and benzyl alcohol (BA)

| PRJNA141173 | ENA

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Project description:This is a mathematical model of heat shock protein synthesis induced by an external temperature stimulus. The model consists of a system of nine nonlinear ordinary differential equations describing the temporal evolution of key variables involved in the regulation of HSP synthesis.

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Transcription profiling of mouse model of melanome secreting different amounts of histidine

Project description:We previously showed that transgenic enhancement of histamine production in B16-F10 melanomas strongly supports tumor growth in C57Bl/6 mice (Cancer Res, 2005 Pos et al.). In this array experiment, gene expression profiles of transgenic mouse melanomas, secreting different amounts of histamine, were compared by whole genome microarrays. Experiment Overall Design: By modifying the levels of L-histidine decarboxylase (HDC), the sole enzyme responsible for histamine production, we introduced three novel variants of the B16-F10 mouse melanoma cell line, displaying diminished (B16-F10 HDC-A), unmodified (B16-F10 HDC-M) or enhanced (B16-F10 HDC-S) capacities to produce and secrete histamine. Experiment Overall Design: In this experiment, B16-F10 HDC-A, HDC-M, and HDC-S experimental mouse melanomas were compared by analyzing 6-6 tumors in each group. Experiment Overall Design: In order to reduce the amount of arrays required, equal amounts of randomly chosen RNA sample pairs were pooled in each group, thus, at the end, each group consisted of 3 pooled tumor samples. All samples were biological replicates, no technical replicates or dye swapping were done. Experiment Overall Design: Gene expression patterns of the three tumor groups were compared indirectly, via a common reference samplei n a two-color array design. Arrays shown here represent gene expression patterns of individual tumor samples compared to the reference sample.

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Project description:Mild stress could help cells to survive more severe environmental or pathophysiological conditions. In the current study, we investigated the cellular mechanisms which contribute to the development of stress tolerance upon a prolonged (0-12h) fever-like (40 °C) or a moderate (42.5 °C) hyperthermia in mammalian CHO cells. Our results indicate that mild heat triggers a distinct, dose dependent remodeling of the cellular lipidome followed by the expression of heat shock proteins only at higher heat dosages. A significant elevation in the relative concentration of sat-urated membrane lipid species, specific lysophosphatidylinositol and sphingolipid species sug-gests prompt membrane microdomain reorganization and an overall membrane rigidification in response to the fluidizing heat in a time dependent manner. RNAseq experiments reveal that mild heat initiate endoplasmic reticulum stress-related signaling cascades resulting in lipid re-arrangement and ultimately in an elevated resistance against membrane fluidization by benzyl alcohol. To protect cells against lethal, protein denaturing high temperatures the classical heat shock protein response was required. The different layers of stress response elicited by different heat dosages highlights the capability of cells to utilize multiple tools to gain resistance against or to survive lethal stress conditions.

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

Project description:Heat-Shock Factor 1 (HSF1), master regulator of the heat-shock response, facilitates malignant transformation, cancer cell survival and proliferation in model systems. The common assumption is that these effects are mediated through regulation of heat-shock protein (HSP) expression. However, the transcriptional network that HSF1 coordinates directly in malignancy and its relationship to the heat-shock response have never been defined. By comparing cells with high and low malignant potential alongside their non-transformed counterparts, we identify an HSF1-regulated transcriptional program specific to highly malignant cells and distinct from heat shock. Cancer-specific genes in this program support oncogenic processes: cell-cycle regulation, signaling, metabolism, adhesion and translation. HSP genes are integral to this program, however, even these genes are uniquely regulated in malignancy. This HSF1 cancer program is active in breast, colon and lung tumors isolated directly from human patients and is strongly associated with metastasis and death. Thus, HSF1 rewires the transcriptome in tumorigenesis, with prognostic and therapeutic implications.

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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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The non-canonical small heat shock protein from C. elegans is a molecular aggregase

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