Expression data following mitogen stimulation from Jurkat Cell
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE11118 | GEO | 2009/12/04
SECONDARY ACCESSION(S): PRJNA107015
REPOSITORIES: GEO
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Project description:Gene expression analysis identified 27 of these 744 p300 and pol II associated genes as significantly increased (p? 0.05) within the first hour following mitogen stimulation Experiment Overall Design: Total RNA was purified from Jurkat T-cells treated 0, 30, and 60 min with phorbol ester and ionomycin. Antisense biotin-labeled RNA (aRNA) suitable for application to the Affymetrix microarray platform was generated using the Ambion MessageAmp 2-Biotin Enhanced kit as suggested by the manufacturer (www.Ambion.com). Purified biotin-labeled aRNA was fragmented and hybridized to U133 plus 2 GenechipsTM (Affymetrix), as recommended by the manufacturer. All samples were hybridized as technical replicates. Affymetrix U133 plus 2 GenechipsTM contain probe-sets corresponding to over 56,000 targets.
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Project description:We profiled the dynamic interaction of p300 with proximal promoters of human T cells identified a class of genes that rapidly coassemble p300 and RNA polymerase II following mitogen stimulation. We classified the genes that rapidly coassemble p300 and pol II following mitogen stimulation
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Project description:Acetaminophen (APAP), a widely used analgesic and antipyretic that is considered to be relatively safe at recommended doses, is the leading cause of drug-induced liver failure in the United States. 3M-bM-^@M-^Y-Hydroxyacetanilide (AMAP), a regioisomer of acetaminophen is useful as a comparative tool for studying APAP-induced toxicity since it is non-toxic relative to APAP. TGF-alpha transgenic mouse hepatocytes were treated with both isomers to investigate mitogen-activated protein kinase cascades in order to differentiate their toxicological outcomes. Mitogen-activated protein kinase (MAPK) cascade expression and activation were measured using microarray and Bioplex technologies, respectively. APAP treatment led to c-Jun N-terminal kinase (JNK) activation, whereas AMAP treatment led to the activation of extracellular-signal-regulated protein kinase (ERK). The microarray data suggested APAP treatment may upregulate gene expression at multiple levels of the JNK cascade including a JNK-related scaffold protein. Expression data was related to phosphoprotein levels using the Bioplex system. APAP treatment led to a significant activation of JNK compared to its regioisomer. In contrast, microarray analysis of AMAP showed a slight upregulation of ERK gene activity. Furthermore, Bioplex data showed AMAP treatment led to significant ERK phosphorylation compared to APAP. Cell viability assays confirmed that APAP-induced activation of JNK was related to higher rates of cell death, whereas activation of ERK by AMAP may be cytoprotective. 27 arrays, 9 experimental groups, 2hr AMAP, 2hr APAP, 2hr Control, 6hr AMAP, 6hr APAP, 6hr Control, 24hr AMAP, 24hr APAP, 24hr Control.
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Project description:In mammals, increasing evidence supports the generality of cotranscriptional gene regulation and the idea that genetic control often occurs subsequent to RNA polymerase II (Pol II) recruitment. In our recent experiments, we have used Pol II Chromatin Immunoprecipitation (ChIP) to investigate relationships between the mechanistic events that control acute stress response (ASR) gene activation following stimulation of the alpha1a-Adrenergic Receptor expressed in rat-1 fibroblasts. We validate the temporal accuracy of our Pol II ChIP assay by comparison to major transcriptional events assessable by microarray and PCR analysis of precursor and mature mRNA. Initial temporal microarray analysis of gene activation following agonist addition identified genes that were upregulated and provided a temporal profile of changes in polyadenylated mRNA levels. Combined with PCR analysis of pre-mRNA, total RNA, polyadenylated RNA and the Pol II ChIP data, we demonstrate complex multilevel gene regulation including a diverse set of cotranscriptional mechanisms. Given our data, we propose that analysis of a genes regulation must begin with global assessement of changes in transcriptional behavior to identify events that are actually rate limiting if reductionist mechanistic dissection is to distinguish events that are regulated from the larger set of mechanisms available to most genes.
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