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accession-icon GSE2362
Altered hepatic gene expression in liver-Cpr-null and Cpr-low mice
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

NADPH-cytochrome P450 reductase (CPR) is important for the functions of many enzymes, such as microsomal cytochrome P450 (P450) monooxygenases and heme oxygenases. Two mouse models with deficient CPR expression in adults were recently generated in this laboratory: liver-Cpr-null (with liver-specific Cpr deletion) (Gu et al., J. Biol. Chem., 278, 2589525901, 2003) and Cpr-low (with reduced CPR expression in all organs examined) (Wu et al. J. Pharmacol. Expt. Ther. 312, 35-43, 2005). The phenotypes included a reduced serum cholesterol level and an induction of hepatic P450 in both models, and hepatomegaly and fatty liver in the liver-Cpr-null mouse alone. Our aim was to identify hepatic gene-expression changes related to these phenotypes. Cpr-lox mice, which have normal CPR expression (Wu et al., Genesis, 36, 177-181, 2003.), were used as the control in microarray analysis. A detailed analysis of the gene-expression changes in lipid metabolism and transport pathways revealed potential mechanisms, such as an increased activation of constitutive androstane receptor (CAR) and a decreased activation of peroxisomal proliferators activated receptor alpha (PPAR-gamma) by precursors of cholesterol biosynthesis, that underlie common changes (e.g., induction of multiple P450s and inhibition of genes for fatty acids metabolism) in response to CPR-loss in the two mouse models. Moreover, we also uncovered model-specific gene-expression changes, such as the induction of a lipid translocase (CD36 antigen) and the suppression of carnitine O-palmitoyltransferase 1 (CPT1a) and acyl-CoA synthetase long-chain family member 1 (Acsl1), that are potentially responsible for the severe hepatic lipidosis observed in liver-Cpr-null, but not Cpr-low mice.

Publication Title

Hepatic gene expression changes in mouse models with liver-specific deletion or global suppression of the NADPH-cytochrome P450 reductase gene. Mechanistic implications for the regulation of microsomal cytochrome P450 and the fatty liver phenotype.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE31774
Effect of loss of function of Gal11/Med15 and Med3 from the Mediator tail module in budding yeast
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Gene expression was compared for wild type yeast (BY4741) and yeast lacking Gal11/Med15 and Med3, or from a gal11-myc med3 strain. The gal11-myc allele shows a partial loss of function when combined with med3. Expression was analyzed for yeast grown in YPD as well as in CSM.

Publication Title

Distinct role of Mediator tail module in regulation of SAGA-dependent, TATA-containing genes in yeast.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE1639
Rpd3 and histone H3 and H4 deletions/mutations
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Signal intensity data for rpd3 delete, H3delta(1-28), H3(K4,9,14,18,23,27Q), H4delta(2-26), H4(K5,8,12,16Q), rpd3 delete H3delta(1-28), and rpd3 delete H4(K5,8,12,16Q) yeast grown in rich (YPD) media

Publication Title

Genome-wide analysis of the relationship between transcriptional regulation by Rpd3p and the histone H3 and H4 amino termini in budding yeast.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17638
The Ess1 prolyl isomerase is required for the transcription termination of small non-coding RNAs via Nrd1 pathway
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Genome-wide studies have identified abundant small, non-coding RNAs including snRNAs, snoRNAs, cryptic unstable transcripts (CUTs), and upstream regulatory RNAs (uRNAs) that are transcribed by RNA polymerase II (pol II) and terminated by a Nrd1-dependent pathway. Here, we show that the prolyl isomerase, Ess1, is required for Nrd1-dependent termination of ncRNAs. Ess1 binds the carboxy terminal domain (CTD) of pol II and is thought to regulate transcription by conformational isomerization of Ser-Pro bonds within the CTD. In ess1 mutants, expression of ~10% of the genome was altered, due primarily to defects in termination of snoRNAs, CUTs, SUTs and uRNAs. Ess1 promoted dephosphorylation of Ser5 (but not Ser2) within the CTD, most likely by the Ssu72 phosphatase, and we provide evidence for a competition between Nrd1 and Pcf11 for CTD-binding that is regulated by Ess1-dependent isomerization. This is the first example of a prolyl isomerase required for interpreting the CTD code.

Publication Title

The Ess1 prolyl isomerase is required for transcription termination of small noncoding RNAs via the Nrd1 pathway.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE4135
Wild type yeast and H3del(1-28) and H4del(2-26) yeast grown in complete synthetic media
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Yeast lacking the H3 or H4 amino termini, and corresponding wild type strains, were grown in synthetic media. These conditions induce Gcn4-activated transcription.

Publication Title

Contribution of the histone H3 and H4 amino termini to Gcn4p- and Gcn5p-mediated transcription in yeast.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6073
Rap1 and Abf1 DNA-binding ts mutants and wild type after 1 hr at 37 C
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Abf1 and Rap1 are General Regulatory Factors that contribute to transcriptional activation of a large number of genes, as well as to replication, silencing, and telomere structure in yeast. In spite of their widespread roles in transcription, the scope of their functional targets genome-wide has not been previously determined. We have used microarrays to examine the contribution of these essential GRFs to transcription genome-wide, by using ts mutants that dissociate from their binding sites at 37 C. We combined this data with published ChIP-chip studies and motif analysis to identify probable direct targets for Abf1 and Rap1. We also identified a substantial number of genes likely to bind Rap1 or Abf1, but not affected by loss of GRF binding. Interestingly, the results strongly suggest that Rap1 can contribute to gene activation from farther upstream than can Abf1. Also, consistent with previous work, more genes that bind Abf1 are unaffected by loss of binding than those that bind Rap1. Finally, we showed for several such genes that the Abf1 C-terminal region, which contains the putative activation domain, is not needed to confer this peculiar "memory effect" that allows continued transcription after loss of Abf1 binding.

Publication Title

Genome-wide analysis of transcriptional dependence and probable target sites for Abf1 and Rap1 in Saccharomyces cerevisiae.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26056
Expression data from lateral nasal gland of male B6, 129/Sv and Cyp2g1-null mice
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

In male Cyp2g1-null mice, the lateral nasal gland, one of the largest anterior glands in the nasal cavity, was found to be protected from acetaminophen toxicity. The goal of this study was to identify the genes that are involved in the mechanisms, especially those genes functional in drug metabolism, clearance and post-activation events.

Publication Title

A novel defensive mechanism against acetaminophen toxicity in the mouse lateral nasal gland: role of CYP2A5-mediated regulation of testosterone homeostasis and salivary androgen-binding protein expression.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE71816
Transcriptional dysregulation of inflammatory/immune pathways after active vaccination against Huntingtons disease
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Transcriptome profiling of spleens from the triple peptide-immunized cohort showed substantial HD-specific differences including differential activation of genes associated with innate immune responses, absence of negative feedback control of gene expr

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon SRP167336
Transcriptome analysis of tumors that develop in mice following injection of AGS cell lines
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

RNA-seq study of tumors that develop in mice after injection of gastric carcinoma cell line, AGS, with or without Epstein-Barr virus infection

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Disease, Cell line

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accession-icon E-MEXP-1158
Transcription profiling of mouse embryonic stem cells and primordial germ cells to identify genes up-regulated in pluripotent cells
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Understanding the transcriptional regulation of pluripotent cells is of fundamental interest and will greatly inform efforts aimed at directing differentiation of embryonic stem (ES) cells or reprogramming somatic cells. We first analyzed the transcriptional profiles of mouse ES cells and primordial germ cell (PGCs) and identified genes up-regulated in pluripotent cells both in vitro and in vivo. These genes are enriched for roles in transcription, chromatin remodeling, cell cycle and DNA repair. We developed a novel computational algorithm, CompMoby, which combines analyses of sequences both aligned and non-aligned between different genomes with a probabilistic segmentation model to systematically predict short DNA motifs that regulate gene expression. CompMoby was used to identify conserved over-represented motifs in genes up-regulated in pluripotent cells. We show that the motifs are preferentially active in undifferentiated mouse ES and Embryonic Germ cells in a sequence-specific manner, and that they can act as enhancers in the context of an endogenous promoter. Importantly, the activity of the motifs is conserved in human ES cells. We further show that the transcription factor NF-Y specifically binds to one of the motifs, is differentially expressed during ES cell differentiation and is required for ES cell proliferation. This study provides novel insights into the transcriptional regulatory networks of pluripotent cells. Our results suggest that this systematic approach can be broadly applied to understanding transcriptional networks in mammalian species.

Publication Title

Systematic identification of cis-regulatory sequences active in mouse and human embryonic stem cells.

Sample Metadata Fields

Age, Specimen part, Time

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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