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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Med1 overexpression induces cell proliferation

ABSTRACT: Med1 overexpression leads to induction of a wide spectrum of genes. Adenovirally-driven overexpression of Med1 in mouse liver stimulates hepatocyte DNA synthesis with enhanced expression of DNA replication, cell cycle control and liver specific genes as observed at day 3 and day 5 post injection. Med1 gene is amplified in a number of cancers so in this study we tested the hypothesis that Med1 by itself has the capacity to induce cell proliferation. Analysis of the Med1- induced gene expression showed a robust induction of a wide spectrum of genes involved in hepatocellular proliferation. Med1 floxed mice (Med1fl/fl) were injected with Ad-His-Med1 (adenovirus expressing Med1 gene) via tail vein and killed 3 or 5 days after injection. Ad-LacZ (adenovirus expression beta-galactosidase gene) injected mouse liver served as control. Total RNA were isolated from the liver and subjected to the microarray.

ORGANISM(S): Mus musculus

SUBMITTER: Navin Viswakarma

PROVIDER: E-GEOD-48950 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Med1 overexpression induces cell proliferation

Project description:Med1 overexpression leads to induction of a wide spectrum of genes. Adenovirally-driven overexpression of Med1 in mouse liver stimulates hepatocyte DNA synthesis with enhanced expression of DNA replication, cell cycle control and liver specific genes as observed at day 3 and day 5 post injection. Med1 gene is amplified in a number of cancers so in this study we tested the hypothesis that Med1 by itself has the capacity to induce cell proliferation. Analysis of the Med1- induced gene expression showed a robust induction of a wide spectrum of genes involved in hepatocellular proliferation.

2013-07-18 | GSE48950 | GEO

Expression data from PDK4 overexpressing (Ad-PDK4 infected) and control (Ad-control infected) mouse liver

Project description:We identified PDK4 as a gene with adaptive transcriptional response to chemical stress. Although PDK4 is an energy resource regulator induced by starvation, expression of other fasting-inducible genes was unaffected, indicating additional physiological role of PDK4 for liver adaptation to the chemical stress. We used microarrays to determine genes with altered transcriptional level by PDK4 overexpression. Mice were infected with Ad-control (empty adenovirus vector) or Ad-PDK4 (PDK4 overexpressing adenovirus vector) at a dose of 10^9 PFU/mouse by tail vein injection. 3 days after the infection, mice were sacrificed for RNA preparation from the liver. Ad-control infected = 4, Ad-PDK4 infected = 3. Specimens from mice of each group were pooled, and 10 ug RNA from each pool was used for cRNA synthesis.

2010-12-25 | E-GEOD-22534 | biostudies-arrayexpress

Expression data from mouse liver over-expressing either GFP alone or biotinylated-TRb1 and GFP

Project description:We over-expressed biotinylated-thyroid hormone receptor beta 1 (TRb1) in mouse liver using an adenovirus in order to perform ChIP-seq experiments. These microarrays were performed to determine gene expression changes in response to tri-iodothyronine (thyroid hormone; T3) stimulation. A control GFP adenovirus was used and gene expression from these livers was also done as a comparison. We performed microarrays from Ad-GFP-infected propylthiouracil (PTU)-fed livers injected with either saline or T3 and Ad-TRb1-GFP infected livers injected with either saline or T3. RNA was extracted from livers of biotin ligase (BirA)-expressing mice that had been infected with either Ad-GFP or Ad-TRb1, fed with PTU for 3 weeks followed by saline or T3 injections for 4 consecutive days.

2013-12-18 | E-GEOD-52433 | biostudies-arrayexpress

Ablation of coactivator Med1 regulates bulge keratinocyte stem cells and accelerates epidermal regeneration after injury [skin wound]

Project description:Transcriptional coactivator Mediator complex facilitates transcription of various transcription factors. Previously, we have generated Med1 conditional null mice, where a critical subunit of Mediator, Med1, is removed from keratinocytes. Here we present evidence that ablation of Med1 accelerated epidermal regeneration after injury. As bulge keratinocyte stem cells are important contributors to regenerate epidermis, we first analyzed properties of stem cells in Med1 null mice. BrdU long retaining analysis revealed that deletion of Med1 still maintained quiescence of bulge keratinocyte stem cells, despite of general hyperplasia observed in Med1 deficient keratinocytes. Gene expression analysis demonstrated that a series of niche matrix proteins decreased in Med1 deficient keratinocytes. In contrast, the expression of stem cell marker Sox9 was not altered, suggesting stem cells are present but activated because of abnormal niche surrounding stem cells. In addition, Med1 deletion suppressed injury induced inflammatory reaction, which indirectly regulates epidermal regeneration. We also indicated that TGFβ1 significantly decreased in both bulge and epidermal keratinocytes upon Med1 deletion. Our study demonstrates that coactivator Med1 has a critical role to maintain bulge stem cells and epidermal regeneration presumably through regulation in TGFβ signaling. n=3 WT and KO (each sample contain RNA isolated from wounded or nonwounded skins excised from 3 mice)

2014-01-01 | E-GEOD-50670 | biostudies-arrayexpress

Expression data from mouse liver over-expressing either GFP alone or biotinylated-TRb1 and GFP

2013-12-18 | GSE52433 | GEO

Transcriptome profiling of MED1 wild-type and knockout human pre-B ALL cell line 697 (RNA-seq)

Project description:CRISPR/Cas9 system was used to generate mediator complex subunit 1 (MED1) knockout human pre-B ALL cell line 697. RNA-seq was performed to observe the effects of MED1 deletion on gene expression in 697.

2020-05-13 | E-MTAB-8178 | biostudies-arrayexpress

Ablation of coactivator Med1 switches the cell fate of dental epithelia to that generating hair [mixed stage]

Project description:Cell fate is defined by specific transcriptional program. Here, we provide evidence that the transcriptional coactivator, Mediator 1 (MED1), is critical in determining the cell fate of ectodermal epithelia. MED1 ablation disrupted enamel formation and generated hair adjacent to the incisors. Deletion of MED1 altered the differentiation of dental epithelia to one expressing epidermal and hair genes similar to the skin. The cellular switch from dental to epidermal/hair lineage was characterized by abnormalities in MED1 deficient dental epithelial stem cells residing in cervical loop. MED1 deficiency caused a failure of dental epithelial stem cells to commit to the dental stratum intermedium regulated by Notch signaling. Instead, MED1 deficient cells retained stem cell potentials expressing Sox2. These cells were eventually adopted an epidermal fate probably through calcium provided through capillary networks, which is originally utilized for enamel formation. Our results demonstrate that MED1 regulates Sox2/Notch1 regulated cell lineage determination in dental epithelia. Our study also shows a potential to regenerate hairs by using genetically engineered dental tissues or cells outside of the skin. n=3 WT and KO (each sample contain dissected dental tissues from 3 mice combined)

2013-09-23 | E-GEOD-50503 | biostudies-arrayexpress

Ablation of coactivator Med1 switches the cell fate of dental epithelia to that generating hair [maturation stage]

Project description:Cell fate is defined by specific transcriptional program. Here, we provide evidence that the transcriptional coactivator, Mediator 1 (MED1), is critical in determining the cell fate of ectodermal epithelia. MED1 ablation disrupted enamel formation and generated hair adjacent to the incisors. Deletion of MED1 altered the differentiation of dental epithelia to one expressing epidermal and hair genes similar to the skin. The cellular switch from dental to epidermal/hair lineage was characterized by abnormalities in MED1 deficient dental epithelial stem cells residing in cervical loop. MED1 deficiency caused a failure of dental epithelial stem cells to commit to the dental stratum intermedium regulated by Notch signaling. Instead, MED1 deficient cells retained stem cell potentials expressing Sox2. These cells were eventually adopted an epidermal fate probably through calcium provided through capillary networks, which is originally utilized for enamel formation. Our results demonstrate that MED1 regulates Sox2/Notch1 regulated cell lineage determination in dental epithelia. Our study also shows a potential to regenerate hairs by using genetically engineered dental tissues or cells outside of the skin. n=4 WT and KO (each group contains dissected dental tissues from 3 mice combined)

2013-09-23 | E-GEOD-50502 | biostudies-arrayexpress

Ablation of coactivator Med1 switches the cell fate of dental epithelia to that generating hair [CL stage]

2013-09-23 | E-GEOD-50501 | biostudies-arrayexpress

Genome-wide analysis of gene expression in lymph nodes and vaccination site in mice vaccinated with adenovirus and MVA mixed formulations

Project description:Gene expression analysis in lymph nodes and site of injection (intradermal) after vaccination with adenovirus (Ad), modified vaccinia Ankara (MVA) or a mixed formulation of Ad+MVA. The hypothesis tested in the present study was that co-administration of two viral vectors induce a differential gene expression in the site of vaccination (dermis) and the draining lymph nodes that ultimately influences the protective ability of a vaccine against pre-erythrocytic malaria. Total RNA was isolated from the vaccination site (dermis) and lymph nodes after vaccination with adenovirus, MVA or Ad+MVA mixed co-administration after 6h and 24h (ear biopsies) and 9h, 24h and 72h for lymph nodes. Differential gene expression was assessed between vaccinated and non-immunized mice. Four ear biopsy samples did not pass quality control, and are not included in this submission.

2012-12-01 | E-GEOD-30564 | biostudies-arrayexpress

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