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Unknown,Transcriptomics,Genomics,Proteomics

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Analysis of MOF under stress conditions

ABSTRACT: We analyzed the role of MOF in primary MEFs and differentiated podocytes in response to Adriamycin. Mof was deleted in MEFs using the Cre-ERT2 trasgene, while Mof was knockdown in podocytes using shRNA infection. Samples were treated with Adriamycin for 24 hours and gene expression changes analysed. Analysis of gene expression changes upon Mof depletion in two cell lines, MEFs and podocytes, with and without Adriamycin

ORGANISM(S): Mus musculus

SUBMITTER: Sarah Diehl

PROVIDER: E-GEOD-70706 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MOF maintains transcriptional programs regulating cellular stress response.

Sheikh B N BN Bechtel-Walz W W Lucci J J Karpiuk O O Hild I I Hartleben B B Vornweg J J Helmstädter M M Sahyoun A H AH Bhardwaj V V Stehle T T Diehl S S Kretz O O Voss A K AK Thomas T T Manke T T Huber T B TB Akhtar A A

Oncogene 20150921 21

MOF (MYST1, KAT8) is the major H4K16 lysine acetyltransferase (KAT) in Drosophila and mammals and is essential for embryonic development. However, little is known regarding the role of MOF in specific cell lineages. Here we analyze the differential role of MOF in proliferating and terminally differentiated tissues at steady state and under stress conditions. In proliferating cells, MOF directly binds and maintains the expression of genes required for cell cycle progression. In contrast, MOF is d ...[more]

PMID: 26387537

Similar Datasets

Analysis of MOF under stress conditions

Project description:We analyzed the role of MOF in primary MEFs and differentiated podocytes in response to Adriamycin. Mof was deleted in MEFs using the Cre-ERT2 trasgene, while Mof was knockdown in podocytes using shRNA infection. Samples were treated with Adriamycin for 24 hours and gene expression changes analysed.

2015-07-10 | GSE70706 | GEO

Nck2 Regulates Adiposity and Adiposity-Related Metabolic Disorders in Mice and Human

Project description:Obesity is linked to the development of metabolic disorders. Expansion of white adipose tissue (WAT) from hypertrophy of pre-existing adipocytes and/or differentiation of precursors into new mature adipocytes contributes to obesity. We found that Nck2 expression is largely restricted to WAT, raising the hypothesis that it may play a unique function in that tissue. Using mice lacking Nck2, we found that Nck2 regulates adipocyte hypertrophy thus contributing to increased adiposity and progressive glucose intolerance, insulin resistance and hepatic steatosis. These findings were recapitulated in humans such that Nck2 expression in omental WAT was inversely correlated with the degree of obesity. Mechanistically, Nck2 deficiency promoted the induction of an adipocyte differentiation program and signaling by the PERK-eIF2Î±-ATF4 pathway in agreement with a role for the unfolded protein response in adipogenesis. These findings uncover Nck2 as a novel regulator of adipogenesis and that perturbation in its functionality contributes to adiposity-related metabolic disorders. Differential gene expression profile between epididymal white adipose tissue of Nck2-/- and Nck2+/+ mice by RNA sequencing (Illumina HiSEq 2000)

2016-07-01 | E-GEOD-63510 | biostudies-arrayexpress

Cyclodextrin protects podocytes in diabetic kidney disease [HumanWG-6 v3.0 array]

Project description:Analysis of gene expression changes in differentiated human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). The hypothesis is that the three groups can be distinghed by their differential gene expression pattern. The results obtained revealed important information regarding differences in gene expression in human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). Human podocytes were contacted with the serum from patients with diabetes and kidney disease (DKD+) or without kidney disease (DKD-) and compared to normal human podocytes contacted with serum from patients without diabetes (C).

2013-07-11 | E-GEOD-46897 | biostudies-arrayexpress

Cyclodextrin protects podocytes in diabetic kidney disease [HumanHT-12 V4.0 array]

2013-07-13 | E-GEOD-46899 | biostudies-arrayexpress

Role of calcium/calmodulin-dependent kinase type IV in podocyte function in lupus nephritis

Project description:Kidney podocytes and their slit diaphragms contribute to prevent urinary protein loss. T cell from patients with systemic lupus erythematosus display increased expression of calcium/calmodulin kinase IV (CaMKIV). Here we evaluated the functional role of CaMKIV in lupus nephritis (LN) using kidney biopsy specimens and human podocyte cell line (AB8/13). We found that exposure of podocytes to IgG from LN patients resulted in entry of IgG into the cytoplasm. CaMKIV expression was found to be increased in podocytes of LN kidney biopsy specimens and exposure to IgG from LN patients. IgG entered podocytes using the FcRn receptor because when podocytes where treated with FcRn siRNA less IgG was found in the cytoplasm. The DNA microarray studies of podocytes exposed to LN IgG revealed that genes that are related to the activation of immune cells or podocyte damage were upregulated. These genes included CD86, CaMKIV, PTPN22, PDE5A, CD47 and MALT1. Interestingly, CD86 expression decreased after silencing CaMKIV in podocytes. Also, in situ hybridization experiments showed that the expression of CD86 was reduced in podocytes from MRL/lpr.camkivM-bM-^HM-^R/M-bM-^HM-^R mice. IgG from LN patients may enter podocytes through the FcRn and causes the upregulation of a distinct set of genes which may alter podocyte function. Upregulation of CaMKIV appears to precede that of genes known to be linked to podocyte damage such as CD86. These findings may indicate that inhibition of CaMKIV may prove of clinical use in patients with LN. IgG Purification Kits (Dojindo Molecular Technologies, Inc.) are used for isolation and purification of immunoglobulin G of healthy and normal individual according to the manufacturerM-bM-^@M-^Ys protocol. Flow through the column was used for non IgG binding samples. Cultured human podocytes with IgG purified from sera of normal individuals and LN patient for 24 hr were collected for RNA.

2014-08-01 | E-GEOD-55768 | biostudies-arrayexpress

E-GEOD-70706

Project description:Transcription profiling to identify the role of MOF in primary MEFs and differentiated podocytes in response to Adriamycin

2019-05-14 | E-GEOD-70706 | ExpressionAtlas

Genome wide map of long noncoding RNA Tug1 binding sites in cultured mouse podocytes

Project description:We generated a genome wide map of instances where the long noncoding RNA, Tug1, binds to DNA in cultured mouse podocytes under normal glucose conditions using Chromatin-RNA Precipitation coupled with high throughput sequencing (ChIRP-Seq) 48 alternating (even, odd) biotynilated probes were designed to span the full length of Tug1 RNA. Chromatin was prepared from gluteraldehyde crosslinked nuclei from early passage podocytes. Chromatin extracts were duplicated with either even or odd probes. Duplicate samples for Input DNA, Even pulldown (PD) and Odd PD DNA was purified following incubation and supplied for Illumina sequencing by ArrayStar (Rockville, MD).

2016-10-24 | E-GEOD-77493 | biostudies-arrayexpress

Glucocorticoid therapy regulates podocyte motility by inhibition of Rac1

Project description:Nephrotic syndrome (NS) occurs when the glomerular filtration barrier becomes excessively permeable leading to massive proteinuria. In childhood NS, dysregulation of the immune system has been implicated and increasing evidence points to the central role of podocytes in the pathogenesis. Children with NS are typically treated with an empiric course of glucocorticoid (Gc) therapy; a class of steroids that are activating ligands for the glucocorticoid receptor (GR) transcription factor. Although Gc-therapy has been the cornerstone of NS management for decades, the mechanism of action, and target cell, remain poorly understood. We tested the hypothesis that Gc acts directly on the podocyte to produce clinically useful effects without involvement of the immune system. In human podocytes, we demonstrated that the basic GR-signalling mechanism is intact and that Gc induced an increase in podocyte barrier function. To gain mechanistic insight we performed RNA microarray and ChIP-sequencing and identified Gc regulation of motility genes.

2017-07-17 | E-MTAB-5235 | biostudies-arrayexpress

Next Generation Sequencing of control (Untreated), PAN injured and Adriamycin injured human podocytes

Project description:Purpose: Next-generation sequencing (NGS) was used to identify cellular pathways and genes through systems-based analysis. The goals of this study are to identify NGS-derived transcriptome profiling (RNA-seq) in control (untreated) and Injured (PAN and Adriamycin) podocyte. These high throughput data were further validated through qRT–PCR methods to confirm the cellular pathways and genes affected due to the podocyte injury. Methods: Human podocytes were differentiated for 14 days by thermoswitching from 33⁰C to 37⁰C and removal of growth factors, insulin-transferrin-selenium from the medium. These podocytes were incubated 4hour in serum free RPMI medium and injury was induced by using PAN (100μg/ml) and Adriamycin (0.25μg/ml) treatment for 48 hours.Further, podocytes were processed for RNA isolation and submitted to Medical University of South Carolina Sequencing Core facility for RNA-Seq. All the experiments were performed in triplicates. Conclusions: Our study is first to describe the detailed analysis of PAN and Adriamycin induced podocyte transcriptomes using the RNA-seq technology. A comparative analysis of the differential expression profile was obtained between control vs PAN injured podocytes, and control vs Adriamycin injured podocytes. Complex genetic network and genes effected due to the injury will provide a platform to define biological pathways participate during podocytes injury process.

2019-03-31 | GSE124622 | GEO

Transcriptomic output of endogenous KRasG12D and modestly overexpressed MYC in MEFs

Project description:We sought to compare the transcriptomic output of Kras activation with that of modestly overexpressed cMYC, to better understand the mechanism of oncogenic cooperation. We isolated fibrobalsts from mouse embryos carrying CRE-inducible alleles for KRasG12D (LSL-KRasG12D) and MYC (Rosa26-LSL-MYC), alongside double positive and wild-type control MEFs. All MEFs were infected at early passage with Adeno-CMV-CRE, to induced expression of conditional alleles, where present, and RNA was isolated 24hrs post infection.

2020-03-16 | E-MTAB-6824 | biostudies-arrayexpress

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