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Quantitative proteomic analysis of proteasome in response to MG132

ABSTRACT: The ubiquitin-proteasome system and autophagy are two major intracellular proteolytic pathways and both remove misfolded and proteotoxic proteins from eukaryotic cells. This study describes the detailed informations about the change in composition and interactome of proteasomes after prolonged MG132 treatment.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Embryonic Cell, Kidney

SUBMITTER: Dohyun Han

LAB HEAD: Dohyun Han

PROVIDER: PXD019193 | Pride | 2021-09-09

REPOSITORIES: Pride

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			Action	DRS
	20180911_PS_MG_0H_1.raw	Raw
	20180911_PS_MG_0H_1_re.raw	Raw
	20180911_PS_MG_0H_2.raw	Raw
	20180911_PS_MG_0H_2_re.raw	Raw
	20180911_PS_MG_0H_3.raw	Raw

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1 - 5 of 27

Publications

Aggresomal sequestration and STUB1-mediated ubiquitylation during mammalian proteaphagy of inhibited proteasomes.

Choi Won Hoon WH Yun Yejin Y Park Seoyoung S Jeon Jun Hyoung JH Lee Jeeyoung J Lee Jung Hoon JH Yang Su-A SA Kim Nak-Kyoon NK Jung Chan Hoon CH Kwon Yong Tae YT Han Dohyun D Lim Sang Min SM Lee Min Jae MJ

Proceedings of the National Academy of Sciences of the United States of America 20200728 32

The 26S proteasome, a self-compartmentalized protease complex, plays a crucial role in protein quality control. Multiple levels of regulatory systems modulate proteasomal activity for substrate hydrolysis. However, the destruction mechanism of mammalian proteasomes is poorly understood. We found that inhibited proteasomes are sequestered into the insoluble aggresome via HDAC6- and dynein-mediated transport. These proteasomes colocalized with the autophagic receptor SQSTM1 and cleared through sel ...[more]

PMID: 32723828

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Impact of proteasome inhibition on nascent transcription of APOBEC3 cytidine deaminases

Project description:To assess the impact of the proteasome inhibitor MG132 on nascent transcription inMDA-MB-453 cells, csRNA-seq was conducted to compare transcript abundances between treated and DMSO control cells. Analysis of transcripts following MG132 treatment showed that APOBEC3A is one of the most differentially expressed genes. Comparison to other APOBEC family genes, revealed APOBEC3A is unique in its transcriptional upregulation by MG132. Analysis of transcription factor binding sites enriched in the promoter regions of genes changed greater than 2-fold in expression highlighted potential transcription factors driving increased APOBEC3A transcription.

2023-12-05 | GSE248016 | GEO

Proteome Composition of Lysosomes and Autophagosomes after Proteasome Inhibition

Project description:Lysosomes are a major site of intracellular acidic hydrolase-mediated proteolysis and cellular degradation in a membrane-enclosed organelle. Alternatively, soluble, ubiquitin-bound proteins are degraded via the proteasome, a megadalton protein complex within the cytoplasm. The interplay between both degradation pathways has been of increasing interest in recent years. To determine the effects of proteasome inhibition on the lysosomal compartment, we investigated enriched lysosomal fractions, autophagosomal fractions and immunoprecipitated proteasomes from HEK293 cells after proteasome inibition by MG132 or bortezomib in comparison to the respective fractions from control cells.

2020-04-20 | PXD015243 | Pride

Transcription profiling of human MCF-7 cells treated with proteasome inhibitor MG132 and either dexamethasone or 17b-estradiol

Project description:The objective of the study was to investigate the effect of proteasome inhibition on glucocorticoid and estrogen receptor regulated gene expression. Experiment Overall Design: MCF-7 cells were treated with proteasome inhibitor (MG132), dexamethasone, 17b-estradiol or MG132 plus dexamethasone or MG132 plus 7b-estardiol. Control cells were not treated. RNA was collected from 2 biological experiments.

2008-06-20 | E-GEOD-8383 | biostudies-arrayexpress

Systemic Comparison of Heat Shock Response Induced by Heat Shock and a Proteasome Inhibitor in Mouse Fibrosarcoma Cells and Their Thermotolerant Counterparts

Project description:Heat shock response (HSR) is a cellular defense mechanism against various stresses. Both heat shock and proteasome inhibitor MG132 cause the induction of heat shock proteins, a distinct feature of HSR. To better understand the molecular basis of HSR, we subjected the mouse fibrosarcoma cell line, RIF-1, and its thermotolerant variant, TR-RIF-1 cells, to heat shock and MG132. We compared mRNA expressions using microarray analysis during recovery after heat shock and MG132 treatment. This study led us to group the 3,245 up-regulated genes by heat shock and MG132 into three families: genes regulated 1) by both heat shock and MG132 (e.g. chaperones); 2) by heat shock (e.g. DNA-binding proteins including histones); and 3) by MG132 (e.g. innate immunity and defense-related molecules). RIF-1 and TR cells were heat shock treated or MG132 treated and harvested after various times of recovery. mRNA expressions were compared to untreated samples. Biological replication was done.

2011-11-09 | E-GEOD-24197 | biostudies-arrayexpress

Systemic Comparison of Heat Shock Response Induced by Heat Shock and a Proteasome Inhibitor in Mouse Fibrosarcoma Cells and Their Thermotolerant Counterparts

2011-11-09 | GSE24197 | GEO

Proteasome dysfunction in alveolar type 2 epithelial cells is associated with acute respiratory distress syndrome

Project description:Proteasomes are a critical component of quality control that regulates turnover of short-lived, unfolded, and misfolded proteins. Proteasome activity has been therapeutically targeted and considered as a treatment option for several chronic lung disorders including pulmonary fibrosis. Though pharmacologic inhibition of proteasome activity effectively prevents the transformation of fibroblasts to myofibroblasts, the effect on alveolar type 2 (AT2) epithelial cells is not clear. To address this knowledge gap, we generated a genetic model in which a proteasome subunit, RPT3, which promotes assembly of active 26S proteasome, was conditionally deleted in AT2 cells of mice. Targeted deletion of RPT3 in AT2 cells resulted in 26S proteasome dysfunction, leading to augmented cell stress and death. Acute loss of AT2 cells resulted in depletion of alveolar surfactant, disruption of the alveolar epithelial barrier and, ultimately, lethal acute respiratory distress syndrome. This study underscores the need for further investigation into the differential effect of proteasome inhibition in lung cell types.

2019-08-29 | GSE123873 | GEO

affy_ath_2012_04-Functional characterization of JMJ24, a putative histone demethylase

Project description:affy_ath_2012_04 - affy_ath_2012_04 - Epigenetic informations include histone post-translational modifications such as acetylation and methylation. The jumoni proteins can remove the methyl group from lysine or arginine residues of histones. The aim of this project is to compare gene expression levels between mutants of two jumonji genes and wild type at seedling stage (12 d old).-- Seeds were sterilized in bleach, washed with ethanol, dried, dispersed on Murashige and Skoog (MS) 0.5X containing 2% sucrose and kept 5 days at 4Â°C. - After 12 days of growth under a cool white fluorescent light (120 Î¼mol m-2 s-1) and long day conditions (16h of light) in a growth chamber, the plants are harvested and stored at -80Â°C. -The RNA are extracted with the RNA Plant NucleoSpin (Machery-Nagel), quantified with Nanodrop and visualised on agarose gel. The samples are stored at -80Â°C. 8 arrays - ATH1; gene knock out

2013-08-01 | E-GEOD-43728 | biostudies-arrayexpress

Chromatin state of MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [histone_mod_chip_seq]

Project description:We report whole genome chromatin immunoprecipitation followed by sequencing (ChIP-seq) of histone modifications in MCF-7 breast cancer cells treated with vehicle (UNTR) or the proteasome inhibitor MG132 for 4 (MG4H) or 24 (MG24H) hours. We find that MG132 treatment results in the spreading of the H3-trimethyl lysine 4 mark into gene bodies of a subset of induced genes in MCF-7 cells. The spreading of the H3K4me3 is concomitant with hyperacetylation (H3K27ac, K122ac and K9/14ac) of the corresponding gene TSS. H3 Lysine 36 trimethylation mark is enriched at genes that are induced by MG132. Finally, we show that proteasome inhibition establishes a chromatin state that enhances antiproliferative, while dampening cell proliferative gene expression programs relevant to breast cancer. The study provides a comprehensive resource of histone modifications in proteasome inhibited cells.

2020-01-07 | GSE142009 | GEO

Transcriptional regulation in MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [rna_polii_chIP-seq]

Project description:We report whole genome chromatin immunoprecipitation followed by sequencing (ChIP-seq) of 3 different RNA Pol II CTD modifications in MCF-7 breast cancer cells treated with vehicle (UNTR) or the proteasome inhibitor MG132 for 4 (MG4H) or 24 (MG24H) hours. We find the non-phosphorylated form of RNA Pol II CTD accumulates at TSS of all expressed genes in proteasome inhibited cells, particularly after 24H of MG132 treatment. Proteasome inhibition enhances Ser5-P and Ser2-P binding at TSS of genes induced by MG132. We note that proteasome inhibition establishes unique Ser2-P 5’ to 3’ gene profiles at induced compared to repressed genes. Overall proteasome inhibition enhances RNA Pol II processivity and expression of gene networks relevant to breast cancer. The study provides a comprehensive resource of RNA Pol II binding in proteasome inhibited cells.

2020-01-07 | GSE142010 | GEO

Chronic administration of non-constitutive proteasome inhibitor modulates plasticity in hippocampus following tetanic stimulation, but not short theta-burst stimulation.

Project description:Proteasomes degrade most intracellular proteins. Several different forms of proteasomes are known. Proteasome inhibitors targeting different proteasome forms are used in clinical practice and were shown to modulate long-term potentiation (LTP) in hippocampal slices of untreated animals. Here we studied the effect of chronic administration of non-constitutive proteasome inhibitor ONX-0914 on the LTP induced by two different protocols: tetanic stimulation and theta-burst stimulation (TBS). Excitatory postsynaptic potentials (fEPSPs) in hippocampal slices from control animals and animals treated with DMSO or ONX-0914 were compared. The TBS stimulation did not change LTP kinetics in hippocampal slices, however chronic administration of ONX-0914 led to the decrease in fEPSP slopes after tetanic stimulation. Observed effects correlated with differential expression of genes involved in synaptic plasticity, glutaminergic synapse and synaptic signaling. Obtained results indicate that non-constitutive proteasomes are likely involved in the tetanus-evoked LTP but not the LTP occurring after TBS, supporting the relevance and complexity of the role of proteasomes in the synaptic plasticity.

2023-04-05 | GSE229000 | GEO

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