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Integration of Thermal Proteome Profiling with phosphoproteomic and transcriptomic data via mechanistic network models decodes the molecular response to PARP inhibition

ABSTRACT: Integration of Thermal Proteome Profiling with phosphoproteomic and transcriptomic data via mechanistic network models decodes the molecular response to PARP inhibition

PROVIDER: PRJNA1017402 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26060451.fastq.gz	Fastqsanger.gz
	SRR26060452.fastq.gz	Fastqsanger.gz
	SRR26060453.fastq.gz	Fastqsanger.gz
	SRR26060454.fastq.gz	Fastqsanger.gz
	SRR26060455.fastq.gz	Fastqsanger.gz

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Integration of Thermal Proteome Profiling with phosphoproteomic and transcriptomic data via mechanistic network models decodes the molecular response to PARP inhibition

Project description:The deregulation of complex diseases often spans multiple molecular processes. A multimodal functional characterization of these processes can shed light on the disease mechanisms and the effect of drugs. Thermal Proteome Profiling (TPP) is a mass-spectrometry based technique assessing changes in thermal protein stability that can serve as proxies of functional changes of the proteome. These unique insights of TPP can complement those obtained by other omics technologies. Here, we show how TPP can be integrated with phosphoproteomics and transcriptomics in a network-based approach using COSMOS, a framework for causal integration of multi-omics, to provide an integrated view of transcription factors, kinases and proteins with altered thermal stability. This allowed us to recover known mechanistic consequences of PARP inhibition in ovarian cancer cells on cell cycle and DNA damage response in detail and to uncover new insights into drug response mechanisms related to interferon and hippo signaling. We found that TPP complements the other omics data and allowed us to obtain a network model with higher coverage of the main underlying mechanisms. These results illustrate the added value of TPP, and more generally the power of network models to integrate the information provided by different omics technologies. We anticipate that this strategy can be used to broadly integrate functional proteomics with other omics to study complex molecular processes.

2024-04-10 | GSE243208 | GEO

Network integration of Thermal Proteome Profiling with multi-omics data decodes PARP inhibition

Project description:Complex disease phenotypes often span multiple molecular processes. Functional characterization of these processes can shed light on disease mechanisms and drug effects. Thermal Proteome Profiling (TPP) is a mass-spectrometry (MS) based technique assessing changes in thermal protein stability that can serve as proxies of functional protein changes. These unique insights of TPP can complement those obtained by other omics technologies. Here, we show how TPP can be integrated with phosphoproteomics and transcriptomics in a network-based approach using COSMOS, a multi-omics integration framework, to provide an integrated view of transcription factors, kinases and proteins with altered thermal stability. This allowed us to recover consequences of Poly (ADP-ribose) polymerase (PARP) inhibition in ovarian cancer cells on cell cycle and DNA damage response as well as interferon and hippo signaling. We found that TPP offers a complementary perspective to other omics data modalities, and that its integration allowed us to obtain a more complete molecular overview of PARP inhibition. We anticipate that this strategy can be used to integrate functional proteomics with other omics to study molecular processes.

| S-SCDT-10_1038-S44320-024-00025-W | biostudies-other

Network integration of thermal proteome profiling with multi-omics data decodes PARP inhibition.

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PARP inhibition

Project description:PARP inhibition and the effect on Arabidopsis thaliana high light tolerance

2012-05-01 | E-MTAB-896 | biostudies-arrayexpress

Depletion of PARP-2 in HepG2 cells

Project description:Poly(ADP-ribose) polymerase-2 (PARP-2) is acknowledged as a DNA repair enzyme; however, recently metabolic properties had been attributed to it. Hereby, we examined the metabolic consequences of PARP-2 ablation in liver. Microarray analysis of PARP-2 knockdown HepG2 cells revealed the dysregulation of lipid and cholesterol metabolism genes. Induction of cholesterol biosynthesis genes stemmed from the enhanced expression of sterol-regulatory element binding protein (SREBP)-1. We revealed that PARP-2 is a suppressor of the SREBP-1 promoter, therefore ablation of PARP-2 induces SREBP-1 expression and consequently cholesterol synthesis. PARP-2-/- mice had higher SREBP-1 expression that was translated into enhanced hepatic and serum cholesterol levels. PARP-2 silencing was performed employing shPARP-2 (small hairpin) and scPARP-2 (scrambled) shRNA by lentiviral delivery (Sigma) using 40 MOI lentiviruses coding shRNA sequence against PARP-2.

2013-12-31 | E-GEOD-43981 | biostudies-arrayexpress

PARP-1 regulation of alternative splicing

Project description:To address the global impact of PARP-1 on alternative splicing, we isolated total RNA in two biological replicates from control (non-treated), PARP-1 siRNA- and PJ-34-treated cells. Sequencing of these RNAs on an Illumina HiSeq 2500, yielded >56 million 100-bp paired-end RNA-seq reads. First we tested if PARP-1 KD was effective at the RNA-seq level. Read aligning to the entire gene body of PARP-1 shown a reduction in PARP-1 expression of about 1.5-fold (P-value < 0.0003), confirming that indeed PARP-1 was depleted after PARP-1 siRNA treatment. We next used these RNA-seq data sets (control, PARP-1 KD and PARylation inhibited) to assess whether these treatments resulted in changes in i) gene expression and ii) alternative splicing.

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2013-12-31 | E-GEOD-51344 | biostudies-arrayexpress

PARP-1/PARP-2 double deficiency results in recurrent early pregnancy loss and decidualization failure in mice

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2021-09-13 | GSE169544 | GEO

PARP-1, H3 and H3K4me3 ChIP-chip from MCF7 cells

Project description:We are examining the mechanisms by which the nuclear enzyme PARP-1 regulates gene expression. We performed ChIP-chip for PARP-1, histone H3 and H3K4me3 (lysine 4 trimethylation on histone H3) in MCF7 breast carcinoma cells, and looked at 23550 RefSeq genes to determine binding patterns of these factors at promoters. Each experiment was performed in duplicate. ChIP-chip biological replicates for PARP-1, H3 and H3K4me3 (2 replicates each) from MCF7 human breast carcinoma cells are included.

2010-09-20 | E-GEOD-19619 | biostudies-arrayexpress

Distinct roles of PARP-1 and PARP-2 in c-Myc-driven B cell Lymphoma in mice

Project description:To study the implication of PARP-1 deficiency or PARP-2 deficiency in the development of c-Myc overexpression-induced B lymphomas, we have studied by RNAseq the gene expression profile in pre-B cells isolated from bone marrow of mice that overexpress c-Myc in their B lymphocytes (WT) and in those mice with PARP-1 (KO1) or PARP-2 (KO2) deficiency

2021-12-31 | GSE144050 | GEO

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