Dataset Information

Host cell proteome analysis follwoing HIV-1 transduction

ABSTRACT: 293T cells were infected with HIV-1 pseudovirions, and 0, 4 and 12 hours post-infection, the cell lysates were collected. Label-free proteomics was applied to examine the protein-level changes. Duplicate samples for six time points were collected (0, 4, and 12 hours post-transduction, virus- and mock transduced samples) and analyzed in duplicates, allowing for the measurement of two technical and two biological replicates for each time point. The results were used for the analysis of protein networks implementing both the qualitative and quantitative information.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Early Embryonic Cell

SUBMITTER: Eva Csosz

LAB HEAD: Eva Csosz

PROVIDER: PXD010436 | Pride | 2019-07-23

REPOSITORIES: Pride

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Publications

Analysis of networks of host proteins in the early time points following HIV transduction.

Csősz Éva É Tóth Ferenc F Mahdi Mohamed M Tsaprailis George G Emri Miklós M Tőzsér József J

BMC bioinformatics 20190717 1

<h4>Background</h4>Utilization of quantitative proteomics data on the network level is still a challenge in proteomics data analysis. Currently existing models use sophisticated, sometimes hard to implement analysis techniques. Our aim was to generate a relatively simple strategy for quantitative proteomics data analysis in order to utilize as much of the data generated in a proteomics experiment as possible.<h4>Results</h4>In this study, we applied label-free proteomics, and generated a network ...[more]

PMID: 31315557

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Project description:The therapeutic benefits of L–3,4–dihydroxyphenylalanine (L-DOPA) in Parkinson’s disease (PD) patients severely diminishes with the onset of L-DOPA-induced dyskinesia (LID), a debilitating motor side effect. LID is mainly due to altered dopaminergic signaling in the striatum, a brain region that controls motor and cognitive functions. However, the molecular mechanisms that promote LID remain unclear. Here, we have reported that increased striatal RasGRP1 (also known as CalDAG-GEF-II) is instrumentally linked to the development of LID in a 6-hydroxydopamine (6-OHDA) lesioned mouse model of PD. L-DOPA treatment rapidly upregulated RasGRP1 in the dopamine-1 receptor positive neurons in the dorsal striatum. RasGRP1 deleted mice (RasGRP1–/–) had drastically diminished LID, and RasGRP1–/– mice did not interfere with the therapeutic benefits of L-DOPA. In terms of its mechanism, RasGRP1 mediated L-DOPA-induced extracellular regulated kinase (ERK), the mammalian target of rapamycin kinase (mTOR) and the cAMP/PKA pathway. RasGRP1 bind directly with and acts 2 as a guanine nucleotide exchange (GEF) for Ras-homolog-enriched in the brain (Rheb), a potent activator of mTOR, both in vitro and in the intact striatum. High-resolution tandem mass tag mass spectrometry analysis of striatal tissue revealed significant targets, such as phosphodiesterase 10a (Pde10a), Pde2a, catechol-o-methyltransferase (Comt), and glutamate decarboxylase 1 and 2 (Gad1 and Gad2), as downstream regulators of RasGRP1 that are linked to LID vulnerability. Moreover, we found that RASGRP1 protein is also upregulated predominantly in the striatum of MPTP-lesioned macaque treated with L-DOPA, emphasizing the translational potential of this protein. Collectively, the findings of this study demonstrated that RasGRP1 is a major regulator of LID in the dorsal striatum. Pharmacological or gene-depletion strategies targeting RasGRP1 may offer novel therapeutic opportunities for preventing LID in PD patients.

Dataset Information

Host cell proteome analysis follwoing HIV-1 transduction

Publications

Analysis of networks of host proteins in the early time points following HIV transduction.

Similar Datasets

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