Evidence map›Paper›PMID 35579911›Full record

ArticleProteomics. Clinical applications2022

Proteomic profiling of idiopathic Parkinson's disease primary patient cells by SWATH-MS.

Stephen A Wood, Peter G Hains, Arnaud Muller, Melissa Hill, Susitha Premarathne, Mariyam Murtaza, Phillip J Robinson, George D Mellick, Alex M Sykes

Open access · hybridAbstract read
In one paragraph

Article in Proteomics. Clinical applications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 39% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Stephen A WoodGriffith Institute for Drug Discovery, Griffith University, Nathan, Queensland, Australia.ORCID 0000-0002-2576-7457
Peter G HainsCell Signalling Unit, Children's Medical Research Institute, The University of Sydney, Westmead, NSW, Australia.ORCID 0000-0002-7276-1760
Arnaud MullerLuxembourg Institute of Health, Dudelange, Luxembourg.
Melissa HillGriffith Institute for Drug Discovery, Griffith University, Nathan, Queensland, Australia.ORCID 0000-0001-8077-0889
Susitha PremarathneGriffith Institute for Drug Discovery, Griffith University, Nathan, Queensland, Australia.
Mariyam MurtazaGriffith Institute for Drug Discovery, Griffith University, Nathan, Queensland, Australia.
Phillip J RobinsonCell Signalling Unit, Children's Medical Research Institute, The University of Sydney, Westmead, NSW, Australia.ORCID 0000-0002-7878-0313
George D MellickGriffith Institute for Drug Discovery, Griffith University, Nathan, Queensland, Australia.ORCID 0000-0002-7211-4651
Alex M SykesGriffith Institute for Drug Discovery, Griffith University, Nathan, Queensland, Australia.ORCID 0000-0001-8981-6652
Griffith University · AUThe University of Sydney · AULuxembourg Institute of Health · LU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeParkinson's disease (PD) is the second most prevalent neurodegenerative disease. It is generally diagnosed clinically after the irreversible loss of dopaminergic neurons and no general biomarkers currently exist. To gain insight into the underlying cellular causes of PD we aimed to quantify the proteomic differences between healthy control and PD patient cells. EXPERIMENTAL

designSequential Window Acquisition of all THeoretical Mass Spectra was performed on primary cells from healthy controls and PD patients.

resultsIn total, 1948 proteins were quantified and 228 proteins were significantly differentially expressed in PD patient cells. In PD patient cells, we identified seven significantly increased proteins involved in the unfolded protein response (UPR) and focused on cells with high and low amounts of PDIA6 and HYOU1. We discovered that PD patients with high amounts of PDIA6 and HYOU1 proteins were more sensitive to endoplasmic reticulum stress, in particular to tunicamycin. Data is available via ProteomeXchange with identifier PXD030723. CONCLUSIONS AND CLINICAL RELEVANCE: This data from primary patient cells has uncovered a critical role of the UPR in patients with PD and may provide insight to the underlying cellular dysfunctions in these patients.

Indexed as

Neurodegenerative DiseasesParkinson DiseaseBiomarkersHumansProteomicsTunicamycinBiomarkersTunicamycinParkinson's diseaseproteomics

Identifiers

PMID35579911
PMCPMC9787017
OpenAlexW4280603773

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.