Evidence map›Paper›PMID 35858317›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

A versatile fluorescence-quenched substrate for quantitative measurement of glucocerebrosidase activity within live cells.

Matthew C Deen, Yanping Zhu, Christina Gros, Na Na, Pierre-André Gilormini, David L Shen, Sandeep Bhosale, Nadia Anastasi, RuiQi Wang, Xiaoyang Shan and 4 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. A Common PD-RiskbioRxiv : the preprint server for biology · 2025
    Article
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  6. Article
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  9. Review
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  12. Review
  13. Article
  14. Live cellFrontiers in cellular neuroscience · 2023
    Article
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

14 authors at 3 institutions in 2 countries.

Matthew C DeenDepartment of Chemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Yanping ZhuDepartment of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Christina GrosDepartment of Chemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Na NaDepartment of Chemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Pierre-André GilorminiDepartment of Chemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
David L ShenDepartment of Chemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Sandeep BhosaleDepartment of Chemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.ORCID 0000-0002-1850-1271
Nadia AnastasiRoche Pharma Research and Early Development, Neuroscience and Rare Diseases Discovery and Translational Area, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
RuiQi WangDepartment of Chemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Xiaoyang ShanDepartment of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.ORCID 0000-0001-9966-9326
Eva HardeRoche Pharma Research and Early Development, Neuroscience and Rare Diseases Discovery and Translational Area, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
Ravi JagasiaRoche Pharma Research and Early Development, Neuroscience and Rare Diseases Discovery and Translational Area, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
Francis C LynnDiabetes Research Group, BC Children's Hospital Research Institute, Vancouver, BC V5Z 4H4, Canada.ORCID 0000-0001-9318-1063
David J VocadloDepartment of Chemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.ORCID 0000-0001-6897-5558
Simon Fraser University · CARoche (Switzerland) · CHBC Children's Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of activity of the lysosomal glycosidase β-glucocerebrosidase (GCase) causes the lysosomal storage disease Gaucher disease (GD) and has emerged as the greatest genetic risk factor for the development of both Parkinson disease (PD) and dementia with Lewy bodies. There is significant interest into how GCase dysfunction contributes to these diseases, however, progress toward a full understanding is complicated by presence of endogenous cellular factors that influence lysosomal GCase activity. Indeed, such factors are thought to contribute to the high degree of variable penetrance of

Indexed as

Gaucher DiseaseGlucosylceramidaseParkinson Diseasealpha-SynucleinHumansLewy BodiesLewy Body DiseaseLysosomesMutationSubstrate Specificityalpha-SynucleinGlucosylceramidaseenzyme kineticsflow cytometryfluorescence-quenched substrateglycoside hydrolaseParkinson disease

Identifiers

PMID35858317
PMCPMC9304032
OpenAlexW4285093339

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.