Evidence map›Paper›PMID 38207075›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production.

Neal K Bennett, Megan Lee, Adam L Orr, Ken Nakamura

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.0field-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

18 citing papers in PubMed, 17 citations in OpenAlex.

  1. Injury polarized CD4Redox biology · 2026
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  18. Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Neal K BennettGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158.ORCID 0000-0003-3120-4164
Megan LeeGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158.
Adam L OrrAppel Alzheimer's Disease Research Institute, Weill Cornell Medicine, New York, NY 10021.
Ken NakamuraGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158.ORCID 0000-0002-9192-182X
Gladstone Institutes · USCornell University · US

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MALLORY O JOHNSON · 1988 to 2026
$93.6M
Defining Strategies to Target Energy Failure in Metabolically Vulnerable Human CellsR01AG065428 · NIA · J. DAVID GLADSTONE INSTITUTES · PI NAKAMURA, KEN · 2020 to 2024
$3.7M
Mitochondrial Complex III Free Radicals in Dementia-Related Proteinopathy and NeuroinflammationR01AG068091 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI ORR, ANNA GOLDSHMIDT · 2020 to 2024
$3.1M
Metabolic Vulnerability and Effects of APOE in Human Neurons with Impaired Endocytic RecyclingK01AG078485 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI Neal Bennett · 2022 to 2026
$643k
BD FACSAria II Flow CytometerS10RR028962 · NCRR · J. DAVID GLADSTONE INSTITUTES · PI CAVROIS, MARIELLE · 2011 to 2011
$544k
Bioenergetic and Proteolytic Impact of Ubiquitin-like Pathways in Metabolically Stressed NeuronsF32AG063457 · NIA · J. DAVID GLADSTONE INSTITUTES · PI BENNETT, NEAL · 2019 to 2021
$155k
NCRR NIH HHS S10 RR028962NIAID NIH HHS P30 AI027763NIA NIH HHS F32 AG063457NIA NIH HHS K01 AG078485NIA NIH HHS R01 AG065428NIA NIH HHS R01 AG068091
6 · The paper itself

Abstract

Respiratory chain dysfunction can decrease ATP and increase reactive oxygen species (ROS) levels. Despite the importance of these metabolic parameters to a wide range of cellular functions and disease, we lack an integrated understanding of how they are differentially regulated. To address this question, we adapted a CRISPRi- and FACS-based platform to compare the effects of respiratory gene knockdown on ROS to their effects on ATP. Focusing on genes whose knockdown is known to decrease mitochondria-derived ATP, we showed that knockdown of genes in specific respiratory chain complexes (I, III, and CoQ10 biosynthesis) increased ROS, whereas knockdown of other low ATP hits either had no impact (mitochondrial ribosomal proteins) or actually decreased ROS (complex IV). Moreover, although shifting metabolic conditions profoundly altered mitochondria-derived ATP levels, it had little impact on mitochondrial or cytosolic ROS. In addition, knockdown of a subset of complex I subunits-including

Indexed as

MitochondriaMitochondrial MembranesAdenosine TriphosphateMitochondrial ProteinsOxidative StressReactive Oxygen SpeciesAdenosine TriphosphateMitochondrial ProteinsReactive Oxygen SpeciesATPCRISPRimetabolismmitochondriaROS

Identifiers

PMID38207075
PMCPMC10801874
OpenAlexW4390734167

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.