Evidence map›Paper›PMID 24556985›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

GLTSCR2/PICT1 links mitochondrial stress and Myc signaling.

John C Yoon, Alvin J Y Ling, Meltem Isik, Dong-Young Donna Lee, Michael J Steinbaugh, Laura M Sack, Abigail N Boduch, T Keith Blackwell, David A Sinclair, Stephen J Elledge

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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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

10 authors at 4 institutions in 1 country.

John C YoonDepartment of Genetics, Harvard Medical School, Boston, MA 02115.
Alvin J Y Ling
Meltem Isik
Dong-Young Donna Lee
Michael J Steinbaugh
Laura M Sack
Abigail N Boduch
T Keith Blackwell
David A Sinclair
Stephen J Elledge
Harvard University · USBrigham and Women's Hospital · USHoward Hughes Medical Institute · USJoslin Diabetes Center · US

Funding

ROLE OF DIETARY CONSTITUENTS ON GENE EXPRESSION IN INTESTINAL EPITHELIUMP30DK040561 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI ALEXANDER A SOUKAS · 1994 to 2026
$31.6M
SIRT1 as a regulator of health and lifespan of mammalsR37AG028730 · NIA · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2012 to 2021
$4.1M
Regulation of C. elegans SKN-1/Nrf activity by the unfolded protein responseR01GM094398 · NIGMS · JOSLIN DIABETES CENTER · PI BLACKWELL, T KEITH · 2012 to 2015
$1.2M
Genetic analysis of mitochondrial regulators in mammalian cellsK08DK081612 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI YOON, JOHN C · 2008 to 2012
$800k
Howard Hughes Medical InstituteNIA NIH HHS R37 AG028730NIDDK NIH HHS K08 DK081612NIDDK NIH HHS K08DK081612NIDDK NIH HHS P30 DK040561NIGMS NIH HHS R01 GM094398NIGMS NIH HHS R01GM094398
6 · The paper itself

Abstract

Mitochondrial defects underlie a multitude of human diseases. Genetic manipulation of mitochondrial regulatory pathways represents a potential therapeutic approach. We have carried out a high-throughput overexpression screen for genes that affect mitochondrial abundance or activity using flow-cytometry-based enrichment of a cell population expressing a high-complexity, concentration-normalized pool of human ORFs. The screen identified 94 candidate mitochondrial regulators including the nuclear protein GLTSCR2, also known as PICT1. GLTSCR2 enhances mitochondrial function and is required for the maintenance of oxygen consumption, consistent with a pivotal role in the control of cellular respiration. RNAi inactivation of the Caenorhabditis elegans ortholog of GLTSCR2 reduces respiration in worms, indicating functional conservation across species. GLTSCR2 controls cellular proliferation and metabolism via the transcription factor Myc, and is induced by mitochondrial stress, suggesting it may constitute a significant component of the mitochondrial signaling pathway.

Indexed as

Stress, PhysiologicalAdenosine TriphosphateAnimalsBlotting, WesternCaenorhabditis elegansCells, CulturedDatabases, GeneticDNA PrimersFlow CytometryHumansImmunoprecipitationMicroarray AnalysisMitochondriaOpen Reading FramesOxygen ConsumptionProto-Oncogene Proteins c-mycAdenosine TriphosphateDNA PrimersMYC protein, humanNOP53 protein, humanProto-Oncogene Proteins c-mycTumor Suppressor Proteins

Identifiers

PMID24556985
PMCPMC3956149
OpenAlexW2081928547

What OpenQuestion holds

Textmetadata
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.