Evidence map›Paper›PMID 28644127›Full record

ArticleeLife2017

MPI depletion enhances O-GlcNAcylation of p53 and suppresses the Warburg effect.

Nataly Shtraizent, Charles DeRossi, Shikha Nayar, Ravi Sachidanandam, Liora S Katz, Adam Prince, Anna P Koh, Adam Vincek, Yoav Hadas, Yujin Hoshida and 5 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  8. Frontiers in pharmacology · 2024
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  19. The Cyclically SeasonalFrontiers in genetics · 2020
    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

15 authors at 4 institutions in 2 countries.

Nataly ShtraizentDepartment of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, United States.
Charles DeRossiDepartment of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, United States.ORCID 0000-0001-5267-6553
Shikha NayarDepartment of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, United States.
Ravi SachidanandamDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, United States.
Liora S KatzDepartment of Medicine, Division of Endocrinology, Diabetes and Bone Disease, Icahn School of Medicine at Mount Sinai, New York, United States.
Adam PrinceDepartment of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, United States.
Anna P KohDepartment of Medicine, Division of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, United States.
Adam VincekDepartment of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, United States.
Yoav HadasDepartment of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, United States.
Yujin HoshidaDepartment of Medicine, Division of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, United States.
Donald K ScottDepartment of Medicine, Division of Endocrinology, Diabetes and Bone Disease, Icahn School of Medicine at Mount Sinai, New York, United States.
Efrat EliyahuDepartment of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, United States.
Hudson H FreezeSanford Children's Health Research Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, United States.
Kirsten C SadlerBiology Program, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates.ORCID 0000-0002-1100-4125
Jaime ChuDepartment of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, United States.ORCID 0000-0002-9291-8630
Icahn School of Medicine at Mount Sinai · USChild Health and Development Institute · USNew York University Abu Dhabi · AESanford Burnham Prebys Medical Discovery Institute · US

Funding

THE TISCH CANCER INSTITUTE - CANCER CENTER SUPPORT GRANTP30CA196521 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Deanna L Benson · 2015 to 2026
$35.4M
Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STREAMSON C CHUA · 2015 to 2026
$27.7M
PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI GREGORY J. GORES · 2009 to 2026
$22.2M
New Congenital Disorders of Glycosylation: Therapy and ModelsR01DK099551 · NIDDK · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI Hudson H. Freeze · 2014 to 2026
$6.7M
Role of Uhrf1 in Liver Development, Regeneration and CarciogenesisR01DK080789 · NIDDK · NEW YORK UNIVERSITY · PI Kirsten C Sadler Edepli · 2009 to 2026
$5.2M
Molecular Prognostic Indicators in Liver Cirrhosis and CancerR01DK099558 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HOSHIDA, YUJIN · 2013 to 2016
$2.6M
Understanding fatty liver disease using the zebrafish mutant, foie grasR01AA018886 · NIAAA · NEW YORK UNIVERSITY · PI SADLER EDEPLI, KIRSTEN C · 2009 to 2017
$2.4M
TRAINING PROGRAM IN INVESTIGATIVE GASTROENTEROLOGYT32DK007792 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CHO, JUDY H. · 2001 to 2016
$2.3M
A novel role for p53 in congenital disorders of glycosylationK08DK101340 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHU, JAIME C · 2013 to 2016
$554k
NIAAA NIH HHS R01 AA018886NIDDK NIH HHS K08 DK101340NIDDK NIH HHS P30 DK020541NIDDK NIH HHS P30 DK084567NIDDK NIH HHS R01 DK080789NIDDK NIH HHS R01 DK099551NIDDK NIH HHS R01 DK099558NIDDK NIH HHS T32 DK007792
6 · The paper itself

Abstract

Rapid cellular proliferation in early development and cancer depends on glucose metabolism to fuel macromolecule biosynthesis. Metabolic enzymes are presumed regulators of this glycolysis-driven metabolic program, known as the Warburg effect; however, few have been identified. We uncover a previously unappreciated role for Mannose phosphate isomerase (MPI) as a metabolic enzyme required to maintain Warburg metabolism in zebrafish embryos and in both primary and malignant mammalian cells. The functional consequences of MPI loss are striking: glycolysis is blocked and cells die. These phenotypes are caused by induction of p53 and accumulation of the glycolytic intermediate fructose 6-phosphate, leading to engagement of the hexosamine biosynthetic pathway (HBP), increased O-GlcNAcylation, and p53 stabilization. Inhibiting the HBP through genetic and chemical methods reverses p53 stabilization and rescues the Mpi-deficient phenotype. This work provides mechanistic evidence by which MPI loss induces p53, and identifies MPI as a novel regulator of p53 and Warburg metabolism.

Indexed as

Protein Processing, Post-TranslationalAcetylglucosamineAnimalsCell Line, TumorFructosephosphatesGlycolysisHumansMannose-6-Phosphate IsomeraseTumor Suppressor Protein p53ZebrafishZebrafish ProteinsAcetylglucosaminefructose-6-phosphateFructosephosphatesMannose-6-Phosphate Isomerasetp53 protein, zebrafishTumor Suppressor Protein p53Zebrafish Proteinscancercancer biologycell biologyglucose metabolismhumanmouseO-GlcNAcp53Warburg effectzebrafishzebrafish embryo

Identifiers

PMID28644127
PMCPMC5495572
OpenAlexW2662007953

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.