Evidence map›Paper›PMID 25876076›Full record

ArticlePloS one2015

Nutritional energy stimulates NAD+ production to promote tankyrase-mediated PARsylation in insulinoma cells.

Linlin Zhong, Tsung-Yin J Yeh, Jun Hao, Nasim Pourtabatabaei, Sushil K Mahata, Jianhua Shao, Steven D Chessler, Nai-Wen Chi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Targeting the NADCell communication and signaling : CCS · 2020
    Article
  5. Review
  6. 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

8 authors at 3 institutions in 2 countries.

Linlin ZhongResearch Service, VA San Diego Healthcare System, San Diego, CA 92161, United States of America; Department of Medicine, University of California San Diego, La Jolla, CA 92093, United States of America.
Tsung-Yin J YehDepartment of Medicine, University of California San Diego, La Jolla, CA 92093, United States of America.
Jun HaoDepartment of Medicine, University of California San Diego, La Jolla, CA 92093, United States of America; Department of Pathology, Hebei Medical University, Shijiazhuang, China.
Nasim PourtabatabaeiDepartment of Medicine, University of California San Diego, La Jolla, CA 92093, United States of America.
Sushil K MahataResearch Service, VA San Diego Healthcare System, San Diego, CA 92161, United States of America; Department of Medicine, University of California San Diego, La Jolla, CA 92093, United States of America.
Jianhua ShaoDepartment of Pediatrics, University of California San Diego, La Jolla, CA 92093, United States of America.
Steven D ChesslerDepartment of Medicine, University of California Irvine, Irvine, CA 92697, United States of America.
Nai-Wen ChiResearch Service, VA San Diego Healthcare System, San Diego, CA 92161, United States of America; Department of Medicine, University of California San Diego, La Jolla, CA 92093, United States of America.
University of California, San Diego · USVA San Diego Healthcare System · USUniversity of California, Irvine · US

Funding

BLRD VA I01 BX000702
6 · The paper itself

Abstract

The poly-ADP-ribosylation (PARsylation) activity of tankyrase (TNKS) regulates diverse physiological processes including energy metabolism and wnt/β-catenin signaling. This TNKS activity uses NAD+ as a co-substrate to post-translationally modify various acceptor proteins including TNKS itself. PARsylation by TNKS often tags the acceptors for ubiquitination and proteasomal degradation. Whether this TNKS activity is regulated by physiological changes in NAD+ levels or, more broadly, in cellular energy charge has not been investigated. Because the NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) in vitro is robustly potentiated by ATP, we hypothesized that nutritional energy might stimulate cellular NAMPT to produce NAD+ and thereby augment TNKS catalysis. Using insulin-secreting cells as a model, we showed that glucose indeed stimulates the autoPARsylation of TNKS and consequently its turnover by the ubiquitin-proteasomal system. This glucose effect on TNKS is mediated primarily by NAD+ since it is mirrored by the NAD+ precursor nicotinamide mononucleotide (NMN), and is blunted by the NAMPT inhibitor FK866. The TNKS-destabilizing effect of glucose is shared by other metabolic fuels including pyruvate and amino acids. NAD+ flux analysis showed that glucose and nutrients, by increasing ATP, stimulate NAMPT-mediated NAD+ production to expand NAD+ stores. Collectively our data uncover a metabolic pathway whereby nutritional energy augments NAD+ production to drive the PARsylating activity of TNKS, leading to autoPARsylation-dependent degradation of the TNKS protein. The modulation of TNKS catalytic activity and protein abundance by cellular energy charge could potentially impose a nutritional control on the many processes that TNKS regulates through PARsylation. More broadly, the stimulation of NAD+ production by ATP suggests that nutritional energy may enhance the functions of other NAD+-driven enzymes including sirtuins.

Indexed as

3T3 CellsAcrylamidesAdenosine TriphosphateAnimalsCatalysisEnergy MetabolismGlucoseHEK293 CellsHumansInsulinomaMiceNADNicotinamide PhosphoribosyltransferasePiperidinesProteasome Endopeptidase ComplexProtein Processing, Post-TranslationalAcrylamidesAdenosine TriphosphateGlucoseN-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamideNADNicotinamide PhosphoribosyltransferasePiperidinesProteasome Endopeptidase Complextankyrase 1, ratTankyrasesTNKS protein, humanUbiquitin

Identifiers

PMID25876076
PMCPMC4395342
OpenAlexW2086030246

What OpenQuestion holds

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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.