Evidence map›Paper›PMID 25515537›Full record

ArticleScience signaling2014

Npr2 inhibits TORC1 to prevent inappropriate utilization of glutamine for biosynthesis of nitrogen-containing metabolites.

Sunil Laxman, Benjamin M Sutter, Lei Shi, Benjamin P Tu

Abstract read
In one paragraph

Article in Science signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Mechanisms and rationales of SAM homeostasis.Trends in biochemical sciences · 2025
    Review
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  20. Metabolic Networks Influencing Skeletal Muscle Fiber Composition.Frontiers in cell and developmental biology · 2018
    Review
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

4 authors at 1 institution in 1 country.

Sunil LaxmanDepartment of Biochemistry, The University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9038, USA.
Benjamin M SutterDepartment of Biochemistry, The University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9038, USA.
Lei ShiDepartment of Biochemistry, The University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9038, USA.
Benjamin P TuDepartment of Biochemistry, The University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9038, USA. benjamin.tu@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · US

Funding

METABOLIC SIGNALS DRIVING CELL GROWTH & PROLIFERATIONR01GM094314 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI TU, BENJAMIN P · 2010 to 2019
$3.2M
NIGMS NIH HHS R01 GM094314NIGMS NIH HHS R01GM094314
6 · The paper itself

Abstract

Cells must be capable of switching between growth and autophagy in unpredictable nutrient environments. The conserved Npr2 protein complex (comprising Iml1, Npr2, and Npr3; also called SEACIT) inhibits target of rapamycin complex 1 (TORC1) kinase signaling, which inhibits autophagy in nutrient-rich conditions. In yeast cultured in media with nutrient limitations that promote autophagy and inhibit growth, loss of Npr2 enables cells to bypass autophagy and proliferate. We determined that Npr2-deficient yeast had a metabolic state distinct from that of wild-type yeast when grown in minimal media containing ammonium as a nitrogen source and a nonfermentable carbon source (lactate). Unlike wild-type yeast, which accumulated glutamine, Npr2-deficient yeast metabolized glutamine into nitrogen-containing metabolites and maintained a high concentration of S-adenosyl methionine (SAM). Moreover, in wild-type yeast grown in these nutrient-limited conditions, supplementation with methionine stimulated glutamine consumption for synthesis of nitrogenous metabolites, demonstrating integration of a sulfur-containing amino acid cue and nitrogen utilization. These data revealed the metabolic basis by which the Npr2 complex regulates cellular homeostasis and demonstrated a key function for TORC1 in regulating the synthesis and utilization of glutamine as a nitrogen source.

Indexed as

Ammonium CompoundsGlutamineIntracellular Signaling Peptides and ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsS-AdenosylmethionineTranscription FactorsAmmonium CompoundsGlutamineIntracellular Signaling Peptides and ProteinsNPR2 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsS-AdenosylmethionineTORC1 protein complex, S cerevisiaeTranscription Factors

Identifiers

PMID25515537
PMCPMC4427238
OpenAlexW2046525620

What OpenQuestion holds

Textmetadata
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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.