Evidence map›Paper›PMID 24397525›Full record

ArticleAnalytical chemistry2014

Quantitation of cellular metabolic fluxes of methionine.

Tomer Shlomi, Jing Fan, Baiqing Tang, Warren D Kruger, Joshua D Rabinowitz

Open access · greenAbstract read
In one paragraph

Article in Analytical chemistry, 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
2.7field-weighted citation impact, top 10% 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, 41 citations in OpenAlex.

  1. Review
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  5. The role of BCancer & metabolism · 2025
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  7. Vitamin BScience advances · 2023
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  10. Review
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  14. Article
  15. Formate metabolism in health and disease.Molecular metabolism · 2020
    Review
  16. Review
  17. Review
  18. Article
  19. Canonical Wnt is inhibited by targeting one-carbon metabolism through methotrexate or methionine deprivation.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  20. 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

5 authors at 4 institutions in 2 countries.

Tomer ShlomiDept. of Computer Science, Technion - Israel Institute of Technology, Haifa 32000, Israel.
Jing Fan
Baiqing Tang
Warren D Kruger
Joshua D Rabinowitz
Fox Chase Cancer Center · USPrinceton University · USRutgers Cancer Institute of New JerseyTechnion – Israel Institute of Technology · IL

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
Tumor cell metabolism in actionR01CA163591 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI JOSHUA D RABINOWITZ, Eileen P. White · 2012 to 2026
$7.0M
The Role of Methylthioadenosine Phosphorylase Loss in TumorigenesisR01CA131024 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI KRUGER, WARREN D · 2009 to 2013
$1.8M
NCI NIH HHS P30 CA072720NCI NIH HHS R01 CA131024NCI NIH HHS R01 CA163591
6 · The paper itself

Abstract

Methionine is an essential proteogenic amino acid. In addition, it is a methyl donor for DNA and protein methylation and a propylamine donor for polyamine biosynthesis. Both the methyl and propylamine donation pathways involve metabolic cycles, and methods are needed to quantitate these cycles. Here, we describe an analytical approach for quantifying methionine metabolic fluxes that accounts for the mixing of intracellular and extracellular methionine pools. We observe that such mixing prevents isotope tracing experiments from reaching the steady state due to the large size of the media pools and hence precludes the use of standard stationary metabolic flux analysis. Our approach is based on feeding cells with (13)C methionine and measuring the isotope-labeling kinetics of both intracellular and extracellular methionine by liquid chromatography-mass spectrometry (LC-MS). We apply this method to quantify methionine metabolism in a human fibrosarcoma cell line and study how methionine salvage pathway enzyme methylthioadenosine phosphorylase (MTAP), frequently deleted in cancer, affects methionine metabolism. We find that both transmethylation and propylamine transfer fluxes amount to roughly 15% of the net methionine uptake, with no major changes due to MTAP deletion. Our method further enables the quantification of flux through the pro-tumorigenic enzyme ornithine decarboxylase, and this flux increases 2-fold following MTAP deletion. The analytical approach used to quantify methionine metabolic fluxes is applicable for other metabolic systems affected by mixing of intracellular and extracellular metabolite pools.

Indexed as

AnimalsCell Line, TumorHumansMetabolic Flux AnalysisMethionineMethylationPurine-Nucleoside Phosphorylase5'-methylthioadenosine phosphorylaseMethioninePurine-Nucleoside Phosphorylase

Identifiers

PMID24397525
PMCPMC4060246
OpenAlexW1992048153

What OpenQuestion holds

Textmetadata
LicenceTDM
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.