Evidence map›Paper›PMID 19833238›Full record

ReviewBiochimica et biophysica acta2010

The logic of the hepatic methionine metabolic cycle.

M V Martinov, V M Vitvitsky, R Banerjee, F I Ataullakhanov

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

47 citing papers in PubMed, 143 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Metabolic kinetic modeling of [European journal of nuclear medicine and molecular imaging · 2023
    Article
  8. Synthesis of 4-(Phenylchalcogenyl)tetrazolo[1,5-Molecules (Basel, Switzerland) · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. New targets for NAFLD.JHEP reports : innovation in hepatology · 2021
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Sulfur Metabolism Under Stress.Antioxidants & redox signaling · 2020
    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

4 authors at 2 institutions in 2 countries.

M V MartinovNational Research Center for Hematology, RAMS, Moscow, Russia.
V M Vitvitsky
R Banerjee
F I Ataullakhanov
Federal State Institution Hematology Research Center · RUUniversity of Michigan–Ann Arbor · US

Funding

Transsulfuration and HyperhomocysteinemiaR01HL058984 · NHLBI · UNIVERSITY OF NEBRASKA LINCOLN · PI BANERJEE, RUMA V · 1997 to 2020
$6.0M
The Sulfur/Glutamate Circuitry in the Neuroimmune SystemR01DK064959 · NIDDK · UNIVERSITY OF NEBRASKA LINCOLN · PI BANERJEE, RUMA V · 2003 to 2009
$2.2M
NHLBI NIH HHS HL58984NHLBI NIH HHS R01 HL058984NIDDK NIH HHS R01 DK064959
6 · The paper itself

Abstract

This review describes our current understanding of the "traffic lights" that regulate sulfur flow through the methionine bionetwork in liver, which supplies two major homeostatic systems governing cellular methylation and antioxidant potential. Theoretical concepts derived from mathematical modeling of this metabolic nexus provide insights into the properties of this system, some of which seem to be paradoxical at first glance. Cellular needs supported by this network are met by use of parallel metabolic tracks that are differentially controlled by intermediates in the pathway. A major task, i.e. providing cellular methylases with the methylating substrate, S-adenosylmethionine, is met by flux through the methionine adenosyltransferase I isoform. On the other hand, a second important function, i.e., stabilization of the blood methionine concentration in the face of high dietary intake of this amino acid, is achieved by switching to an alternative isoform, methionine adenosyltransferase III, and to glycine N-methyl transferase, which together bypass the first two reactions in the methionine cycle. This regulatory strategy leads to two metabolic modes that differ in metabolite concentrations and metabolic rates almost by an order of magnitude. Switching between these modes occurs in a narrow trigger zone of methionine concentration. Complementary experimental and theoretical analyses of hepatic methionine metabolism have been richly informative and have the potential to illuminate its response to oxidative challenge, to methionine restriction and lifespan extension studies and to diseases resulting from deficiencies at specific loci in this pathway.

Indexed as

Amino Acid Metabolism, Inborn ErrorsAnimalsGlycine N-MethyltransferaseHumansLiverMetabolic Networks and PathwaysMethionineMethionine AdenosyltransferaseMethylationMethyltransferasesModels, BiologicalS-AdenosylmethionineGlycine N-MethyltransferaseMethionineMethionine AdenosyltransferaseMethyltransferasesS-Adenosylmethionine

Identifiers

PMID19833238
PMCPMC2787964
OpenAlexW2001779904

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.