S-adenosylmethionine and proliferation

New pathways, new targets

Nuria Martínez-López, Marta Varela-Rey, Usue Ariz, Nieves Embade, Mercedes Vazquez-Chantada, David Fernandez-Ramos, Laura Gomez-Santos, Shelly C. Lu, Jose M. Mato, Maria L. Martinez-Chantar

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

SAMe (S-adenosylmethionine) is the main methyl donor group in the cell. MAT (methionine adenosyl-transferase) is the unique enzyme responsible for the synthesis of SAMe from methionine and ATP, and SAMe is the common point between the three principal metabolic pathways: polyamines, transmethylation and transsulfuration that converge into the methionine cycle. SAMe is now also considered a key regulator of metabolism, proliferation, differentiation, apoptosis and cell death. Recent results show a new signalling pathway implicated in the proliferation of the hepatocyte, where AMPK (AMP-activated protein kinase) and HuR, modulated by SAMe, take place in HGF (hepatocyte growth factor)-mediated cell growth. Abnormalities in methionine metabolism occur in several animal models of alcoholic liver injury, and it is also altered in patients with liver disease. Both high and low levels of SAMe predispose to liver injury. In this regard, knockout mouse models have been developed for the enzymes responsible for SAMe synthesis and catabolism, MAT1A and GNMT (glycine N-methyltransferase) respectively. These knockout mice develop steatosis and HCC (hepatocellular carcinoma), and both models closely replicate the pathologies of human disease, which makes them extremely useful to elucidate the mechanism underlying liver disease. These new findings open a wide range of possibilities to discover novel targets for clinical applications.

Original languageEnglish (US)
Pages (from-to)848-852
Number of pages5
JournalBiochemical Society Transactions
Volume36
Issue number5
DOIs
StatePublished - Oct 2008
Externally publishedYes

Fingerprint

S-Adenosylmethionine
Methionine
Liver
Metabolism
Knockout Mice
Liver Diseases
Glycine N-Methyltransferase
AMP-Activated Protein Kinases
Hepatocyte Growth Factor
Wounds and Injuries
Polyamines
Cell growth
Pathology
Cell death
Enzymes
Transferases
Metabolic Networks and Pathways
Hepatocytes
Hepatocellular Carcinoma
Animals

Keywords

  • Glycine N-methyltransferase (GNMT)
  • HuR
  • Liver
  • Methionine adenosyltransferase (MAT)
  • Non-alcoholic steatohepatitis (NASH)
  • S-adenosylmethionine (SAMe)

ASJC Scopus subject areas

  • Biochemistry

Cite this

Martínez-López, N., Varela-Rey, M., Ariz, U., Embade, N., Vazquez-Chantada, M., Fernandez-Ramos, D., ... Martinez-Chantar, M. L. (2008). S-adenosylmethionine and proliferation: New pathways, new targets. Biochemical Society Transactions, 36(5), 848-852. https://doi.org/10.1042/BST0360848

S-adenosylmethionine and proliferation : New pathways, new targets. / Martínez-López, Nuria; Varela-Rey, Marta; Ariz, Usue; Embade, Nieves; Vazquez-Chantada, Mercedes; Fernandez-Ramos, David; Gomez-Santos, Laura; Lu, Shelly C.; Mato, Jose M.; Martinez-Chantar, Maria L.

In: Biochemical Society Transactions, Vol. 36, No. 5, 10.2008, p. 848-852.

Research output: Contribution to journalArticle

Martínez-López, N, Varela-Rey, M, Ariz, U, Embade, N, Vazquez-Chantada, M, Fernandez-Ramos, D, Gomez-Santos, L, Lu, SC, Mato, JM & Martinez-Chantar, ML 2008, 'S-adenosylmethionine and proliferation: New pathways, new targets', Biochemical Society Transactions, vol. 36, no. 5, pp. 848-852. https://doi.org/10.1042/BST0360848
Martínez-López N, Varela-Rey M, Ariz U, Embade N, Vazquez-Chantada M, Fernandez-Ramos D et al. S-adenosylmethionine and proliferation: New pathways, new targets. Biochemical Society Transactions. 2008 Oct;36(5):848-852. https://doi.org/10.1042/BST0360848
Martínez-López, Nuria ; Varela-Rey, Marta ; Ariz, Usue ; Embade, Nieves ; Vazquez-Chantada, Mercedes ; Fernandez-Ramos, David ; Gomez-Santos, Laura ; Lu, Shelly C. ; Mato, Jose M. ; Martinez-Chantar, Maria L. / S-adenosylmethionine and proliferation : New pathways, new targets. In: Biochemical Society Transactions. 2008 ; Vol. 36, No. 5. pp. 848-852.
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