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English Journal

A metabolomics-driven approach reveals metabolic responses and mechanisms in the rat heart following myocardial infarction.

Nam M1, Jung Y2, Ryu DH3, Hwang GS4.
International journal of cardiology.Int J Cardiol.2017 Jan 15;227:239-246. doi: 10.1016/j.ijcard.2016.11.127. Epub 2016 Nov 11.
BACKGROUND: Myocardial infarction (MI) is caused by myocardial necrosis resulting from prolonged ischemia. However, the biological mechanisms underlying MI remain unclear.METHODS: We evaluated metabolic and lipidomic changes in rat heart tissue from sham and MI at 1h, 1day and 10day after coronary l
PMID 27852445

Transient Kinetics Define a Complete Kinetic Model for Protein Arginine Methyltransferase 1.

Hu H1, Luo C2, Zheng YG3.
The Journal of biological chemistry.J Biol Chem.2016 Dec 23;291(52):26722-26738. doi: 10.1074/jbc.M116.757625. Epub 2016 Nov 10.
Protein arginine methyltransferases (PRMTs) are the enzymes responsible for posttranslational methylation of protein arginine residues in eukaryotic cells, particularly within the histone tails. A detailed mechanistic model of PRMT-catalyzed methylation is currently lacking, but it is essential for
PMID 27834681

Short term methionine restriction increases hepatic global DNA methylation in adult but not young male C57BL/6J mice.

Mattocks DA1, Mentch SJ2, Shneyder J1, Ables GP1, Sun D3, Richie JP Jr4, Locasale JW2, Nichenametla SN5.
Experimental gerontology.Exp Gerontol.2016 Dec 7;88:1-8. doi: 10.1016/j.exger.2016.12.003. [Epub ahead of print]
Despite well-documented evidence for lifespan extension by methionine restriction (MR), underlying mechanisms remain unknown. As methionine can alter S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), the substrate and product of DNA methyltransferase-1 (DNMT1), we hypothesized that MR die
PMID 27940170

Relationship between blood levels of methyl donor and folate and mild cognitive impairment in Chinese patients with type 2 diabetes: a case-control study