Psychiatry related information on Mtr

• Similar treatment with MS also increased the latency period, though the delay was not as striking as that observed after DEM administration [1].

High impact information on Mtr

• Topical administration of diethyl maleate (DEM) and L-methionine sulfoximine (MS) reduced the L-glutathione (GSH) levels in kidneys, livers, and skin of inbred BALB/c mice [1].
• Thus, in this animal model, an acute dose of ethanol does not alter methionine synthase activity nor does it enhance the inactivation produced by nitrous oxide [2].
• Moreover, in mice that were not exposed to nitrous oxide, methionine synthase activity was not altered by the acute administration of ethanol alone or in combination with 0.4% atm isoflurane [2].
• The methionine synthase (Mtr) gene maps to proximal mouse chromosome 13 [3].
• Dimethylthiourea, a hydroxyl radical scavenger, impedes the inactivation of methionine synthase by nitrous oxide in mice [4].

Biological context of Mtr

• CONCLUSIONS: These findings demonstrate that defective homocysteine remethylation caused by deficiency of either MS or folate produces oxidative stress and endothelial dysfunction in the cerebral microcirculation of mice [5].

Anatomical context of Mtr

• Muscle damage was estimated by the total activity of beta-glucuronidase and water content from the red parts of m. quadriceps femoris (MQF), m. soleus (MS), m. rectus femoris (MRF), and from m. triceps brachii (MTB) [6].

Associations of Mtr with chemical compounds

• Dilatation of cerebral arterioles to the endothelium-dependent dilator, acetylcholine (10 micromol/L) was blunted in Mtr(+/-) mice compared with Mtr(+/+) mice fed the control diet (21+/-4 versus 32+/-4%; P<0.05) [5].
• The side chain, 4-methoxy-2,3,6-trimethylbenzenesulphonyl (Mtr), is a protective group coupled to arginine to mask the omega-nitrogen, in order to protect the guanidino function during peptide synthesis by the 9-fluorenylmethoxycarbonyl (Fmoc) procedure (Walker, 1994) [7].
• Methionine synthase activities in mice following acute exposures to ethanol and nitrous oxide [2].
• We investigated the effect of consecutive administration with lower-dose CDDP on intracellular accumulation of reduced folate and the activity of methionine synthase, a key enzyme in intracellular methionine synthesis [8].
• Distinct age-dependence in the activities of betaine methyltransferase, methylenetetrahydrofolate reductase and methionine synthase were found both in normal and tumour-bearing mice [9].

Other interactions of Mtr

• Methionine synthase assay based on coupling with thymidylate synthase reaction [10].
• The pattern of a "nonprotective" profile was composed of enolase (Eno1p), transketolase, heat shock protein and methionine synthase [11].

Analytical, diagnostic and therapeutic context of Mtr

• Elevated levels of superoxide and hydrogen peroxide were detected by confocal microscopy in cerebral arterioles of Mtr(+/-) mice fed the control diet and in both Mtr(+/+) and Mtr(+/-) mice fed the LF diet [5].
• To better study the pathophysiology of methionine synthase deficiency, we utilized gene-targeting technology to inactivate the methionine synthase gene in mice [12].
• Proteins of a liver extract taken from a metabolically (13)C-labeled mouse were separated by 2D-PAGE and identified after tryptic digestion by MALDI-TOF MS peptide mass fingerprinting [13].
• Methylenetetrahydrofolate reductase activity was elevated while methionine synthase was impaired in atherogenic diet fed group [14].

References