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1 re found for red blood cell folate and other sulfur amino acids.
2 variations associated with dietary intake of sulfur amino acids.
3  indistinguishable from sulfate derived from sulfur amino acids.
4  the terminal reaction in the degradation of sulfur amino acids.
5 ng normal food (protein, 0.8 g kg(-1) d(-1); sulfur amino acids, 20 mg kg(-1) d(-1)) at standardized
6 netics of leucine, phenylalanine, glutamine, sulfur amino acid, and threonine and their relation to w
7 hogen responses, two to proteins involved in sulfur amino acid biosynthesis, and two having significa
8  is sufficient for degradation, and specific sulfur amino acids can promote the degradation by destab
9                         Thus, in addition to sulfur amino acid catabolism, ETHE1 also affects the oxi
10 , membrane transport activities of the three sulfur amino acids cysteine, cystine and methionine, and
11 al capacity according to the availability of sulfur amino acids, establishing a functional significan
12 This experiment marks the first synthesis of sulfur amino acids from spark discharge experiments desi
13 ntribution to homocysteine remethylation and sulfur amino acid homeostasis is not known.
14 ntrations were not affected by the amount of sulfur amino acids in the three diets.
15 e cytosolic disulfide-reducing power and all sulfur amino acids in TR/GR-null livers.
16 thionine is the precursor of homocysteine, a sulfur amino acid intermediate in the methylation and tr
17                     Vitamin B12, folate, and sulfur amino acids may be modifiable risk factors for st
18 previously underappreciated link between the sulfur amino acid metabolic pathway and obesity and card
19 l homocystinuria (HCU) is an inborn error of sulfur amino acid metabolism caused by deficient activit
20  the physiological significance of BHMT-2 in sulfur amino acid metabolism.
21 BS) deficiency, is the most common defect of sulfur amino acid metabolism.
22 omocystinuria, the most frequent disorder of sulfur amino acid metabolism.
23      Examples of metabolomics evaluations of sulfur amino-acid metabolism in psychiatry, neurology, a
24 The first six deal with the functionality of sulfur amino acids (methionine and cysteine) and related
25  selenomethionine of mutants impaired in the sulfur amino acid pathway, we excluded a toxic effect of
26 thesis are the availability of cysteine, the sulfur amino acid precursor, and the activity of the rat
27                                Understanding sulfur amino acid precursor-dependent cellular mechanism
28  the extra- and intracellular equilibrium of sulfur amino acids, resulting in a decrease of approxima
29 supplying an adequate amino acid intake or a sulfur amino acid (SAA) (methionine and cysteine) free m
30 creases in seven transcripts occurred in the sulfur amino acid (SAA) biosynthetic pathway and the iro
31 DR-mediated stress resistance, we found that sulfur amino acid (SAA) restriction increased expression
32 flux and oxidation rates were determined and sulfur amino acid (SAA, methionine plus cysteine) balanc
33 ning normal or low amounts of acid-producing sulfur amino acids (SAA) and examined how this adaption
34 w these rates compare with those when either sulfur amino acids (SAAs: methionine and cyst(e)ine) or
35                   Methionine is an essential sulfur amino acid that is engaged in key cellular functi
36                            Homocysteine is a sulfur amino acid whose metabolism stands at the interse

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