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1 variations associated with dietary intake of sulfur amino acids.
2  indistinguishable from sulfate derived from sulfur amino acids.
3  the terminal reaction in the degradation of sulfur amino acids.
4 re found for red blood cell folate and other 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 cysteine dioxygenase (cdo-1), members of the sulfur amino acid catabolism pathway required for produc
10                         Thus, in addition to sulfur amino acid catabolism, ETHE1 also affects the oxi
11 n a mouse model of CKD, we found that a high sulfur amino acid-containing diet resulted in posttransl
12  of soybean seeds as a proxy for the overall sulfur amino acid content of soybean seeds.
13 cost-effective method to predict the overall sulfur amino acid content of soybean seeds.
14 nhibitor activities and elemental sulfur and sulfur amino acid content of the seeds.
15 s to develop soybean cultivars with enhanced sulfur amino acid content.
16 , membrane transport activities of the three sulfur amino acids cysteine, cystine and methionine, and
17                Furthermore, a diet devoid of sulfur amino acids does not require GCN2 for the ISR to
18 al capacity according to the availability of sulfur amino acids, establishing a functional significan
19 This experiment marks the first synthesis of sulfur amino acids from spark discharge experiments desi
20 ntribution to homocysteine remethylation and sulfur amino acid homeostasis is not known.
21 ntrations were not affected by the amount of sulfur amino acids in the three diets.
22 e cytosolic disulfide-reducing power and all sulfur amino acids in TR/GR-null livers.
23         Here we report that fatty liver is a sulfur amino acid insufficient state that promotes metab
24 thionine is the precursor of homocysteine, a sulfur amino acid intermediate in the methylation and tr
25          In contrast, dietary removal of the sulfur amino acids lowered serum methionine, but not int
26                     Vitamin B12, folate, and sulfur amino acids may be modifiable risk factors for st
27 previously underappreciated link between the sulfur amino acid metabolic pathway and obesity and card
28 l homocystinuria (HCU) is an inborn error of sulfur amino acid metabolism caused by deficient activit
29 gs support a pathogenic link of dysregulated sulfur amino acid metabolism to metabolic inflexibility
30 pathway, which links cell proliferation with sulfur amino acid metabolism, was significantly affected
31 omocystinuria, the most frequent disorder of sulfur amino acid metabolism.
32  the physiological significance of BHMT-2 in sulfur amino acid metabolism.
33 BS) deficiency, is the most common defect of sulfur amino acid metabolism.
34 gs support a role for LdmS in Staphylococcal sulfur amino acid metabolism.
35 odermis where it is also sufficient to drive sulfur amino acid metabolism.
36      Examples of metabolomics evaluations of sulfur amino-acid metabolism in psychiatry, neurology, a
37 The first six deal with the functionality of sulfur amino acids (methionine and cysteine) and related
38 e diet or a diet devoid of either leucine or sulfur amino acids (methionine and cysteine).
39  selenomethionine of mutants impaired in the sulfur amino acid pathway, we excluded a toxic effect of
40 thesis are the availability of cysteine, the sulfur amino acid precursor, and the activity of the rat
41                                Understanding sulfur amino acid precursor-dependent cellular mechanism
42                                              Sulfur amino acid restriction (SAAR)-the reduction of me
43  the extra- and intracellular equilibrium of sulfur amino acids, resulting in a decrease of approxima
44 supplying an adequate amino acid intake or a sulfur amino acid (SAA) (methionine and cysteine) free m
45 creases in seven transcripts occurred in the sulfur amino acid (SAA) biosynthetic pathway and the iro
46                         We show that hepatic sulfur amino acid (SAA) metabolism is under transcriptio
47 DR-mediated stress resistance, we found that sulfur amino acid (SAA) restriction increased expression
48                 Evidence suggests inadequate sulfur amino acid (SAA) status may explain many signs of
49 flux and oxidation rates were determined and sulfur amino acid (SAA, methionine plus cysteine) balanc
50 ning normal or low amounts of acid-producing sulfur amino acids (SAA) and examined how this adaption
51 w these rates compare with those when either sulfur amino acids (SAAs: methionine and cyst(e)ine) or
52                   Methionine is an essential sulfur amino acid that is engaged in key cellular functi
53 rence Intake (DRI) Recommendations for total sulfur amino acids (TSAAs; methionine + cysteine) during
54                            Homocysteine is a sulfur amino acid whose metabolism stands at the interse