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1 phyllide reductase mRNA and immunodetectable enzyme protein.
2 olysis and resulting in irreversible loss of enzyme protein.
3 time-dependent conformational change in the enzyme protein.
4 mogenates reflects the steady state level of enzyme protein.
5 -hour incorporation of [3H]-leucine into the enzyme protein.
6 ic conformational constraints imposed on the enzyme protein.
7 after incorporation of [3H]-leucine into the enzyme protein.
8 t these drugs did not affect the mass of the enzyme protein.
9 cids from the C-terminus of the 11 beta-HSD2 enzyme protein.
10 GSAT, or by the cellular abundance of these enzyme proteins.
11 ignificant increases in mitochondrial marker enzyme proteins.
12 e further extended to the detection of other enzyme proteins.
13 code antioxidant and Phase II detoxification enzymes/proteins.
14 orated into newly synthesized zinc-requiring enzymes/proteins.
16 ect of urocortin to a decrease in a specific enzyme protein and a subsequent decrease in the concentr
17 generally modest, when the patterns for the enzyme protein and mRNA levels for GST pi were correlate
18 octapeptide and reduced pancreatic digestive enzyme protein and mRNA levels, thus suggesting mild pan
20 pEG on plasmids may result in an increase of enzyme protein and overproduction of this essential amin
23 cates that this property is intrinsic to the enzyme protein, and cannot be attributed to the lipid en
27 sily eluted in a buffer, indicating that the enzyme proteins are probably secreted from, and deposite
30 Cells transduced with NO synthase expressed enzyme protein at consistently high levels for several p
31 hed clinical testing, including gene-editing enzymes, protein-based inhibitors, and RNA-based therape
32 ires LexA repressor, and the RecA and RecBCD enzymes--proteins best known for their role as initiator
36 cing the unproductive hydrolytic cleavage of enzyme-protein covalent intermediates that form during t
37 tween genetic mutations, endogenous residual enzyme proteins (cross-reactive immunologic material), d
40 rsional motions of multiple hydrogens of the enzyme protein during the conformational change that acc
43 k for potential off-target inhibition of the enzyme protein farnesyltransferase (PFTase) by commercia
44 s have exploited the high specificity of the enzyme protein farnesyltransferase (PFTase) to site-spec
46 lation is carried out by a pair of cytosolic enzymes, protein farnesyltransferase (FTase) and protein
47 as the recognition motif for two prenylation enzymes, protein farnesyltransferase (FTase) and protein
49 nd selectivity toward FTase over the related enzyme, protein geranylgeranyltransferase type I (GGTase
52 to assess the in vivo turnover rate of AAAD enzyme protein in the rhesus macaque striatum by monitor
55 e) storage rates and fatty acid (FA) storage enzymes/proteins in omental and abdominal subcutaneous f
58 at wild-type levels, indicating that another enzyme protein is responsible for the physiologically re
59 lead to selective inhibitors of the related enzyme protein kinase A (PKA), and several specific modi
64 nsgenic flies specifically inhibited for the enzyme protein kinase C dissociate the acquisition of le
65 -7 that expresses a transgene coding for the enzyme protein kinase C-alpha (PKC-alpha), is both malig
68 lly dependent on the cytosolic dsRNA-binding enzyme protein kinase R and does not require signalling
70 and binding studies demonstrate that a third enzyme, protein kinase C (PKC), binds AKAP79 at a site d
71 hat control the activation of DNA processing enzymes, protein kinases, and scaffold proteins to coord
72 cellular proteins, including lipid modifying enzymes, protein kinases, GTPases, and proteins involved
73 ast Tup1p repressor is one of only a few non-enzyme proteins known to interact directly with the amin
77 p in cells is limited by a ubiquitous repair enzyme, protein l-isoaspartyl methyltransferase (PIMT).
78 -l-methionine and the commercially available enzyme, protein l-isoaspartyl-O-methyltransferase, and (
79 ental temporal changes in enzyme activities, enzyme protein level, and steady-state transcript abunda
80 by a radioisotope incorporation method) and enzyme protein mass (determined by Western blotting and
81 ase-1 (but similar amounts of ADMA-producing enzyme, protein methyltransferase-1) in the human failin
82 ase, a disorder that is caused by loss of an enzyme (protein O-mannose beta-1,2-N-acetylglucosaminylt
83 iated by the endoplasmic reticulum-localized enzyme protein-O-fucosyltransferase 2 (POFUT2) was descr
84 as mendelian traits involving structural or enzyme proteins of the respiratory chain, mitochondrial
85 tive and/or positive feedback, bi-functional enzymes, protein oligomerization and discrete or continu
86 evels of PSY and several other carotenogenic enzyme proteins overaccumulate in the clpc1, clpp4, and
88 an inhibitor screen for one such target, the enzyme protein phosphatase methylesterase-1 (PME-1), whi
89 structures of both calcineurin and a related enzyme, protein phosphatase-1, revealed that this class
92 terial activity was obtained at a DH of 30% (enzyme/protein ratio 0.04 U/mg of protein, enzyme activi
93 of nuclear genes encoding heme biosynthetic enzymes, proteins required for mitochondrial genome tran
94 mage bioluminescence from Renilla luciferase enzyme/protein (RL) by injecting the substrate coelenter
95 dynamics of hydration at the surface of the enzyme protein Subtilisin Carlsberg, whose single Trp re
96 rect correlation between enzyme activity and enzyme protein, suggesting that the dynamic time course
98 oforms within the same subclass of signaling enzyme, proteins that have a high degree of structural s
100 enetic deletion of the insulin-desensitizing enzyme protein tyrosine phosphatase (PTP)1B in db/db mic
101 project to discover novel inhibitors for the enzyme protein tyrosine phosphatase-1B (PTP1B), a tyrosi
104 ts of PEPC mRNA, PEPC specific activity, and enzyme protein were greater in proteoid roots than in no
106 activity often occurs without a reduction in enzyme protein, which negates the use of immunocytochemi
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