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1 GPT (10 U/ml) decreased neuronal death caused by exposur
2 GPT and changes of JTH scores at onset of PN were signif
3 GPT has also been predicted to act on the cytosolic face
4 GPT is an effective neuroprotectant against glutamate ex
5 GPT was again neuroprotective, decreasing neuronal death
9 ctural models supported associations between GPT and improved survival in the overall cohort (adjuste
17 and synthesis of the DPAGT1 encoded enzyme, GPT, in determining the abundance of cytoplasmic beta-ca
19 20.6 improved to adjusted means of 17.6 for GPT and 16.5 for CM, with no significant difference betw
23 hs per 100 person-years for patients who had GPT vs. those who did not have GPT; adjusted HR, 0.60 [C
26 ients who had GPT vs. those who did not have GPT; adjusted HR, 0.60 [CI, 0.43 to 0.82]; P = 0.002) an
32 or a histidine in GPT-1 and an asparagine in GPT-2, which causes a gain or loss of an NlaIII restrict
34 ution in codon 14, coding for a histidine in GPT-1 and an asparagine in GPT-2, which causes a gain or
35 spans is the largest hydrophilic segment in GPT and, as judged by site-directed mutagenesis, has a n
36 GPT sequences or epitope tags inserted into GPT, after selective permeabilization of the plasma memb
37 egulated; transcription of the mouse mammary GPT gene is stimulated by the lactogenic hormones, insul
40 ts in regulating the expression of the mouse GPT (mGPT) gene was investigated by transient transfecti
41 croscopy with antibodies specific for native GPT sequences or epitope tags inserted into GPT, after s
48 s were detected by chemical cross-linking of GPT and by a dominant-negative effect caused by co-expre
55 and the SLO system showed that overexpressed GPT was not functional in vivo, although it was highly a
58 ) of liver injury, as measured by both serum GPT levels and percent hepatocellular necrosis, was dram
60 unction (JTH) and the Grooved Pegboard Test (GPT), were performed at baseline and during subsequent c
61 typic and phenotypic susceptibility testing (GPT) optimizes antiretroviral selection, but its effect
62 The more abundant expression of GPT2 than GPT, especially in muscle and fat, suggests a unique and
70 determination of the molecular basis of the GPT isozyme variants will permit PCR-based detection of
71 decades, although chromosomal mapping of the GPT locus in the 1980s produced conflicting results.
73 TP inhibition increased transcription of the GPT/GOT1 genes through up-regulation of the IRE1alpha/cJ
75 superior to placebo in patients assigned to GPT (difference, -1.7; 95% CI, -3.2 to -0.1; P = .04) or
77 ase (GOT) and glutamic pyruvic transaminase (GPT) levels were determined by enzymatic method, and the
79 r damage as measured by serum transaminases (GPT) demonstrate similar acute (3-6 h) post-I/R response
80 DP-GlcNAc:dolichol-P GlcNAc-1-P transferase (GPT) is an endoplasmic reticulum (ER) enzyme responsible
81 th LLO initiation by GlcNAc-1-P transferase (GPT), mannose-P-dolichol synthase, glucose-P-dolichol sy
82 DP-GlcNAc:dolichol-P GlcNAc-1-P transferase (GPT), which initiates N-linked glycosylation by catalyzi
83 N-acetylglucosamine-1-phosphate transferase (GPT), the enzyme that initiates the pathway for the bios
84 variants of glutamate pyruvate transminase (GPT) (E.C.2.6.1.2) have been used as genetic markers in
86 igated by transient transfections of various GPT promoter/luciferase (Luc) constructs into primary mo
87 xpressed in muscle, fat, and kidney, whereas GPT is mainly expressed in kidney, liver, and heart.
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