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1                                              GOT knockdown abrogated this effect and caused ATP loss
2                                              GOT overexpression increased anaplerotic refilling of tr
3 te (Asp) via aspartate aminotransferase (AST/GOT).
4                                 Furthermore, GOT overexpression not only reduced ischemic stroke lesi
5  under hypoglycemic conditions and increased GOT-mediated metabolism in vitro Correction of stroke-in
6  Immunohistochemistry demonstrated increased GOT protein expression in the brain.
7                  BCA significantly increased GOT mRNA and protein expression at 24 h and protected ag
8  mitigates stroke-induced injury by inducing GOT expression.
9 was identified as the most potent inducer of GOT gene expression in neural cells.
10  seek to identify small-molecule inducers of GOT expression to mitigate ischemic stroke injury.
11 asmid, which demonstrated transactivation of GOT.
12 MS/MS in combination with either targeted or GOT approaches can be a useful tool for monitoring gut m
13                                       Plasma GOT, GPT, and hepatic MMP-9 activity increased 2.5-fold,
14  SESI-MS/MS and metabolic features from SESI-GOT-MS/MS have significant differences when comparing sa
15                        As a result, the SESI-GOT-MS/MS method detected a similar number of metabolic
16       The analytical performance of the SESI-GOT-MS/MS method, as well as its biological capability,
17 SESI-MS/MS panel and 75 features in the SESI-GOT-MS/MS panel) were established.
18 obally optimized targeted mass spectrometry (GOT-MS), to sensitively detect volatile metabolites from
19 her, our results support a new paradigm that GOT enables metabolism of otherwise neurotoxic extracell
20                                          The GOT activity expressed as the ratio with and without pyr
21                                          The GOT-dependent metabolism of glutamate was studied in pri
22 aluated glutamate-oxaloacetate transaminase (GOT) activity in hemolysates with and without pyridoxal
23 ized by glutamate oxaloacetate transaminase (GOT) to maintain cellular energetics and protect the bra
24 lity of glutamate oxaloacetate transaminase (GOT) to metabolize neurotoxic glutamate in the stroke-af
25    Plasma glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) levels were
26 plasm, glutamate oxaloacetate transaminases (GOT), and malate dehydrogenases (MDH).
27    This was a randomized single-blind trial (GOT ICE [Cognitive Effects of Body Temperature During Hy
28       Of note, this protection was lost when GOT was knocked down.
29 motor function-this protection was lost with GOT knockdown.