1                                              GOT knockdown abrogated this effect and caused ATP loss

2                                              GOT overexpression increased anaplerotic refilling of tr

3                                 Furthermore, GOT overexpression not only reduced ischemic stroke lesi

4  under hypoglycemic conditions and increased GOT-mediated metabolism in vitro Correction of stroke-in

5  Immunohistochemistry demonstrated increased GOT protein expression in the brain.

6                  BCA significantly increased GOT mRNA and protein expression at 24 h and protected ag

7  mitigates stroke-induced injury by inducing GOT expression.

8 was identified as the most potent inducer of GOT gene expression in neural cells.

9  seek to identify small-molecule inducers of GOT expression to mitigate ischemic stroke injury.

10 asmid, which demonstrated transactivation of GOT.

11                                       Plasma GOT, GPT, and hepatic MMP-9 activity increased 2.5-fold,

12 her, our results support a new paradigm that GOT enables metabolism of otherwise neurotoxic extracell

13                                          The GOT-dependent metabolism of glutamate was studied in pri

14 ized by glutamate oxaloacetate transaminase (GOT) to maintain cellular energetics and protect the bra

15 lity of glutamate oxaloacetate transaminase (GOT) to metabolize neurotoxic glutamate in the stroke-af

16    Plasma glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) levels were

17 plasm, glutamate oxaloacetate transaminases (GOT), and malate dehydrogenases (MDH).

18       Of note, this protection was lost when GOT was knocked down.

19 motor function-this protection was lost with GOT knockdown.