EC Number |
General Information |
Reference |
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2.8.3.5 | malfunction |
insulinoma cell lines with more than 70% knockdown of enzyme activity shows more than 70% reduction in glucose- or methyl succinate-plus-beta-hydroxybutyrate-stimulated insulin release |
724109 |
2.8.3.5 | malfunction |
loss of succinyl-CoA:3-ketoacid CoA transferase protein in aged rats may attenuate the capacity of kidney mitochondria to utilize ketone bodies for energy production |
703810 |
2.8.3.5 | malfunction |
overexpression of OXCT1 enhances sensitivity to cisplatin in the SK-OV-3 OC cell line |
762068 |
2.8.3.5 | malfunction |
succinyl-CoA:3-ketoacid CoA transferase deficiency is an inborn error of ketone body metabolism and causes episodic ketoacidosis |
724424 |
2.8.3.5 | metabolism |
SCOT is a key enzyme involved in ketone body metabolism |
705310 |
2.8.3.5 | metabolism |
SCOT is a rate-limiting enzyme in the degradation of ketone bodies |
703810 |
2.8.3.5 | more |
low enzyme expression is correlated with diabetis type 2 |
703384 |
2.8.3.5 | physiological function |
3-oxoacid-CoA transferase 1 (OXCT1) is a homodimeric mitochondrial matrix enzyme that serves a central role in extrahepatic ketone body catabolism (ketone bodies to acetyl-CoA to mitochondrial tricarboxylic acid cycle entrance). OXCT1 overexpression in a cisplatin-resistant cell line improves sensitivity to cisplatin. Natural sensitivity to cisplatin is observed in the eight human ovarian cell lines SK-OV-3, PA-1, Caov-3, TOV-21 G, TOV-112D, OV-90, OVCAR-3 and A2780 |
762068 |
2.8.3.5 | physiological function |
loss of SCOT protein in the aged rats may attenuate the capacity of kidney mitochondria to utilize ketone bodies for energy production |
703810 |
2.8.3.5 | physiological function |
role of SCOT in insulin secretion |
703384 |