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Associations between DNA variants of the dopamine beta hydroxylase gene and measures of sustained attention accord well with cognitive-neuroanatomical models of sustained attention.
A recent example of a study of a predictive genetic biomarker in cocaine dependence examined the relationship between genetic variation of the dopamine beta hydroxylase (DBH) gene and the response to the medication disulfiram.
Dopamine beta hydroxylase (DBH) is responsible for maintaining dopamine-to-norepinephrine ratio implicated in migraine pathophysiology.
Finally, we excluded any correlation between polymorphisms rs4818 and rs4680 of Catechol-O-Methyltransferase (COMT) gene and migraine, suggesting to look over COMT to explain catecholamine derangement in migraine, exploring enzymes involved in catecholamines synthesis and catabolism such as monoamine-oxidase, dopamine beta hydroxylase, tyrosine hydroxylase or tyrosine decarboxylase[6].
Indeed, even in mice lacking both HCRT and the norepinephrine synthesizing enzyme, dopamine beta hydroxylase, i.e., a double knockout, there is no additive effect [38].
In contrast, dopamine beta hydroxylase (DβH), the critical enzyme required to transform dopamine into noradrenalin was down-regulated during differentiation (Fig. 2B).
Similar(45)
Pharmacogenetic randomized trial for cocaine abuse: disulfiram and dopamine beta-hydroxylase.
In contrast to amine oxidases, dopamine beta-monooxyegnase contains only copper as a cofactor.
For example, dopamine beta-monooxygenase catalyzes the formation of the hormone/neurotransmitter norepinephrine from dopamine.
Dopamine beta-hydroxylase (DBH) is an intracellular enzyme catalyzing the conversion of dopamine to noradrenaline.
Disruption of the dopamine beta-hydroxylase gene in mice suggests roles for norepinephrine in motor function, learning and memory.
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