Keiko Sawabe

TL;DR: It is found that TPH1 is expressed preferentially during the late developmental stage in the mouse brain, and showed higher affinity to tryptophan and stronger enzyme activity than TPH2 in a condition reflecting that of the developing brainstem.

TL;DR: Results indicated that the exogenous BH4 was oxidized and the resultant 7,8BH2 circulated through the tissues, and then it was incorporated by various other tissues and organs through a pathway shared by theExogenous sepiapterin and 7, 8BH 2 in their uptake.

TL;DR: It was concluded that the elevation in BH4 by supplementation was mainly through a "salvage pathway" that included BH2 as the key intermediate in the production of BH 4 through the action of dihydrofolate reductase.

TL;DR: Cellular uptake of sepiapterin resulted in an efficient accumulation of tetrahydrobiopterin in the cytosol in continuous manner, suggesting that this route opens into the cytOSolic compartment where use of the salvage pathway was strongly driven by sepi adapterin reductase and dihydrofolate reduct enzyme with a supply of NADPH which favors tetrahyllabopterin accumulation.

TL;DR: It is concluded that 26S proteasomes are mainly involved in the degradation of TPH, and a PEST sequence that is widely shared among short-lived proteins has been recognized.