Hasegawa H, Kojima M, Iida Y, Oguro K, Nakanishi N
Department of Biosciences, Teikyo University of Science, Uenohara, Yamanashi, Japan.
FEBS Lett. 1996 Sep 2;392(3):289-92. doi: 10.1016/0014-5793(96)00834-4.
RBL2H3 cells showed a remarkable increase in their level of tryptophan hydroxylase (up to 25-fold), the rate-limiting enzyme in serotonin biosynthesis, by stimulation with intracellular calcium mobilizers A23187, thapsigargin, and tBuBHQ as well as by stimulation with an antigen in the presence of IgE. The increase in the enzyme protein was visualized by Western blot analysis using anti-tryptophan hydroxylase antiserum. The enzyme turnover (Hasegawa et al., FEBS Lett., 368 (1995) 151-154) was not slowed down during the rise in tryptophan hydroxylase. Actinomycin D prevented the stimulation-induced elevation of the enzyme. These findings strongly suggest that this stimulation was achieved by the accelerated biosynthesis of tryptophan hydroxylase.
用细胞内钙动员剂A23187、毒胡萝卜素和叔丁基对苯二酚刺激，以及在存在IgE的情况下用抗原刺激，RBL2H3细胞中色氨酸羟化酶（血清素生物合成中的限速酶）水平显著增加（高达25倍）。使用抗色氨酸羟化酶抗血清通过蛋白质印迹分析可视化酶蛋白的增加。在色氨酸羟化酶增加过程中，酶周转（Hasegawa等人，《欧洲生物化学学会联合会快报》，368 (1995) 151 - 154）并未减慢。放线菌素D可阻止刺激诱导的酶升高。这些发现有力地表明，这种刺激是通过色氨酸羟化酶的生物合成加速实现的。
