本组对二乙基亚硝胺所诱导的大鼠原发性肝癌组织中的组氨酸酶活性及酶蛋白表达进行了研究。
The catalytic activity of histidase and the expression of the enzyme protein were investigated in rat hepatomas induced by diethylnitrosamine.
这个激酶从自我磷酸的组氨酸上转移磷酸基,因此(为什么是这样)通常是可逆的,这个激酶也作为一个去磷酸酶。
The kinase transfers the phosphate from an autophosphorylated histidine and thus (why thus?) is often reversible, with the kinase acting as a phosphatase as well.
针对HRP2(富组氨酸蛋白2)抗原的恶性疟原虫检测方法表现出最高的检出率,但有些针对pLDH(疟原虫乳酸脱氢酶)的检测方法也展示出很高的检出率。
P. falciparum tests targeting HRP2 antigen demonstrated the highest detection rates, but some tests targeting pLDH also exhibited high detection rates.
组氨酸残基被修饰后酶活力基本不变,酶的荧光强度也不改变。
Modification of histidine residue did not change the activity of enzyme and its fluorescence emission peak intensity.
组氨酸残基被修饰后酶活力基本不变,酶的荧光强度也不改变。
Modification of histidine residue did not change the activity of the enzyme and its fluorescence emission peak intensity.
目的探讨胃黏膜内组氨酸脱羧酶(HDC)和H+,K+-ATP酶的表达与大鼠乙酸性胃溃疡自愈过程的关系。
To determine the expression change of histidine decarboxylase (HDC) and H+, K+-ATPase in gastric mucosa during the healing of acetic acid-induced gastric ulcer in rats.
其它:染料木素有抑制组氨酸脱羧酶,儿茶酚-O-甲基转移酶作用。
Other: The dyewood is known as the suppression histidine decarboxylase, the catecha phenol-O-methyl shift enzyme action.
目的探讨胃黏膜内组氨酸脱羧酶(HDC)和H+,K+-ATP酶的表达与大鼠乙酸性胃溃疡自愈过程的关系。
Objective To investigate the expression changes of histidine decarboxylase(HDC)and H+, K+-ATPase in gastric mucosa during the healing of experimental gastric ulcer in rats.
酪氨酸修饰剂的作用引起酶活力下降,初步证明,组氨酸残基是该酶活力的必需基因。
Modifying reagents of tyrosine caused remarkable decrease in the enzyme activity. And histidyl-residues were essential groups for enzyme activity.
低温可以通过质膜流动性的改变被质膜感知,也可以通过质膜上的钙离子通透性通道、组氨酸激酶、受体激酶和磷酸酯酶感知。
Cold can be perceived by plasma membrane either due to changes in membrane fluidity or with the help of sensors like Ca 2+ permeable channels, histidine kinases, receptor kinases and phospholipases .
低温可以通过质膜流动性的改变被质膜感知,也可以通过质膜上的钙离子通透性通道、组氨酸激酶、受体激酶和磷酸酯酶感知。
Cold can be perceived by plasma membrane either due to changes in membrane fluidity or with the help of sensors like Ca 2+ permeable channels, histidine kinases, receptor kinases and phospholipases .
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