• 本组二乙基亚硝胺诱导大鼠原发性肝癌组织中的组氨酸活性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.

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  • 这个自我磷酸组氨酸转移磷酸基,因此为什么是这样通常可逆的,这个激也作为一个去磷酸

    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.

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  • 针对HRP2(富组氨酸蛋白2)抗原的恶性疟原虫检测方法表现最高的检出率,有些针对pLDH(疟原虫乳酸脱氢)的检测方法展示很高的检出率。

    P. falciparum tests targeting HRP2 antigen demonstrated the highest detection rates, but some tests targeting pLDH also exhibited high detection rates.

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  • 组氨酸残基被修饰活力基本不变,荧光强度改变

    Modification of histidine residue did not change the activity of enzyme and its fluorescence emission peak intensity.

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  • 组氨酸残基被修饰活力基本不变,荧光强度改变

    Modification of histidine residue did not change the activity of the enzyme and its fluorescence emission peak intensity.

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  • 目的探讨黏膜组氨酸脱羧HDCH+,K+-ATP表达大鼠乙酸胃溃疡过程关系。

    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.

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  • 其它染料木素有抑制组氨酸脱羧,儿茶酚-O-甲基转移作用

    Other: The dyewood is known as the suppression histidine decarboxylase, the catecha phenol-O-methyl shift enzyme action.

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  • 目的探讨黏膜内组氨酸脱羧HDCH+,K+-ATP表达大鼠乙酸性胃溃疡过程的关系。

    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.

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  • 酪氨酸修饰作用引起活力下降,初步证明,组氨酸残基活力的必需基因。

    Modifying reagents of tyrosine caused remarkable decrease in the enzyme activity. And histidyl-residues were essential groups for enzyme activity.

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  • 低温可以通过流动性改变被质膜感知可以通过质膜上的离子通透性通道组氨酸受体磷酸酯感知。

    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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  • 低温可以通过流动性改变被质膜感知可以通过质膜上的离子通透性通道组氨酸受体磷酸酯感知。

    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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