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首页> 外文期刊>Archives of Biochemistry and Biophysics >Peptidylglycine-alpha-amidating monooxygenase activity and protein are lower in copper-deficient rats and suckling copper-deficient mice
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Peptidylglycine-alpha-amidating monooxygenase activity and protein are lower in copper-deficient rats and suckling copper-deficient mice

机译:缺铜大鼠和哺乳期缺铜小鼠的肽基甘氨酸-α-酰胺化单加氧酶活性和蛋白质较低

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摘要

Peptidylglycine-alpha-amidating monooxygenase (PAM) is a copper-dependent enzyme involved in peptide posttranslational activation. Dietary Cu deficiency (Cu-) was studied to determine if lower PAM activity was due to reduction in protein or cofactor limitation. PAM activity was lower in cardiac atria of Cu- rats than Cu-adequate (Cu+) rats and there was a 50% equivalent reduction in PAM protein. No reduction in Cu- rat midbrain PAM protein was detected although PAM activity was reduced 40%. In 12-day-old (P12) mouse pups derived from dams that began Cu deficiency on day 7 of gestation, there was a parallel reduction in brain PAM activity and protein of 40-50%. PAM mRNA levels assessed in atria and brains from Cu+ and Cu- rats and mice were not altered by dietary treatment, suggesting a posttranscriptional mechanism for lower PAM protein when Cu is limiting in the cell, perhaps due to enhanced apoprotein turnover. (C) 2004 Elsevier Inc. All rights reserved.
机译:肽基甘氨酸-α-酰胺化单加氧酶(PAM)是一种铜依赖性酶,参与肽翻译后激活。研究了饮食中的铜缺乏症(Cu-),以确定较低的PAM活性是否是由于蛋白质或辅助因子限制的降低所致。在Cu-大鼠的心脏心房中,PAM活性低于在Cu-充足的(Cu +)大鼠中,PAM蛋白降低了50%。尽管PAM活性降低了40%,但未检测到Cu-大鼠中脑PAM蛋白降低。在源自大坝的12日龄(P12)小鼠幼仔中,在妊娠的第7天开始出现铜缺乏症,其大脑PAM活性和蛋白质平行降低40-50%。饮食治疗不会改变Cu +和Cu-大鼠和小鼠的心房和大脑中PAM mRNA的水平,这表明当铜在细胞中受到限制时,PAM蛋白含量较低的转录后机制可能是由于载脂蛋白更新所致。 (C)2004 Elsevier Inc.保留所有权利。

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