Dopamine metabolism in hypoxanthine-guanine phosphoribosyltransferase-deficient variants of PC12 cells.

Dopamine metabolism in hypoxanthine-guanine phosphoribosyltransferase-deficient variants of PC12 cells.
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PC12 细胞次黄嘌呤鸟嘌呤磷酸核糖转移酶缺陷变体中的多巴胺代谢。

DOI:
10.1111/j.1471-4159.1986.tb02837.x
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发表时间:
1986
影响因子:
4.7
通讯作者:
Howard,BD
Howard,BD
中科院分区:
医学2区
文献类型:
--
作者:
Bitler,CM;Howard,BD

文献摘要

相似文献

Lesch‐Nyhan syndrome results from a deficiency of hypoxanthine‐guanine phosphoribosyltrans‐ferase (HPRT). It is manifest by behavioral abnormalities, including self‐mutilation, and evidence of abnormal 3,4‐dihydroxyphenylethylamine (dopamine) metabolism. To assess whether an HPRT deficiency in a dopaminergic cell can adversely affect dopamine metabolism in that cell, dopamine metabolism was examined in HPRT‐defi‐cient variants of PC12 pheochromocytoma cells and in cells that had regained HPRT activity by virtue of transformation with a recombinant retrovirus containing the human gene for HPRT. There was no correlation between HPRT activity and endogenous dopamine levels, dopamine uptake, dopamine release, or monoamine oxidase activity. Transformation with the HPRT retrovirus did not adversely affect dopamine metabolism.