PC12 variants deficient in catecholamine transport.
PC12 variants deficient in catecholamine transport.
复制标题
PC12 变体缺乏儿茶酚胺转运。
DOI：
10.1111/j.1471-4159.1986.tb00752.x
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发表时间：
1986
影响因子：
4.7
通讯作者：
Howard,BD
中科院分区：
文献类型：
--
作者：
Bitler,CM;Zhang,MB;Howard,BD
We have isolated PC12 cell variants deficient in transporter‐mediated uptake of 3,4‐dihydroxyphenylethylamine (dopamine). The variants either were obtained nonselectively, or they were selected by resistance to guanethidine orN‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP). Dopamine uptake into guanethidine‐resistant cells occurred with a decreasedVmax; theKmfor dopamine and inhibition by guanethidine were normal. MPTP‐resistant cells lacked the capacity to take up dopamine. Most of the variants resembled wild‐type PC12 in their response to nerve growth factor and the storage and secretion of dopamine. MPTP‐resistant cells exhibited several deficiencies in addition to dopamine transport, i.e., no measurable storage of dopamine or acetylcholine and no observable response to nerve growth factor. Wild‐type and variant cells were compared with respect to the labeling of cell proteins with [3H]xylamine, which binds covalently to certain proteins apparently only after entering PC12 via the catecholamine transporter. When intact variant cells were used, there was markedly reduced labeling of the proteins by [3H]xylamine. Almost all of these proteins were readily labeled when cell homogenates were exposed to [3H]xylamine. However, MPTP‐resistant cells were missing three of these proteins. Northern blot analysis with cDNA clones revealed that the MPTP‐resistant cells had markedly reduced levels of several specific mRNA species.
