Institute of Pharmacology and Toxicology, Biomedical Centre, University of Bonn, Sigmund-Freud-Str. 25, 53105, Bonn, Germany.
Neurochem Res. 2013 Jul;38(7):1303-14. doi: 10.1007/s11064-013-1022-3. Epub 2013 Mar 23.
The thiol reagent N-ethylmaleimide (NEM) is known to inhibit irreversibly ligand binding by the norepinephrine transporter (NET), while the simultaneous presence of NET substrates or ligands protects from this inhibition. Therefore, cysteine residues located within the substrate binding pocket of the NET were assumed to play an important role in ligand binding. To examine which (if any) of the 10 cysteines (Cys) of the human (h) NET might be involved in transport and/or binding function, we mutated all hNET cysteines to alanine. Using transfected HEK293 cells we studied NEM effects on the hNET with respect to [(3)H]nisoxetine binding. Two cysteines (Cys176 and Cys185) within the extracellular loop of the NET have been proposed to form a disulfide bond. We could demonstrate that this is of crucial importance as corresponding hNET mutants, in which these cysteines have been replaced, showed a lack of plasma membrane expression. However, due to their oxidized state in the native NET protein, Cys176 and Cys185 may not be targets for NEM. All other Cys-to-Ala hNET mutants were fully active and showed no change in inhibition of [(3)H]nisoxetine binding by NEM. These observations clearly exclude cysteines as being involved in hNET ligand binding. Since NEM also interacts with histidin (His), we mutated all 13 histidins of the hNET to alanine and examined the NET mutants in functional and binding assays. His222 within the large extracellular loop of the transporter was identified as an interaction partner of NEM since in the corresponding hNET mutant NEM exhibited a significantly reduced inhibitory potency. Furthermore, we could show that histidins in position 296, 370 and 372 are important for nisoxetine binding, while His220, 441, 598 and 599 are crucial for plasma membrane expression of the hNET.
巯基试剂 N-乙基马来酰亚胺(NEM)已知可不可逆地抑制去甲肾上腺素转运体(NET)的配体结合,而 NET 底物或配体的同时存在则可防止这种抑制。因此,假定位于 NET 底物结合口袋内的半胱氨酸残基在配体结合中起重要作用。为了研究人 NET 中的 10 个半胱氨酸(Cys)中的哪些(如果有)可能参与转运和/或结合功能,我们将所有 hNET 半胱氨酸突变为丙氨酸。使用转染的 HEK293 细胞,我们研究了 NEM 对 hNET 的影响,以研究 [(3)H]去甲烟碱结合。NET 细胞外环中的两个半胱氨酸(Cys176 和 Cys185)已被提议形成二硫键。我们可以证明这一点至关重要,因为相应的 hNET 突变体中,这些半胱氨酸已被取代,显示出缺乏质膜表达。然而,由于在天然 NET 蛋白中处于氧化状态,Cys176 和 Cys185 可能不是 NEM 的靶标。所有其他 Cys-to-Ala hNET 突变体均完全活跃,并且在 NEM 抑制 [(3)H]去甲烟碱结合方面没有变化。这些观察结果清楚地排除了半胱氨酸参与 hNET 配体结合。由于 NEM 还与组氨酸(His)相互作用,我们将 hNET 的 13 个组氨酸突变为丙氨酸,并在功能和结合测定中检查 NET 突变体。转运体大细胞外环中的 His222 被鉴定为 NEM 的相互作用伙伴,因为在相应的 hNET 突变体中,NEM 的抑制效力显著降低。此外,我们可以证明位置 296、370 和 372 的组氨酸对去甲烟碱结合很重要,而 His220、441、598 和 599 对 hNET 的质膜表达至关重要。