Igo R P, Ash J F
Department of Neurobiology and Anatomy, School of Medicine, University of Utah, Salt Lake City 84132.
Biochim Biophys Acta. 1995 Feb 15;1233(2):153-62. doi: 10.1016/0005-2736(94)00246-l.
Pathways of L-glutamate and L-aspartate import by HeLa S3 cells were investigated before and after the cells were depleted of internal amino acids by starvation. Two new regulations of transport were observed in starved cells. Aspartate entered nonstarved cells by two routes, one non-saturable and one, an apparent analog of saturable system X-AG, that was sodium-dependent and competitively inhibited by glutamate. Starvation for one hour in saline increased the efficiency of saturable aspartate import, increasing Vmax and decreasing Km, an effect not previously reported for system X-AG. Glutamate uptake by nonstarved cells appeared to occur through system X-AG; through an analog of system X-C, which was sodium-independent, cystine- and quisqualate-inhibitable; as well as through one or more nonsaturable pathways. Starvation in saline for one hour resulted in the appearance of a new low-affinity saturable glutamate uptake system. This new system was sodium-dependent but not inhibited by aspartate.
在通过饥饿使HeLa S3细胞内氨基酸耗尽之前和之后，对其L-谷氨酸和L-天冬氨酸的导入途径进行了研究。在饥饿细胞中观察到了两种新的转运调节方式。天冬氨酸通过两条途径进入未饥饿细胞，一条是非饱和途径，另一条是明显类似于饱和系统X-AG的途径，该途径依赖于钠并受到谷氨酸的竞争性抑制。在盐溶液中饥饿一小时会提高饱和天冬氨酸导入的效率，增加Vmax并降低Km，这是系统X-AG以前未报道过的效应。未饥饿细胞对谷氨酸的摄取似乎通过系统X-AG发生；通过系统X-C的类似物，该类似物不依赖于钠，可被胱氨酸和喹啉酸抑制；以及通过一条或多条非饱和途径。在盐溶液中饥饿一小时导致出现一种新的低亲和力饱和谷氨酸摄取系统。这个新系统依赖于钠，但不受天冬氨酸抑制。
