Thyrotropin-releasing hormone stimulates GTP hydrolysis by membranes from GH4C1 rat pituitary tumor cells.
Thyrotropin-releasing hormone stimulates GTP hydrolysis by membranes from GH4C1 rat pituitary tumor cells.
复制标题
促甲状腺激素释放激素通过 GH4C1 大鼠垂体肿瘤细胞膜刺激 GTP 水解。
DOI：
10.1073/pnas.81.19.6183
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发表时间：
1984
影响因子：
11.1
通讯作者：
Phillips,WJ
中科院分区：
文献类型：
--
作者：
Hinkle,PM;Phillips,WJ
促甲状腺激素释放激素（TRH）刺激GH4 C1大鼠垂体瘤细胞产生催乳素，该细胞具有对该肽的高亲和力膜受体。TRH引起高达50%的增加，从GH4 C1细胞膜中的低Km GTdR的活性。TRH刺激效应在GTP浓度为1 μ M或更低时最大。TRH引起的GTP酶活性增加0.2和20 pmol之间的GTP水解每毫克蛋白质每分钟，这取决于GTP浓度，而TRH结合是0.3 pmol/毫克蛋白质。TRH没有刺激GH 12 C1或GH-Y细胞膜中的GT3活性，这两种垂体细胞系缺乏TRH受体。GT3的刺激依赖于TRH受体的占有率; GT3活性的半数最大增加需要46 nM TRH和25 nM [N3-甲基-His]TRH，但TRH游离酸无活性。当在相同条件下测量时，这些肽对受体的表观Kd相似。TRH与受体的结合受鸟苷酸调节，以及TRH刺激低Km GTdR活性的证明表明TRH受体与乳营养细胞膜中的鸟苷酸调节蛋白相关。
Thyrotropin-releasing hormone (TRH) stimulates prolactin production by GH4C1 rat pituitary tumor cells, which possess high-affinity membrane receptors for the peptide. TRH caused up to a 50% increase in the activity of a low-Km GTPase in membranes from GH4C1 cells. The TRH stimulatory effect was maximal at GTP concentrations of 1 microM or lower. TRH caused an increase in GTPase activity of between 0.2 and 20 pmol of GTP hydrolyzed per mg of protein per min, depending on GTP concentration, while TRH binding was 0.3 pmol/mg of protein. TRH did not stimulate GTPase activity in membranes from GH12C1, or GH-Y cells, two pituitary lines lacking TRH receptors. Stimulation of GTPase depended on occupancy of the TRH receptor; half-maximal increases in GTPase activity required 46 nM TRH and 25 nM [N3-methyl-His]TRH, but the TRH free acid was inactive. The apparent Kds of these peptides for receptors were similar when measured under the same conditions. The fact that TRH binding to receptors is regulated by guanyl nucleotides, together with the demonstration of TRH stimulation of low-Km GTPase activity, suggests that the TRH receptor is associated with a guanyl nucleotide regulatory protein in the lactotroph membrane.