Growth and protein phosphorylation in the Nb2 lymphoma: effect of prolactin, cAMP, and agents that activate adenylate cyclase.
Growth and protein phosphorylation in the Nb2 lymphoma: effect of prolactin, cAMP, and agents that activate adenylate cyclase.
复制标题
Nb2 淋巴瘤中的生长和蛋白质磷酸化：催乳素、cAMP 和激活腺苷酸环化酶的药物的作用。
DOI：
10.1002/jcb.240430405
复制
发表时间：
1990
影响因子：
4
通讯作者：
Prentice,DA
中科院分区：
文献类型：
--
作者：
Rayhel,EJ;Hughes,JP;Svihla,DA;Prentice,DA
Nb2 T淋巴瘤的独特之处在于这些淋巴细胞对催乳素和白细胞介素2的反应是增殖的。在这项研究中，我们研究了腺苷酸环化酶系统在Nb2细胞的反应性和这个信号系统在调节增殖和蛋白磷酸化的作用。cAMP类似物抑制催乳素刺激的增殖，并阻断催乳素诱导的蛋白磷酸化减少。Forskolin是T淋巴细胞中腺苷酸环化酶的有效激活剂，不会升高Nb 2细胞中的cAMP水平，也不是催乳素诱导增殖的有效抑制剂。事实上，毛喉素的一种制剂刺激了静止的Nb2细胞的增殖。与毛喉素一样，前列腺素E2不能刺激Nb 2细胞产生cAMP，尽管它能增加大鼠外周血淋巴细胞中的cAMP。霍乱毒素似乎能使Nb 2细胞中的一种刺激性鸟嘌呤核苷酸结合蛋白ADP核糖基化，但该毒素既不能增加细胞内cAMP水平，也不是一种有效的抗有丝分裂剂。百日咳毒素是一种通过抑制抑制性鸟嘌呤核苷酸结合蛋白增加cAMP产生的药物，对催乳素刺激的Nb 2细胞仅产生轻微的抗增殖作用。这些数据表明，cAMP抑制Nb 2细胞增殖和催乳素诱导的蛋白磷酸化变化，但我们的Nb 2细胞克隆中的腺苷酸环化酶系统对通常增加cAMP的药物反应不佳。
The Nb2 T lymphoma is unique in that these lymphocytes proliferate in response to prolactin as well as in response to interleukin‐2. In this study, we have examined the responsiveness of the adenylate cyclase system in Nb2 cells and the role of this signaling system in regulating proliferation and protein phosphorylation. An analog of cAMP inhibited prolactin‐stimulated proliferation and blocked a prolactin‐induced decrease in protein phosphorylation. Forskolin, a potent activator of adenylate cyclase in T lymphocytes, did not elevate cAMP levels in Nb2 cells and was not an effective inhibitor of prolactin‐induced proliferation. In fact, one preparation of forskolin stimulated proliferation of quiescent Nb2 cells. Like forskolin, prostaglandin E2did not stimulate cAMP production in Nb2 cells even though, it increased cAMP in a preparation of rat peripheral blood lymphocytes. Cholera toxin appeared to ADP‐ribosylate a stimulatory guanine nucleotide‐binding protein in Nb2 cells, but the toxin did not increase intracellular levels of cAMP nor was it a potent anti‐mitogenic agent. Pertussis toxin, an agent that can increase cAMP production through suppression of the inhibitory guanine nucleotide‐binding protein, exerted only minor anti‐proliferative actions on prolactin‐stimulated Nb2 cells. These data suggest that cAMP inhibits Nb2 cell proliferation and prolactin‐induced changes in protein phosphorylation but that the adenylate cyclase system in our clone of Nb2 cells responds poorly to agents that normally increase cAMP.