Lu M L, Sato M, Cao B, Richie J P
Division of Urologic Surgery, Brigham and Women's Hospital, Boston, MA 02115, USA.
Proc Natl Acad Sci U S A. 1996 Aug 20;93(17):8977-82. doi: 10.1073/pnas.93.17.8977.
UV irradiation induces apoptosis (or programmed cell death) in HL-60 promyelocytic leukemia cells within 3 h. UV-induced apoptosis is accompanied by activation of a 36-kDa myelin basic protein kinase (p36 MBP kinase). This kinase is also activated by okadaic acid and retinoic acid-induced apoptosis. Irrespective of the inducing agent, p36 MBP kinase activation is restricted to the subpopulation of cells actually undergoing apoptosis. Activation of p36 MBP kinase occurs in enucleated cytoplasts, indicating no requirement for a nucleus or fragmented DNA in signaling. We also demonstrate the activation of p36 kinase in tumor necrosis factor-alpha- and serum starvation-induced cell death using the human prostatic tumor cell line LNCap and NIH 3T3 fibroblasts, respectively. We postulate that p36 MBP kinase is a common component in diverse signaling pathways leading to apoptosis.
紫外线照射可在3小时内诱导HL - 60早幼粒细胞白血病细胞发生凋亡（或程序性细胞死亡）。紫外线诱导的凋亡伴随着一种36 kDa髓鞘碱性蛋白激酶（p36 MBP激酶）的激活。该激酶也可被冈田酸和视黄酸诱导的凋亡激活。无论诱导剂是什么，p36 MBP激酶的激活都局限于实际正在经历凋亡的细胞亚群。p36 MBP激酶的激活发生在去核的胞质体中，这表明信号传导不需要细胞核或片段化的DNA。我们还分别使用人前列腺肿瘤细胞系LNCap和NIH 3T3成纤维细胞，证明了在肿瘤坏死因子-α和血清饥饿诱导的细胞死亡中p36激酶的激活。我们推测p36 MBP激酶是导致凋亡的多种信号通路中的一个共同成分。
