Molecular cloning of gene sequences regulated by tumor promoters and mitogens through protein kinase C.

M D Johnson; G M Housey; P T Kirschmeier; I B Weinstein

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Molecular cloning of gene sequences regulated by tumor promoters and mitogens through protein kinase C.

机译：通过蛋白激酶C克隆由肿瘤启动子和有丝分裂原调控的基因序列。

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cDNA clones representing genes whose expression is modulated by treatment with mitogens and tumor promoters were isolated and characterized. TPA-S1 corresponds to an mRNA species whose abundance was increased markedly within 1 h of exposure to the tumor promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA), and TPA-R1 represents an mRNA that was decreased in TPA-treated cells. The induction of TPA-S1 was blocked by actinomycin D but was not affected by cycloheximide, and it was specific for phorbol esters with tumor-promoting activity. The role of protein kinase C in the induction of TPA-S1 is supported by the following lines of evidence. (i) Agents that activated protein kinase C (TPA, platelet-derived growth factor, and diacylglycerol) also increased TPA-S1 mRNA levels. (ii) A potent PKC inhibitor blocked the induction of TPA-S1. (iii) Down-regulation of PKC activity, by treatment of cells with TPA for 24 h, resulted in a loss of responsiveness to TPA-S1 induction by subsequent TPA treatment. DNA sequence analysis of TPA-S1 predicts a cysteine-rich, secreted protein with a molecular weight of 22.6 X 10(3) that exhibits homology with sequences representing a protein with human erythroid-potentiating activity and protease inhibitory activity.

机译：分离并表征了代表基因的cDNA克隆，这些基因的表达受有丝分裂原处理后被调节。 TPA-S1对应于在与肿瘤启动子12-O-十四烷酰佛波醇13-乙酸盐（TPA）接触后1小时内丰度显着增加的mRNA物种，而TPA-R1代表在TPA处理的过程中降低的mRNA细胞。 TPA-S1的诱导被放线菌素D阻断，但不受环己酰亚胺的影响，并且它对具有促肿瘤活性的佛波酯具有特异性。以下证据支持了蛋白激酶C在TPA-S1诱导中的作用。（i）激活蛋白激酶C（TPA，血小板衍生的生长因子和二酰基甘油）的药物也增加了TPA-S1 mRNA水平。（ii）一种有效的PKC抑制剂阻断了TPA-S1的诱导。（iii）通过用TPA处理细胞24小时，PKC活性的下调导致随后TPA处理对TPA-S1诱导的反应性丧失。 TPA-S1的DNA序列分析预测了分子量为22.6 X 10（3）的富含半胱氨酸的分泌蛋白，该蛋白与代表具有人类红素增强活性和蛋白酶抑制活性的蛋白质的序列具有同源性。

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《Molecular and Cellular Biology》 |1987年第8期|共9页
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M D Johnson; G M Housey; P T Kirschmeier; I B Weinstein;
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中图分类细胞生物学;
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1. Molecular cloning of gene sequences regulated by tumor promoters and mitogens through protein kinase C. [J] . M D Johnson, G M Housey, P T Kirschmeier, Molecular and Cellular Biology . 1987,第8期

机译：通过蛋白激酶C克隆由肿瘤启动子和有丝分裂原调控的基因序列。
2. Molecular cloning and characterization of the mitogen-activated protein kinase kinase gene (MKK4) and its promoter sequence from oilseed rape (Brassica campestris L.) [J] . Teng Guo Zhang, Qiong Qiong Chen, Ning Wang, Plant Cell, Tissue and Organ Culture (PCTOC) . 2013,第3期

机译：油菜油菜（Brassica campestris L.）的丝裂原活化蛋白激酶激酶基因（MKK4）及其启动子序列的分子克隆和表征
3. Molecular cloning and characterization of the mitogen-activated protein kinase kinase gene (MKK4) and its promoter sequence from oilseed rape (Brassica campestris L.) [J] . Zhang Teng Guo, Chen Qiong Qiong, Wang Ning, Plant Cell, Tissue and Organ Culture: An International Journal on in Vitro Culture of Higher Plants . 2013,第3期

机译：油菜油菜（Brassica campestris L.）的丝裂原活化蛋白激酶激酶基因（MKK4）及其启动子序列的分子克隆和表征
4. Cloning and characterization of three homoeologous genes encoding PDI (Protein Disulfide Isomerase) and their promoter sequences in wheat. [C] . M. Ciaffi, A. Zanotti, A. R. Paolacci, International Wheat Genetics Symposium . 2003

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5. Heterodimeric deoxyguanosine/deoxyadenosine kinase from Lactobacillus acidophilus R-26: Affinity protein purification, molecular cloning, sequence of the genes, and expression in Escherichia coli. [D] . Ma, Grace Tak-Yi. 1993

机译：嗜酸乳杆菌R-26的异二聚体脱氧鸟苷/脱氧腺苷激酶：亲和蛋白纯化，分子克隆，基因序列和在大肠杆菌中的表达。
6. Molecular cloning of gene sequences regulated by tumor promoters and mitogens through protein kinase C. [O] . M D Johnson, G M Housey, P T Kirschmeier, 1987

机译：通过蛋白激酶C克隆受肿瘤启动子和有丝分裂原调控的基因序列。
7. Molecular cloning of gene sequences regulated by tumor promoters and mitogens through protein kinase C. [O] . Johnson, M D, Housey, G M, Kirschmeier, P T, 1987

机译：通过蛋白激酶C克隆受肿瘤启动子和有丝分裂原调控的基因序列。
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Molecular cloning of gene sequences regulated by tumor promoters and mitogens through protein kinase C.

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