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raf family serine/threonine protein kinases in mitogen signal transduction.

作者信息

Rapp U R, Heidecker G, Huleihel M, Cleveland J L, Choi W C, Pawson T, Ihle J N, Anderson W B

机构信息

Laboratory of Viral Carcinogenesis, National Cancer Institute-Frederick Cancer Research Facility, Maryland 21701.

出版信息

Cold Spring Harb Symp Quant Biol. 1988;53 Pt 1:173-84. doi: 10.1101/sqb.1988.053.01.023.

DOI:10.1101/sqb.1988.053.01.023
PMID:2978288
Abstract
摘要

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1
raf family serine/threonine protein kinases in mitogen signal transduction.丝裂原信号转导中的raf家族丝氨酸/苏氨酸蛋白激酶
Cold Spring Harb Symp Quant Biol. 1988;53 Pt 1:173-84. doi: 10.1101/sqb.1988.053.01.023.
2
Tyrosine phosphorylation in signal transduction.信号转导中的酪氨酸磷酸化。
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Signal transduction from membrane to cytoplasm: growth factors and membrane-bound oncogene products increase Raf-1 phosphorylation and associated protein kinase activity.从细胞膜到细胞质的信号转导：生长因子和膜结合癌基因产物增加Raf-1磷酸化及相关蛋白激酶活性。
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A dominant role for the Raf-MEK pathway in forskolin, 12-O-tetradecanoyl-phorbol acetate, and platelet-derived growth factor-induced CREB (cAMP-responsive element-binding protein) activation, uncoupled from serine 133 phosphorylation in NIH 3T3 cells.Raf-MEK通路在毛喉素、十四酰佛波醇乙酸酯及血小板衍生生长因子诱导的NIH 3T3细胞中cAMP反应元件结合蛋白（CREB）激活过程中起主导作用，且该激活与丝氨酸133磷酸化无关。
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pim-1 proto-oncogene expression in anti-CD3-mediated T cell activation is associated with protein kinase C activation and is independent of Raf-1.抗CD3介导的T细胞活化过程中pim-1原癌基因的表达与蛋白激酶C活化相关，且不依赖于Raf-1。
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Zeta PKC plays a critical role during stromelysin promoter activation by platelet-derived growth factor through a novel palindromic element.ζ蛋白激酶C通过一种新的回文元件，在血小板衍生生长因子激活基质溶解素启动子的过程中发挥关键作用。
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[The c-raf oncogene].[c-raf原癌基因]
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Activation of Raf-1 and mitogen-activated protein kinase in murine macrophages partially mimics lipopolysaccharide-induced signaling events.鼠巨噬细胞中Raf-1和丝裂原活化蛋白激酶的激活部分模拟了脂多糖诱导的信号事件。
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Genomic response to growth factors.对生长因子的基因组反应。
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Inhibition of oncogene expression by green tea and (-)-epigallocatechin gallate in mice.绿茶和（-）-表没食子儿茶素没食子酸酯对小鼠癌基因表达的抑制作用。
Nutr Cancer. 1995;24(2):203-9. doi: 10.1080/01635589509514408.

引用本文的文献

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A-RAF kinase functions in ARF6 regulated endocytic membrane traffic.A-RAF激酶在ARF6调节的内吞膜运输中发挥作用。
PLoS One. 2009;4(2):e4647. doi: 10.1371/journal.pone.0004647. Epub 2009 Feb 27.
2
Drosophila-raf acts to elaborate dorsoventral pattern in the ectoderm of developing embryos.果蝇raf蛋白在发育中胚胎的外胚层中发挥作用，细化背腹模式。
Genetics. 2001 Nov;159(3):1031-44. doi: 10.1093/genetics/159.3.1031.
3
Insulin signal transduction through protein kinase cascades.胰岛素通过蛋白激酶级联反应进行信号转导。
Mol Cell Biochem. 1998 May;182(1-2):31-48.
4
Hepatitis B virus X protein induces RNA polymerase III-dependent gene transcription and increases cellular TATA-binding protein by activating the Ras signaling pathway.乙型肝炎病毒X蛋白通过激活Ras信号通路诱导RNA聚合酶III依赖性基因转录并增加细胞中的TATA结合蛋白。
Mol Cell Biol. 1997 Dec;17(12):6838-46. doi: 10.1128/MCB.17.12.6838.
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3pK, a novel mitogen-activated protein (MAP) kinase-activated protein kinase, is targeted by three MAP kinase pathways.3pK是一种新型的丝裂原活化蛋白（MAP）激酶激活的蛋白激酶，受三种MAP激酶途径调控。
Mol Cell Biol. 1996 Dec;16(12):6687-97. doi: 10.1128/MCB.16.12.6687.
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Bcl-2 interacting protein, BAG-1, binds to and activates the kinase Raf-1.Bcl-2相互作用蛋白BAG-1与激酶Raf-1结合并激活它。
Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):7063-8. doi: 10.1073/pnas.93.14.7063.
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Mitogen-activated protein kinases p42mapk and p44mapk are required for fibroblast proliferation.丝裂原活化蛋白激酶p42mapk和p44mapk是成纤维细胞增殖所必需的。
Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8319-23. doi: 10.1073/pnas.90.18.8319.
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Growth factors induce nuclear translocation of MAP kinases (p42mapk and p44mapk) but not of their activator MAP kinase kinase (p45mapkk) in fibroblasts.生长因子可诱导成纤维细胞中丝裂原活化蛋白激酶（p42mapk和p44mapk）发生核转位，但不会诱导其激活剂丝裂原活化蛋白激酶激酶（p45mapkk）发生核转位。
J Cell Biol. 1993 Sep;122(5):1079-88. doi: 10.1083/jcb.122.5.1079.
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Raf-1 and p21v-ras cooperate in the activation of mitogen-activated protein kinase.Raf-1与p21v-ras协同激活丝裂原活化蛋白激酶。
Proc Natl Acad Sci U S A. 1993 Jun 15;90(12):5772-6. doi: 10.1073/pnas.90.12.5772.
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Oncogene activation of HIV-LTR-driven expression via the NF-kappa B binding sites.通过核因子κB结合位点实现HIV长末端重复序列驱动表达的癌基因激活。
Nucleic Acids Res. 1993 Nov 11;21(22):5229-34. doi: 10.1093/nar/21.22.5229.