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本文引用的文献

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JNK2 is a positive regulator of the cJun transcription factor.JNK2是cJun转录因子的正向调节因子。
Mol Cell. 2006 Sep 15;23(6):899-911. doi: 10.1016/j.molcel.2006.07.028.
2
Cell apoptosis: requirement of H2AX in DNA ladder formation, but not for the activation of caspase-3.细胞凋亡:H2AX是DNA梯状条带形成所必需的,但对caspase-3的激活并非必需。
Mol Cell. 2006 Jul 7;23(1):121-32. doi: 10.1016/j.molcel.2006.05.023.
3
COOH-terminal Src kinase-mediated c-Jun phosphorylation promotes c-Jun degradation and inhibits cell transformation.羧基末端Src激酶介导的c-Jun磷酸化促进c-Jun降解并抑制细胞转化。
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Chemical genetic analysis of the time course of signal transduction by JNK.JNK信号转导时间进程的化学遗传学分析
Mol Cell. 2006 Mar 3;21(5):701-10. doi: 10.1016/j.molcel.2006.01.018.
5
The tumor suppressor p16(INK4a) prevents cell transformation through inhibition of c-Jun phosphorylation and AP-1 activity.肿瘤抑制因子p16(INK4a)通过抑制c-Jun磷酸化和AP-1活性来阻止细胞转化。
Nat Struct Mol Biol. 2005 Aug;12(8):699-707. doi: 10.1038/nsmb960. Epub 2005 Jul 10.
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Interaction of phosphorylated c-Jun with TCF4 regulates intestinal cancer development.磷酸化的c-Jun与TCF4的相互作用调节肠道癌的发展。
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Cross-talk between JIP3 and JIP1 during glucose deprivation: SEK1-JNK2 and Akt1 act as mediators.葡萄糖剥夺期间JIP3与JIP1之间的相互作用:SEK1-JNK2和Akt1作为介质发挥作用。
J Biol Chem. 2005 Jul 22;280(29):26845-55. doi: 10.1074/jbc.M502318200. Epub 2005 May 23.
8
The nucleolus as a stress sensor: JNK2 inactivates the transcription factor TIF-IA and down-regulates rRNA synthesis.核仁作为一种应激传感器:JNK2使转录因子TIF-IA失活并下调rRNA合成。
Genes Dev. 2005 Apr 15;19(8):933-41. doi: 10.1101/gad.333205. Epub 2005 Apr 1.
9
JNK1 and JNK2 oppositely regulate p53 in signaling linked to apoptosis triggered by an altered fibronectin matrix: JNK links FAK and p53.在与由改变的纤连蛋白基质引发的凋亡相关的信号传导中,JNK1和JNK2对p53的调节作用相反:JNK连接FAK和p53。
J Biol Chem. 2005 May 20;280(20):19992-9. doi: 10.1074/jbc.M500331200. Epub 2005 Mar 18.
10
c-Jun N-terminal kinase (JNK) positively regulates NFATc2 transactivation through phosphorylation within the N-terminal regulatory domain.c-Jun氨基末端激酶(JNK)通过在N末端调节域内的磷酸化正向调节NFATc2反式激活。
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JNK的功能相反性

The functional contrariety of JNK.

作者信息

Bode Ann M, Dong Zigang

机构信息

Hormel Institute, University of Minnesota, Austin, Minnesota 55912, USA.

出版信息

Mol Carcinog. 2007 Aug;46(8):591-8. doi: 10.1002/mc.20348.

DOI:10.1002/mc.20348
PMID:17538955
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2832829/
Abstract

The JNK proteins are activated by multiple and diverse stimuli, leading to varied and seemingly contradictory cellular responses. In particular, JNKs have been reported to have a role in the induction of apoptosis, but have also been implicated in enhancing cell survival and proliferation. Thus the JNK proteins seem to represent an archetype of contrariety of intracellular signaling. The opposing roles of JNKs have been attributed to the observation that JNKs activate different substrates based on specific stimulus, cell type or temporal aspects. Because of their analogous expression in apparently almost every tissue, JNK1 and JNK2 have most often been considered to have overlapping or redundant functions. In spite of this assessment, research evidence suggests that the functions of JNKs should be addressed in a manner that differentiates between their precise contributions. Specifically in this review, we examine evidence regarding whether the JNKs proteins might play distinctive roles in cellular processes associated with carcinogenesis.

摘要

JNK蛋白可被多种不同的刺激激活,从而导致多样且看似矛盾的细胞反应。特别是,据报道JNK在诱导细胞凋亡中发挥作用,但也与增强细胞存活和增殖有关。因此,JNK蛋白似乎代表了细胞内信号转导矛盾性的一个典型例子。JNK的相反作用归因于这样的观察结果,即JNK根据特定的刺激、细胞类型或时间因素激活不同的底物。由于JNK1和JNK2在几乎每个组织中都有类似的表达,它们最常被认为具有重叠或冗余的功能。尽管有这样的评估,但研究证据表明,JNK的功能应以区分其精确贡献的方式来探讨。具体而言,在本综述中,我们研究了有关JNK蛋白是否可能在与致癌作用相关的细胞过程中发挥独特作用的证据。