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CK2 磷酸化 TNFAIP1 以影响其亚细胞定位和与 PCNA 的相互作用。

CK2 phosphorylates TNFAIP1 to affect its subcellular localization and interaction with PCNA.

机构信息

Key laboratory of Protein Chemistry and Developmental Biology, Ministry of Education of China, Department of Biochemistry and Molecular Biology, College of Life Science, Hunan Normal University, Changsha, China.

出版信息

Mol Biol Rep. 2010 Jul;37(6):2967-73. doi: 10.1007/s11033-009-9863-1. Epub 2009 Oct 23.

DOI:10.1007/s11033-009-9863-1
PMID:19851886
Abstract

TNFAIP1 is a protein which can be induced by tumor necrosis factoralpha (TNFalpha) and interleukin-6 (IL-6), it may play roles in DNA synthesis, DNA repair, cell apoptosis and human diseases. However, very little has been known about how TNFAIP1 acts in these physiological processes. In this paper, CK2beta was identified as a partner of TNFAIP1 by screening the HeLa cDNA library in yeast two-hybrid system with TNFAIP1 as a bait. Furthermore, it was demonstrated that CK2 could phosphorylate TNFAIP1 in vitro and in vivo, which facilitated the distribution of TNFAIP1 in nucleus and enhanced its interaction with PCNA. It is suggested that the phosphorylation of TNFAIP1 may be required for its functions.

摘要

TNFAIP1 是一种可被肿瘤坏死因子α(TNFα)和白细胞介素-6(IL-6)诱导的蛋白,它可能在 DNA 合成、DNA 修复、细胞凋亡和人类疾病中发挥作用。然而,关于 TNFAIP1 在这些生理过程中如何发挥作用的信息知之甚少。在本文中,我们通过酵母双杂交系统用 TNFAIP1 作为诱饵筛选 HeLa cDNA 文库,鉴定出 CK2β是 TNFAIP1 的一个伴侣。此外,我们还证明 CK2 可以在体外和体内使 TNFAIP1 磷酸化,这促进了 TNFAIP1 在核内的分布,并增强了它与 PCNA 的相互作用。这表明 TNFAIP1 的磷酸化可能是其发挥功能所必需的。

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本文引用的文献

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Functional characterization of the promoter region of human TNFAIP1 gene.人 TNFAIP1 基因启动子区的功能特征分析。
Mol Biol Rep. 2010 Apr;37(4):1699-705. doi: 10.1007/s11033-009-9588-1. Epub 2009 Jul 11.
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KCTD10 interacts with proliferating cell nuclear antigen and its down-regulation could inhibit cell proliferation.钾通道四聚体化结构域包含蛋白10(KCTD10)与增殖细胞核抗原相互作用,其下调可抑制细胞增殖。
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LncRNA NKILA Exacerbates Alzheimer's Disease Progression by Regulating the FOXA1-Mediated Transcription of TNFAIP1.长链非编码 RNA NKILA 通过调控 FOXA1 介导的 TNFAIP1 转录加重阿尔茨海默病进展。
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Downregulation of TNFAIP1 alleviates OGD/R‑induced neuronal damage by suppressing Nrf2/GPX4‑mediated ferroptosis.TNFAIP1的下调通过抑制Nrf2/GPX4介导的铁死亡减轻氧糖剥夺/复氧诱导的神经元损伤。
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miR-29c-3p Increases Cell Viability and Suppresses Apoptosis by Regulating the TNFAIP1/NF-κB Signaling Pathway via TNFAIP1 in Aβ-Treated Neuroblastoma Cells.miR-29c-3p通过在Aβ处理的神经母细胞瘤细胞中经由TNFAIP1调节TNFAIP1/NF-κB信号通路来增加细胞活力并抑制细胞凋亡。
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