Identification of nucleolar and coiled-body phosphoprotein 1 (NOLC1) minimal promoter regulated by NF-κB and CREB

Gao, Xue Song; Wang, Qi; Li, Wei; Yang, Biao; Song, Hao; Ju, Wei; Liu, Shu Nai; Cheng, Jun

doi:10.5483/bmbrep.2011.44.1.70

Cited by 18 publications

(19 citation statements)

References 16 publications

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“…HCV NS5A has also been implicated in HCV‐induced liver fibrogenesis. Our previous study revealed that NF‐κB and CREB, but not E2F, could bind to the promoter region of NS5ATP13 gene [Gao et al, ]. In the current study, pNS5ATP13 and pNF‐κB p65 (RelA) were markedly upregulated by NS5A overexpression in HepG2 cells (Fig.…”

Section: Resultssupporting

confidence: 55%

“…Recent study reported that H5N1 viral NS1 interacts with host NS5ATP13 protein [Zhu et al, ]. Previously, we revealed that NF‐κB and CREB could bind to the promoter region of the NS5ATP13 gene [Gao et al, ]. In an early study, we demonstrated that NS5ATP13 amounts are low in both liver cancer tissues and hepatoma cell lines [Duan et al, ], implying the crucial role of NS5ATP13 in liver diseases.…”

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confidence: 85%

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NS5ATP13 Promotes Liver Fibrogenesis Via Activation of Hepatic Stellate Cells

Liu

Han

et al. 2017

J. Cell. Biochem.

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Liver fibrosis is a reversible wound-healing response to any etiology of chronic hepatic injuries. Activation of hepatic stellate cells (HSCs) is the key event in liver fibrogenesis. Generally, persistent activation and proliferation of HSCs results in liver fibrosis progression, while primary mechanisms of liver fibrosis resolution are apoptosis and reversion to a quiescent phenotype of activated HSCs. NS5ATP13 (HCV NS5A-transactivated protein 13) is involved in nucleologenesis and tumorigenesis, but its role in liver fibrosis and HSC activation remains unclear. This study found that NS5ATP13 was upregulated in both fibrotic liver tissues and activated human HSCs induced by TGF-β1. Moreover, NS5ATP13 enhanced extracellular matrix (ECM) production and HSC activation, with or without TGF-β1 treatment, likely involving the TGF-β1/Smad3 signaling pathway. Additionally, NS5ATP13 boosted HSC proliferation by inhibiting cell apoptosis. Furthermore, HCV NS5A promoted the profibrogenic effect of NS5ATP13 partly through TGF-β1 and NF-κB p65 (RelA) upregulation. Meanwhile, NS5ATP13 was required for the pro-fibrogenic effect of NF-κB. Moreover, NS5ATP13 and NF-κB phosphorylation as well as HSC activation were reduced by CX-4945, a CK2 specific inhibitor. These findings indicated that NS5ATP13 acts as a profibrogenic factor, providing a potential target for antifibrotic therapies. J. Cell. Biochem. 118: 2463-2473, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Resultssupporting

confidence: 55%

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confidence: 85%

NS5ATP13 Promotes Liver Fibrogenesis Via Activation of Hepatic Stellate Cells

Liu

Han

et al. 2017

J. Cell. Biochem.

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“…ChIP analyses were performed as described previously with the following modifications (Gao et al, 2011; Park and Park, 2010). Briefly, hADSC, 3T3-L1, and MEF cells were cross-linked in 1% formaldehyde at 37°C for 10 min, and then the nuclei were isolated (Kouskouti et al, 2004).…”

Section: Methodsmentioning

confidence: 99%

HIF-1-Dependent Induction of Jumonji Domain-Containing Protein (JMJD) 3 under Hypoxic Conditions

Lee¹,

Choi²,

Oh³

et al. 2014

Molecules and Cells

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Jumonji domain-containing proteins (JMJD) catalyze the oxidative demethylation of a methylated lysine residue of histones by using O2, α-ketoglutarate, vitamin C, and Fe(II). Several JMJDs are induced by hypoxic stress to compensate their presumed reduction in catalytic activity under hypoxia. In this study, we showed that an H3K27me3 specific histone demethylase, JMJD3 was induced by hypoxia-inducible factor (HIF)-1α/β under hypoxia and that treatment with Clioquinol, a HIF-1α activator, increased JMJD3 expression even under normoxia. Chromatin immunoprecipitation (ChIP) analyses showed that both HIF-1α and its dimerization partner HIF-1β/Arnt occupied the first intron region of the mouse JMJD3 gene, whereas the HIF-1α/β heterodimer bound to the upstream region of the human JMJD3, indicating that human and mouse JMJD3 have hypoxia-responsive regulatory regions in different locations. This study shows that both mouse and human JMJD3 are induced by HIF-1.

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“…Mechanistically, we speculate that H1 acts through chromatin-coupled protein-protein interactions [59] rather than by modulating the higher order structure of rDNA chromatin as proposed by others [80]. NolC1 and snoRNPS are H1.0 binding proteins that function in rRNA processing [86,87]. The affinity binding studies also identified many nucleolar H1.0 binding proteins involved in Pol II transcription (transcription factors, elongation factors, histone chaperones, chromatin remodelers), pre-mRNA splicing (snRNPS, hnRNPS, many splicing factors), and mRNA processing (PAPBC1, matrin).…”

Section: H1-dependent Protein-protein Interactions and The Nucleolusmentioning

confidence: 99%

Linker histone H1 and protein–protein interactions

Kalashnikova

Rogge

Hansen

2016

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

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Linker histones H1 are ubiquitous chromatin proteins that play important roles in chromatin compaction, transcription regulation, nucleosome spacing and chromosome spacing. H1 function in DNA and chromatin structure stabilization is well studied and established. The current paradigm of linker histone mode of function considers all other cellular roles of linker histones to be a consequence from H1 chromatin compaction and repression. Here we review the multiple processes regulated by linker histones and the emerging importance of protein interactions in H1 functioning. We propose a new paradigm which explains the multi functionality of linker histones through linker histones protein interactions as a way to directly regulate recruitment of proteins to chromatin.

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Identification of nucleolar and coiled-body phosphoprotein 1 (NOLC1) minimal promoter regulated by NF-κB and CREB

Cited by 18 publications

References 16 publications

NS5ATP13 Promotes Liver Fibrogenesis Via Activation of Hepatic Stellate Cells

NS5ATP13 Promotes Liver Fibrogenesis Via Activation of Hepatic Stellate Cells

HIF-1-Dependent Induction of Jumonji Domain-Containing Protein (JMJD) 3 under Hypoxic Conditions

Linker histone H1 and protein–protein interactions

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