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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=NOLC1</id>
	<title>NOLC1 - История изменений</title>
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	<updated>2026-04-19T10:48:38Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
	<generator>MediaWiki 1.43.6</generator>
	<entry>
		<id>https://transhumanist.ru/index.php?title=NOLC1&amp;diff=4699&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Nucleolar and coiled-body phosphoprotein 1 (140 kDa nucleolar phosphoprotein) (Nopp140) (Hepatitis C virus NS5A-transactivated protein 13) (HCV NS5A-transactivate...»</title>
		<link rel="alternate" type="text/html" href="https://transhumanist.ru/index.php?title=NOLC1&amp;diff=4699&amp;oldid=prev"/>
		<updated>2021-04-29T19:30:29Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Nucleolar and coiled-body phosphoprotein 1 (140 kDa nucleolar phosphoprotein) (Nopp140) (Hepatitis C virus NS5A-transactivated protein 13) (HCV NS5A-transactivate...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Nucleolar and coiled-body phosphoprotein 1 (140 kDa nucleolar phosphoprotein) (Nopp140) (Hepatitis C virus NS5A-transactivated protein 13) (HCV NS5A-transactivated protein 13) (Nucleolar 130 kDa protein) (Nucleolar phosphoprotein p130) [KIAA0035] [NS5ATP13]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Enhanced [[NOLC1]] promotes cell senescence and represses hepatocellular carcinoma cell proliferation by disturbing the organization of nucleolus.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28493459&lt;br /&gt;
|abstract=The nucleolus is a key organelle that is responsible for the synthesis of rRNA and assembly of ribosomal subunits, which is also the center of metabolic control because of the critical role of ribosomes in protein synthesis. Perturbations of rRNA biogenesis are closely related to cell senescence and tumor progression; however, the underlying molecular mechanisms are not well understood. Here, we report that cellular senescence-inhibited gene (CSIG) knockdown up-regulated [[NOLC1]] by stabilizing the 5&amp;#039;UTR of [[NOLC1]] mRNA, and elevated [[NOLC1]] induced the retention of NOG1 in the nucleolus, which is responsible for rRNA processing. Besides, the expression of [[NOLC1]] was negatively correlated with CSIG in the aged mouse tissue and replicative senescent 2BS cells, and the down-regulation of [[NOLC1]] could rescue CSIG knockdown-induced 2BS senescence. Additionally, [[NOLC1]] expression was decreased in human hepatocellular carcinoma (HCC) tissue, and the ectopic expression of [[NOLC1]] repressed the proliferation of HCC cells and tumor growth in a HCC xenograft model.&lt;br /&gt;
|mesh-terms=* 5&amp;#039; Untranslated Regions&lt;br /&gt;
* Aging&lt;br /&gt;
* Animals&lt;br /&gt;
* Carcinoma, Hepatocellular&lt;br /&gt;
* Cell Line, Tumor&lt;br /&gt;
* Cell Nucleolus&lt;br /&gt;
* Cell Proliferation&lt;br /&gt;
* Cellular Senescence&lt;br /&gt;
* Fibroblasts&lt;br /&gt;
* GTP Phosphohydrolases&lt;br /&gt;
* Gene Expression Regulation, Neoplastic&lt;br /&gt;
* HEK293 Cells&lt;br /&gt;
* Humans&lt;br /&gt;
* Liver Neoplasms&lt;br /&gt;
* Mice&lt;br /&gt;
* Mice, Inbred BALB C&lt;br /&gt;
* Mice, Nude&lt;br /&gt;
* Neoplasm Transplantation&lt;br /&gt;
* Nuclear Proteins&lt;br /&gt;
* Phosphoproteins&lt;br /&gt;
* RNA, Ribosomal&lt;br /&gt;
* RNA, Small Interfering&lt;br /&gt;
* Ribosomal Proteins&lt;br /&gt;
|keywords=* &lt;br /&gt;
CSIG&lt;br /&gt;
&lt;br /&gt;
* NOLC1&lt;br /&gt;
* aging&lt;br /&gt;
* hepatocellular carcinoma&lt;br /&gt;
* nucleolus&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5506443&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
	</entry>
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