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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=CDC73</id>
	<title>CDC73 - История изменений</title>
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	<updated>2026-09-23T18:17:46Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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		<id>https://transhumanist.ru/index.php?title=CDC73&amp;diff=6152&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Parafibromin (Cell division cycle protein 73 homolog) (Hyperparathyroidism 2 protein) [C1orf28] [HRPT2]  ==Publications==  {{medline-entry |title=Down-regulation...»</title>
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		<updated>2021-05-12T15:14:20Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Parafibromin (Cell division cycle protein 73 homolog) (Hyperparathyroidism 2 protein) [C1orf28] [HRPT2]  ==Publications==  {{medline-entry |title=Down-regulation...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Parafibromin (Cell division cycle protein 73 homolog) (Hyperparathyroidism 2 protein) [C1orf28] [HRPT2]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Down-regulation of cancer-associated gene [[CDC73]] contributes to cellular senescence.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29621547&lt;br /&gt;
|abstract=Dysregulated gene expression is another important contributor in explaining cancer-related phenotypes in addition to mutations. Cellular senescence is a mechanism for the prevention of cancer and thus it is important to understand the regulation of gene expression in senescence due to its potential in anti-cancer therapy. Here, we found that [[CDC73]], which encodes the cell division cycle 73 and acts as a tumor suppressor, was unexpectedly up-regulated in several cancer types but down-regulated in a variety of senescent cells. Importantly, depletion of [[CDC73]] could induce senescence-associated phenotypes in both normal and cancer cells, with an increase in p21 expression. In terms of molecular mechanism, alternative polyadenylation (APA)-mediated 3&amp;#039; untranslated region (3&amp;#039; UTR) lengthening explained, at least in part, the decreased [[CDC73]] expression in senescent cells because longer 3&amp;#039; UTR had a higher rate of RNA degradation compared to the shorter one. Our work discovered that post-transcriptional down-regulation of [[CDC73]] contributed to cellular senescence.&lt;br /&gt;
|mesh-terms=* 3&amp;#039; Untranslated Regions&lt;br /&gt;
* Base Sequence&lt;br /&gt;
* Cell Line&lt;br /&gt;
* Cellular Senescence&lt;br /&gt;
* Cyclin-Dependent Kinase Inhibitor p21&lt;br /&gt;
* Down-Regulation&lt;br /&gt;
* Gene Expression Regulation, Neoplastic&lt;br /&gt;
* Gene Knockdown Techniques&lt;br /&gt;
* Humans&lt;br /&gt;
* Neoplasms&lt;br /&gt;
* Tumor Suppressor Proteins&lt;br /&gt;
* Up-Regulation&lt;br /&gt;
|keywords=* 3′ UTR&lt;br /&gt;
* CDC73&lt;br /&gt;
* Cancer&lt;br /&gt;
* Cellular senescence&lt;br /&gt;
* Gene expression&lt;br /&gt;
|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2018.03.228&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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