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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=CCNA1</id>
	<title>CCNA1 - История изменений</title>
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	<updated>2026-04-12T19:43:00Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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	<entry>
		<id>https://transhumanist.ru/index.php?title=CCNA1&amp;diff=6093&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Cyclin-A1  ==Publications==  {{medline-entry |title=Age-dependent human β cell proliferation induced by glucagon-like peptide 1 and calcineurin signaling. |pubme...»</title>
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		<updated>2021-05-12T15:11:24Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Cyclin-A1  ==Publications==  {{medline-entry |title=Age-dependent human β cell proliferation induced by glucagon-like peptide 1 and calcineurin signaling. |pubme...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Cyclin-A1&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Age-dependent human β cell proliferation induced by glucagon-like peptide 1 and calcineurin signaling.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28920919&lt;br /&gt;
|abstract=Inadequate pancreatic β cell function underlies type 1 and type 2 diabetes mellitus. Strategies to expand functional cells have focused on discovering and controlling mechanisms that limit the proliferation of human β cells. Here, we developed an engraftment strategy to examine age-associated human islet cell replication competence and reveal mechanisms underlying age-dependent decline of β cell proliferation in human islets. We found that exendin-4 (Ex-4), an agonist of the glucagon-like peptide 1 receptor (GLP-1R), stimulates human β cell proliferation in juvenile but not adult islets. This age-dependent responsiveness does not reflect loss of GLP-1R signaling in adult islets, since Ex-4 treatment stimulated insulin secretion by both juvenile and adult human β cells. We show that the mitogenic effect of Ex-4 requires calcineurin/nuclear factor of activated T cells (NFAT) signaling. In juvenile islets, Ex-4 induced expression of calcineurin/NFAT signaling components as well as target genes for proliferation-promoting factors, including [[NFATC1]], [[FOXM1]], and [[CCNA1]]. By contrast, expression of these factors in adult islet β cells was not affected by Ex-4 exposure. These studies reveal age-dependent signaling mechanisms regulating human β cell proliferation, and identify elements that could be adapted for therapeutic expansion of human β cells.&lt;br /&gt;
|mesh-terms=* Adult&lt;br /&gt;
* Aging&lt;br /&gt;
* Animals&lt;br /&gt;
* Calcineurin&lt;br /&gt;
* Cyclin A1&lt;br /&gt;
* Exenatide&lt;br /&gt;
* Female&lt;br /&gt;
* Forkhead Box Protein M1&lt;br /&gt;
* Glucagon-Like Peptide 1&lt;br /&gt;
* Glucagon-Like Peptide-1 Receptor&lt;br /&gt;
* Humans&lt;br /&gt;
* Insulin&lt;br /&gt;
* Insulin Secretion&lt;br /&gt;
* Insulin-Secreting Cells&lt;br /&gt;
* Male&lt;br /&gt;
* Mice, Inbred NOD&lt;br /&gt;
* Middle Aged&lt;br /&gt;
* NFATC Transcription Factors&lt;br /&gt;
* Peptides&lt;br /&gt;
* Signal Transduction&lt;br /&gt;
* Venoms&lt;br /&gt;
&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5617654&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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