<?xml version="1.0"?>
<feed xmlns="http://www.w3.org/2005/Atom" xml:lang="ru">
	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=KDR</id>
	<title>KDR - История изменений</title>
	<link rel="self" type="application/atom+xml" href="https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=KDR"/>
	<link rel="alternate" type="text/html" href="https://transhumanist.ru/index.php?title=KDR&amp;action=history"/>
	<updated>2026-08-23T12:31:24Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
	<generator>MediaWiki 1.43.6</generator>
	<entry>
		<id>https://transhumanist.ru/index.php?title=KDR&amp;diff=4376&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Vascular endothelial growth factor receptor 2 precursor (EC 2.7.10.1) (VEGFR-2) (Fetal liver kinase 1) (FLK-1) (Kinase insert domain receptor) (KDR) (Protein-tyro...»</title>
		<link rel="alternate" type="text/html" href="https://transhumanist.ru/index.php?title=KDR&amp;diff=4376&amp;oldid=prev"/>
		<updated>2021-04-29T19:14:57Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Vascular endothelial growth factor receptor 2 precursor (EC 2.7.10.1) (VEGFR-2) (Fetal liver kinase 1) (FLK-1) (Kinase insert domain receptor) (KDR) (Protein-tyro...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Vascular endothelial growth factor receptor 2 precursor (EC 2.7.10.1) (VEGFR-2) (Fetal liver kinase 1) (FLK-1) (Kinase insert domain receptor) (KDR) (Protein-tyrosine kinase receptor flk-1) (CD309 antigen) [FLK1] [VEGFR2]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Regulation of endothelial progenitor cell differentiation and function by dimethylarginine dimethylaminohydrolase 2 in an asymmetric dimethylarginine-independent manner.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24764313&lt;br /&gt;
|abstract=Endothelial progenitor cells (EPCs) are involved in the repair of vessels and angiogenesis and are useful in the treatment of ischemic diseases. The dimethylarginine dimethylaminohydrolase (DDAH)/asymmetric dimethylarginine (ADMA) pathway is regulated by silent information regulator 1 ([[SIRT1]]), leading to the senescence of endothelial cells (ECs). Here, we demonstrated that peripheral blood EPCs predominantly expressed [[DDAH2]] that increased with EPC differentiation. EPC senescence and dysfunction were induced on interruption of [[DDAH2]] expression, whereas the mRNA expression of vascular endothelial growth factor (VEGF) and kinase-domain insert containing receptor ([[KDR]]) were downregulated. Moreover, [[SIRT1]] expression increased with EPC differentiation. Interruption of [[SIRT1]] inhibited [[DDAH2]], VEGF, and [[KDR]] expression, but had no effect on the level of ADMA. From our data, we concluded that [[DDAH2]] is involved in the differentiation of EPCs and regulates the senescence and function of EPCs through the VEGF/[[KDR]] pathway by activation of [[SIRT1]]. &lt;br /&gt;
|mesh-terms=* Amidohydrolases&lt;br /&gt;
* Arginine&lt;br /&gt;
* Cell Differentiation&lt;br /&gt;
* Cells, Cultured&lt;br /&gt;
* Cellular Senescence&lt;br /&gt;
* Endothelial Progenitor Cells&lt;br /&gt;
* Humans&lt;br /&gt;
* RNA Interference&lt;br /&gt;
* RNA, Messenger&lt;br /&gt;
* RNA, Small Interfering&lt;br /&gt;
* Sirtuin 1&lt;br /&gt;
* Vascular Endothelial Growth Factor A&lt;br /&gt;
* Vascular Endothelial Growth Factor Receptor-2&lt;br /&gt;
|keywords=* SIRT1&lt;br /&gt;
* dimethylarginine dimethylaminohydrolase&lt;br /&gt;
* endothelial progenitor cells&lt;br /&gt;
* senescence&lt;br /&gt;
|full-text-url=https://sci-hub.do/10.1002/cbin.10288&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
	</entry>
</feed>