<?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=ESAM</id>
	<title>ESAM - История изменений</title>
	<link rel="self" type="application/atom+xml" href="https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=ESAM"/>
	<link rel="alternate" type="text/html" href="https://transhumanist.ru/index.php?title=ESAM&amp;action=history"/>
	<updated>2026-11-08T15:00:26Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
	<generator>MediaWiki 1.43.6</generator>
	<entry>
		<id>https://transhumanist.ru/index.php?title=ESAM&amp;diff=5238&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Endothelial cell-selective adhesion molecule precursor [UNQ220/PRO246]  ==Publications==  {{medline-entry |title=The endothelial antigen ESAM marks primitive...»</title>
		<link rel="alternate" type="text/html" href="https://transhumanist.ru/index.php?title=ESAM&amp;diff=5238&amp;oldid=prev"/>
		<updated>2021-05-12T13:35:29Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Endothelial cell-selective adhesion molecule precursor [UNQ220/PRO246]  ==Publications==  {{medline-entry |title=The endothelial antigen &lt;a href=&quot;/ESAM&quot; title=&quot;ESAM&quot;&gt;ESAM&lt;/a&gt; marks primitive...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Endothelial cell-selective adhesion molecule precursor [UNQ220/PRO246]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=The endothelial antigen [[ESAM]] marks primitive hematopoietic progenitors throughout life in mice.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19096010&lt;br /&gt;
|abstract=Although recent advances have enabled hematopoietic stem cells (HSCs) to be enriched to near purity, more information about their characteristics will improve our understanding of their development and stage-related functions. Here, using microarray technology, we identified endothelial cell-selective adhesion molecule ([[ESAM]]) as a novel marker for murine HSCs in fetal liver. Esam was expressed at high levels within a Rag1(-) c-kit(Hi) Sca1( ) HSC-enriched fraction, but sharply down-regulated with activation of the Rag1 locus, a valid marker for the most primitive lymphoid progenitors in E14.5 liver. The HSC-enriched fraction could be subdivided into 2 on the basis of [[ESAM]] levels. Among endothelial antigens on hematopoietic progenitors, [[ESAM]] expression showed intimate correlation with HSC activity. The [[ESAM]](Hi) population was highly enriched for multipotent myeloid-erythroid progenitors and primitive progenitors with lymphopoietic activity, and exclusively reconstituted long-term lymphohematopoiesis in lethally irradiated recipients. Tie2( ) c-kit( ) lymphohematopoietic cells in the E9.5-10.5 aorta-gonad-mesonephros region also expressed high levels of [[ESAM]]. Furthermore, [[ESAM]] was detected on primitive hematopoietic progenitors in adult bone marrow. Interestingly, [[ESAM]] expression in the HSC-enriched fraction was up-regulated in aged mice. We conclude that [[ESAM]] marks HSC in murine fetal liver and will facilitate studies of hematopoiesis throughout life.&lt;br /&gt;
|mesh-terms=* Aging&lt;br /&gt;
* Animals&lt;br /&gt;
* Biomarkers&lt;br /&gt;
* Cell Adhesion Molecules&lt;br /&gt;
* Cells, Cultured&lt;br /&gt;
* Embryo, Mammalian&lt;br /&gt;
* Endothelial Cells&lt;br /&gt;
* Female&lt;br /&gt;
* Fetus&lt;br /&gt;
* Gene Expression Profiling&lt;br /&gt;
* Gene Expression Regulation, Developmental&lt;br /&gt;
* Gene Knock-In Techniques&lt;br /&gt;
* Hematopoiesis&lt;br /&gt;
* Hematopoietic Stem Cells&lt;br /&gt;
* Liver&lt;br /&gt;
* Male&lt;br /&gt;
* Mice&lt;br /&gt;
* Mice, Inbred C57BL&lt;br /&gt;
* Mice, Transgenic&lt;br /&gt;
* Oligonucleotide Array Sequence Analysis&lt;br /&gt;
&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2974489&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
	</entry>
</feed>