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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=ACMSD</id>
	<title>ACMSD - История изменений</title>
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	<updated>2026-04-08T05:13:29Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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	<entry>
		<id>https://transhumanist.ru/index.php?title=ACMSD&amp;diff=3978&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «2-amino-3-carboxymuconate-6-semialdehyde decarboxylase (EC 4.1.1.45) (Picolinate carboxylase)  ==Publications==  {{medline-entry |title=De novo NAD  synthesis enh...»</title>
		<link rel="alternate" type="text/html" href="https://transhumanist.ru/index.php?title=ACMSD&amp;diff=3978&amp;oldid=prev"/>
		<updated>2021-04-29T18:54:38Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «2-amino-3-carboxymuconate-6-semialdehyde decarboxylase (EC 4.1.1.45) (Picolinate carboxylase)  ==Publications==  {{medline-entry |title=De novo NAD  synthesis enh...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;2-amino-3-carboxymuconate-6-semialdehyde decarboxylase (EC 4.1.1.45) (Picolinate carboxylase)&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=De novo NAD  synthesis enhances mitochondrial function and improves health.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30356218&lt;br /&gt;
|abstract=Nicotinamide adenine dinucleotide (NAD ) is a co-substrate for several enzymes, including the sirtuin family of NAD -dependent protein deacylases. Beneficial effects of increased NAD  levels and sirtuin activation on mitochondrial homeostasis, organismal metabolism and lifespan have been established across species. Here we show that α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase ([[ACMSD]]), the enzyme that limits spontaneous cyclization of α-amino-β-carboxymuconate-ε-semialdehyde in the de novo NAD  synthesis pathway, controls cellular NAD  levels via an evolutionarily conserved mechanism in Caenorhabditis elegans and mouse. Genetic and pharmacological inhibition of [[ACMSD]] boosts de novo NAD  synthesis and sirtuin 1 activity, ultimately enhancing mitochondrial function. We also characterize two potent and selective inhibitors of [[ACMSD]]. Because expression of [[ACMSD]] is largely restricted to kidney and liver, these inhibitors may have therapeutic potential for protection of these tissues from injury. In summary, we identify [[ACMSD]] as a key modulator of cellular NAD  levels, sirtuin activity and mitochondrial homeostasis in kidney and liver.&lt;br /&gt;
|mesh-terms=* Animals&lt;br /&gt;
* Caenorhabditis elegans&lt;br /&gt;
* Carboxy-Lyases&lt;br /&gt;
* Cell Line&lt;br /&gt;
* Choline&lt;br /&gt;
* Conserved Sequence&lt;br /&gt;
* Disease Models, Animal&lt;br /&gt;
* Evolution, Molecular&lt;br /&gt;
* Female&lt;br /&gt;
* Gene Knockdown Techniques&lt;br /&gt;
* Health&lt;br /&gt;
* Hepatocytes&lt;br /&gt;
* Homeostasis&lt;br /&gt;
* Humans&lt;br /&gt;
* Kidney&lt;br /&gt;
* Liver&lt;br /&gt;
* Longevity&lt;br /&gt;
* Male&lt;br /&gt;
* Methionine&lt;br /&gt;
* Mice&lt;br /&gt;
* Mice, Inbred C57BL&lt;br /&gt;
* Mitochondria&lt;br /&gt;
* NAD&lt;br /&gt;
* Non-alcoholic Fatty Liver Disease&lt;br /&gt;
* Rats&lt;br /&gt;
* Sirtuins&lt;br /&gt;
&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448761&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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