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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=FLCN</id>
	<title>FLCN - История изменений</title>
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	<updated>2026-04-03T22:48:12Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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	<entry>
		<id>https://transhumanist.ru/index.php?title=FLCN&amp;diff=6570&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Folliculin (BHD skin lesion fibrofolliculoma protein) (Birt-Hogg-Dube syndrome protein) [BHD]  ==Publications==  {{medline-entry |title=Loss of the Birt-Hogg-Dub...»</title>
		<link rel="alternate" type="text/html" href="https://transhumanist.ru/index.php?title=FLCN&amp;diff=6570&amp;oldid=prev"/>
		<updated>2021-05-12T15:37:42Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Folliculin (BHD skin lesion fibrofolliculoma protein) (Birt-Hogg-Dube syndrome protein) [BHD]  ==Publications==  {{medline-entry |title=Loss of the Birt-Hogg-Dub...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Folliculin (BHD skin lesion fibrofolliculoma protein) (Birt-Hogg-Dube syndrome protein) [BHD]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Loss of the Birt-Hogg-Dubé gene product folliculin induces longevity in a hypoxia-inducible factor-dependent manner.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23566034&lt;br /&gt;
|abstract=Signaling through the hypoxia-inducible factor hif-1 controls longevity, metabolism, and stress resistance in Caenorhabditis elegans. Hypoxia-inducible factor (HIF) protein levels are regulated through an evolutionarily conserved ubiquitin ligase complex. Mutations in the [[VHL]] gene, encoding a core component of this complex, cause a multitumor syndrome and renal cell carcinoma in humans. In the nematode, deficiency in vhl-1 promotes longevity mediated through HIF-1 stabilization. However, this longevity assurance pathway is not yet understood. Here, we identify folliculin ([[FLCN]]) as a novel interactor of the hif-1/vhl-1 longevity pathway. [[FLCN]] mutations cause Birt-Hogg-Dubé syndrome in humans, another tumor syndrome with renal tumorigenesis reminiscent of the [[VHL]] disease. Loss of the C. elegans ortholog of [[FLCN]] F22D3.2 significantly increased lifespan and enhanced stress resistance in a hif-1-dependent manner. F22D3.2, vhl-1, and hif-1 control longevity by a mechanism distinct from insulin-like signaling. Daf-16 deficiency did not abrogate the increase in lifespan mediated by flcn-1. These findings define [[FLCN]] as a player in HIF-dependent longevity signaling and connect organismal aging, stress resistance, and regulation of longevity with the formation of renal cell carcinoma.&lt;br /&gt;
|mesh-terms=* Animals&lt;br /&gt;
* Birt-Hogg-Dube Syndrome&lt;br /&gt;
* Caenorhabditis elegans&lt;br /&gt;
* Caenorhabditis elegans Proteins&lt;br /&gt;
* Cullin Proteins&lt;br /&gt;
* Forkhead Transcription Factors&lt;br /&gt;
* Gene Expression Regulation, Developmental&lt;br /&gt;
* Humans&lt;br /&gt;
* Longevity&lt;br /&gt;
* Mutation&lt;br /&gt;
* Protein Stability&lt;br /&gt;
* Proto-Oncogene Proteins&lt;br /&gt;
* RNA, Messenger&lt;br /&gt;
* Sequence Homology, Amino Acid&lt;br /&gt;
* Transcription Factors&lt;br /&gt;
* Tumor Suppressor Proteins&lt;br /&gt;
|keywords=* Birt-Hogg-Dubé&lt;br /&gt;
* C. elegans&lt;br /&gt;
* Vhl&lt;br /&gt;
* folliculin&lt;br /&gt;
* hif&lt;br /&gt;
* longevity&lt;br /&gt;
|full-text-url=https://sci-hub.do/10.1111/acel.12081&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
	</entry>
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