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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=BNC1</id>
	<title>BNC1 - История изменений</title>
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		<title>OdysseusBot: Новая страница: «Zinc finger protein basonuclin-1 [BNC]  ==Publications==  {{medline-entry |title=Basonuclin 1 deficiency causes testicular premature aging: BNC1 cooperates wi...»</title>
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		<updated>2021-04-29T19:33:36Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Zinc finger protein basonuclin-1 [BNC]  ==Publications==  {{medline-entry |title=Basonuclin 1 deficiency causes testicular premature aging: &lt;a href=&quot;/BNC1&quot; title=&quot;BNC1&quot;&gt;BNC1&lt;/a&gt; cooperates wi...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Zinc finger protein basonuclin-1 [BNC]&lt;br /&gt;
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==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Basonuclin 1 deficiency causes testicular premature aging: [[BNC1]] cooperates with [[TAF7]]L to regulate spermatogenesis.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31065688&lt;br /&gt;
|abstract=Basonuclin ([[BNC1]]) is expressed primarily in proliferative keratinocytes and gametogenic cells. However, its roles in spermatogenesis and testicular aging were not clear. Previously we discovered a heterozygous [[BNC1]] truncation mutation in a premature ovarian insufficiency pedigree. In this study, we found that male mice carrying the truncation mutation exhibited progressively fertility loss and testicular premature aging. Genome-wide expression profiling and direct binding studies (by chromatin immunoprecipitation sequencing) with [[BNC1]] in mouse testis identified several spermatogenesis-specific gene promoters targeted by [[BNC1]] including kelch-like family member 10 (Klhl10), testis expressed 14 (Tex14), and spermatogenesis and centriole associated 1 (Spatc1). Moreover, biochemical analysis showed that [[BNC1]] was associated with TATA-box binding protein-associated factor 7 like ([[TAF7]]L), a germ cell-specific paralogue of the transcription factor IID subunit [[TAF7]], both in vitro and in testis, suggesting that [[BNC1]] might directly cooperate with [[TAF7]]L to regulate spermatogenesis. The truncation mutation disabled nuclear translocation of the [[BNC1]]/[[TAF7]]L complex, thus, disturbing expression of related genes and leading to testicular premature aging. Similarly, expressions of [[BNC1]], [[TAF7]]L, Y-box-binding protein 2 (YBX2), outer dense fiber of sperm tails 1 (ODF1), and glyceraldehyde-3-phosphate dehydrogenase, spermatogenic (GAPDHS) were significantly decreased in the testis of men with non-obstructive azoospermia. The present study adds to the understanding of the physiology of male reproductive aging and the mechanism of spermatogenic failure in infertile men.&lt;br /&gt;
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|keywords=* BNC1&lt;br /&gt;
* TAF7L&lt;br /&gt;
* gene mutation&lt;br /&gt;
* spermatogenesis&lt;br /&gt;
* testicular aging&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7052986&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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