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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=FBXW7</id>
	<title>FBXW7 - История изменений</title>
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	<updated>2026-05-18T07:09:40Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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		<id>https://transhumanist.ru/index.php?title=FBXW7&amp;diff=4344&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «F-box/WD repeat-containing protein 7 (Archipelago homolog) (hAgo) (F-box and WD-40 domain-containing protein 7) (F-box protein FBX30) (SEL-10) (hCdc4) [FBW7] [FBX...»</title>
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		<updated>2021-04-29T19:13:22Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «F-box/WD repeat-containing protein 7 (Archipelago homolog) (hAgo) (F-box and WD-40 domain-containing protein 7) (F-box protein FBX30) (SEL-10) (hCdc4) [FBW7] [FBX...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;F-box/WD repeat-containing protein 7 (Archipelago homolog) (hAgo) (F-box and WD-40 domain-containing protein 7) (F-box protein FBX30) (SEL-10) (hCdc4) [FBW7] [FBX30] [SEL10]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=[[MYC]] Modulation around the CDK2/p27/SKP2 Axis.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28665315&lt;br /&gt;
|abstract=[[MYC]] is a pleiotropic transcription factor that controls a number of fundamental cellular processes required for the proliferation and survival of normal and malignant cells, including the cell cycle. [[MYC]] interacts with several central cell cycle regulators that control the balance between cell cycle progression and temporary or permanent cell cycle arrest (cellular senescence). Among these are the cyclin E/A/cyclin-dependent kinase 2 (CDK2) complexes, the CDK inhibitor p27  (p27) and the E3 ubiquitin ligase component S-phase kinase-associated protein 2 (SKP2), which control each other by forming a triangular network. [[MYC]] is engaged in bidirectional crosstalk with each of these players; while [[MYC]] regulates their expression and/or activity, these factors in turn modulate [[MYC]] through protein interactions and post-translational modifications including phosphorylation and ubiquitylation, impacting on [[MYC]]&amp;#039;s transcriptional output on genes involved in cell cycle progression and senescence. Here we elaborate on these network interactions with [[MYC]] and their impact on transcription, cell cycle, replication and stress signaling, and on the role of other players interconnected to this network, such as [[CDK1]], the retinoblastoma protein (pRB), protein phosphatase 2A (PP2A), the F-box proteins [[FBXW7]] and [[FBXO28]], the RAS oncoprotein and the ubiquitin/proteasome system. Finally, we describe how the [[MYC]]/CDK2/p27/SKP2 axis impacts on tumor development and discuss possible ways to interfere therapeutically with this system to improve cancer treatment.&lt;br /&gt;
&lt;br /&gt;
|keywords=* cancer&lt;br /&gt;
* cell cycle&lt;br /&gt;
* cellular senescence&lt;br /&gt;
* oncogenes&lt;br /&gt;
* phosphorylation&lt;br /&gt;
* post-translational modifications&lt;br /&gt;
* protein–protein interactions&lt;br /&gt;
* the ubiquitin/proteasome system&lt;br /&gt;
* transcription&lt;br /&gt;
* tumor suppressor genes&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5541307&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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