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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=RNF111</id>
	<title>RNF111 - История изменений</title>
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	<updated>2026-08-29T20:59:56Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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		<id>https://transhumanist.ru/index.php?title=RNF111&amp;diff=4151&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «E3 ubiquitin-protein ligase Arkadia (EC 2.3.2.27) (RING finger protein 111) (hRNF111) (RING-type E3 ubiquitin transferase Arkadia)  ==Publications==  {{medline-en...»</title>
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		<updated>2021-04-29T19:03:16Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «E3 ubiquitin-protein ligase Arkadia (EC 2.3.2.27) (RING finger protein 111) (hRNF111) (RING-type E3 ubiquitin transferase Arkadia)  ==Publications==  {{medline-en...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;E3 ubiquitin-protein ligase Arkadia (EC 2.3.2.27) (RING finger protein 111) (hRNF111) (RING-type E3 ubiquitin transferase Arkadia)&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Global-genome Nucleotide Excision Repair Controlled by Ubiquitin/Sumo Modifiers.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27200078&lt;br /&gt;
|abstract=Global-genome nucleotide excision repair (GG-NER) prevents genome instability by excising a wide range of different DNA base adducts and crosslinks induced by chemical carcinogens, ultraviolet (UV) light or intracellular side products of metabolism. As a versatile damage sensor, xeroderma pigmentosum group C ([[XPC]]) protein initiates this generic defense reaction by locating the damage and recruiting the subunits of a large lesion demarcation complex that, in turn, triggers the excision of aberrant DNA by endonucleases. In the very special case of a DNA repair response to UV radiation, the function of this [[XPC]] initiator is tightly controlled by the dual action of cullin-type CRL4(DDB2) and sumo-targeted [[RNF111]] ubiquitin ligases. This twofold protein ubiquitination system promotes GG-NER reactions by spatially and temporally regulating the interaction of [[XPC]] protein with damaged DNA across the nucleosome landscape of chromatin. In the absence of either CRL4(DDB2) or [[RNF111]], the DNA excision repair of UV lesions is inefficient, indicating that these two ubiquitin ligases play a critical role in mitigating the adverse biological effects of UV light in the exposed skin. &lt;br /&gt;
&lt;br /&gt;
|keywords=* DNA repair&lt;br /&gt;
* UV radiation&lt;br /&gt;
* aging&lt;br /&gt;
* cyclobutane pyrimidine dimer&lt;br /&gt;
* genomic instability&lt;br /&gt;
* photoproducts&lt;br /&gt;
* skin cancer&lt;br /&gt;
* sunburns&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4848295&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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