https://transhumanist.ru/index.php?action=history&feed=atom&title=UVRAGUVRAG - История изменений2026-08-29T09:55:47ZИстория изменений этой страницы в викиMediaWiki 1.43.6https://transhumanist.ru/index.php?title=UVRAG&diff=4751&oldid=prevOdysseusBot: Новая страница: «UV radiation resistance-associated gene protein (p63) ==Publications== {{medline-entry |title=Essential role for UVRAG in autophagy and maintenance of cardi...»2021-04-29T19:33:17Z<p>Новая страница: «UV radiation resistance-associated gene protein (p63) ==Publications== {{medline-entry |title=Essential role for <a href="/UVRAG" title="UVRAG">UVRAG</a> in autophagy and maintenance of cardi...»</p>
<p><b>Новая страница</b></p><div>UV radiation resistance-associated gene protein (p63)<br />
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==Publications==<br />
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{{medline-entry<br />
|title=Essential role for [[UVRAG]] in autophagy and maintenance of cardiac function.<br />
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24081163<br />
|abstract=Ultraviolet irradiation resistance-associated gene ([[UVRAG]]) is a tumour suppressor candidate that regulates cell autophagy and endocytosis. However, the in vivo function of [[UVRAG]] remains poorly understood. We sought to determine the physiological role of [[UVRAG]] in the heart. We characterized mice with disruption of the [[UVRAG]] gene by piggyBac (PB) transposon insertion. PB construct was inserted into intron 14 of the [[UVRAG]] gene and disruption of [[UVRAG]] transcript was confirmed by reverse transcript-polymerase chain reaction. Immunoblotting revealed that [[UVRAG]] was deficient in multiple tissues. Autophagic flux was attenuated in [[UVRAG]]-deficient ([[UVRAG]](PB/PB)) mouse embryonic fibroblasts. In [[UVRAG]]-deficient hearts, autophagosomes were accumulated and autophagic flux, assessed as the increased protein abundance of LC3 II in chloroquine-treated animals, was impaired. [[UVRAG]]-deficient mice were viable, fertile, and developmentally normal. However, they developed age-related cardiomyopathy associated with compromised cardiac function. In addition, inflammatory response was enhanced in [[UVRAG]]-deficient hearts. Collectively, our findings suggest that [[UVRAG]] is essential for the regulation of autophagy and maintenance of cardiac function.<br />
|mesh-terms=* Aging<br />
* Animals<br />
* Autophagy<br />
* Cardiomyopathies<br />
* Cells, Cultured<br />
* Female<br />
* Heart<br />
* Inflammation<br />
* Male<br />
* Mice<br />
* Pregnancy<br />
* Tumor Suppressor Proteins<br />
|keywords=* Autophagosome<br />
* Autophagy<br />
* Cardiomyopathy<br />
* Inflammation<br />
* UVRAG<br />
|full-text-url=https://sci-hub.do/10.1093/cvr/cvt223<br />
}}</div>OdysseusBot