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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=ADCK1</id>
	<title>ADCK1 - История изменений</title>
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	<updated>2026-04-11T09:32:55Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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		<id>https://transhumanist.ru/index.php?title=ADCK1&amp;diff=5819&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «domain-containing protein kinase 1 precursor (EC 2.7.-.-)  ==Publications==  {{medline-entry |title=Functional analysis of Aarf domain-containing kinase 1 in Dros...»</title>
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		<updated>2021-05-12T14:54:14Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «domain-containing protein kinase 1 precursor (EC 2.7.-.-)  ==Publications==  {{medline-entry |title=Functional analysis of Aarf domain-containing kinase 1 in Dros...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;domain-containing protein kinase 1 precursor (EC 2.7.-.-)&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Functional analysis of Aarf domain-containing kinase 1 in Drosophila melanogaster.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31175694&lt;br /&gt;
|abstract=The ADCK proteins are predicted mitochondrial kinases. Most studies of these proteins have focused on the Abc1/Coq8 subfamily, which contributes to Coenzyme Q biosynthesis. In contrast, little is known about [[ADCK1]] despite its evolutionary conservation in yeast, Drosophila, Caenorhabditis elegans and mammals. We show that Drosophila [[ADCK1]] mutants die as second instar larvae with double mouth hooks and tracheal breaks. Tissue-specific genetic rescue and RNAi studies show that [[ADCK1]] is necessary and sufficient in the trachea for larval viability. In addition, tracheal-rescued [[ADCK1]] mutant adults have reduced lifespan, are developmentally delayed, have reduced body size, and normal levels of basic metabolites. The larval lethality and double mouth hooks seen in [[ADCK1]] mutants are often associated with reduced levels of the steroid hormone ecdysone, suggesting that this gene could contribute to controlling ecdysone levels or bioavailability. Similarly, the tracheal defects in these animals could arise from defects in intracellular lipid trafficking. These studies of [[ADCK1]] provide a new context to define the physiological functions of this poorly understood member of the ADCK family of predicted mitochondrial proteins.&lt;br /&gt;
|mesh-terms=* Abnormalities, Multiple&lt;br /&gt;
* Animals&lt;br /&gt;
* Drosophila Proteins&lt;br /&gt;
* Drosophila melanogaster&lt;br /&gt;
* Ecdysone&lt;br /&gt;
* Larva&lt;br /&gt;
* Longevity&lt;br /&gt;
* Mitochondrial Proteins&lt;br /&gt;
* Mutant Proteins&lt;br /&gt;
* Protein Kinases&lt;br /&gt;
* Trachea&lt;br /&gt;
|keywords=* metabolism&lt;br /&gt;
* mitochondria&lt;br /&gt;
* molting&lt;br /&gt;
* trachea&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7271681&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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