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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=DLG1</id>
	<title>DLG1 - История изменений</title>
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	<subtitle>История изменений этой страницы в вики</subtitle>
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		<id>https://transhumanist.ru/index.php?title=DLG1&amp;diff=6386&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Disks large homolog 1 (Synapse-associated protein 97) (SAP-97) (SAP97) (hDlg)  ==Publications==  {{medline-entry |title=Altered expression of genes for Kir ion ch...»</title>
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		<updated>2021-05-12T15:27:46Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Disks large homolog 1 (Synapse-associated protein 97) (SAP-97) (SAP97) (hDlg)  ==Publications==  {{medline-entry |title=Altered expression of genes for Kir ion ch...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Disks large homolog 1 (Synapse-associated protein 97) (SAP-97) (SAP97) (hDlg)&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Altered expression of genes for Kir ion channels in dilated cardiomyopathy.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23889090&lt;br /&gt;
|abstract=Dilated cardiomyopathy (DCM) is a multifactorial disease characterized by left ventricular dilation that is associated with systolic dysfunction and increased action potential duration. The Kir2.x K⁺ channels (encoded by KCNJ genes) regulate the inward rectifier current (IK1) contributing to the final repolarization in cardiac muscle. Here, we describe the transitions in the gene expression profiles of 4 KCNJ genes from healthy or dilated cardiomyopathic human hearts. In the healthy adult ventricles, [[KCNJ2]], [[KCNJ12]], and [[KCNJ4]] (Kir2.1-2.3, respectively) genes were expressed at high levels, while expression of the [[KCNJ14]] (Kir2.4) gene was low. In DCM ventricles, the levels of Kir2.1 and Kir2.3 were upregulated, but those of Kir2.2 channels were downregulated. Additionally, the expression of the [[DLG1]] gene coding for the synapse-associated protein 97 (SAP97) anchoring molecule exhibited a 2-fold decline with increasing age in normal hearts, and it was robustly downregulated in young DCM patients. These adaptations could offer a new aspect for the explanation of the generally observed physiological and molecular alterations found in DCM.&lt;br /&gt;
|mesh-terms=* Adolescent&lt;br /&gt;
* Adult&lt;br /&gt;
* Aging&lt;br /&gt;
* Blotting, Western&lt;br /&gt;
* Cardiomyopathy, Dilated&lt;br /&gt;
* Female&lt;br /&gt;
* Gene Expression&lt;br /&gt;
* Heart Ventricles&lt;br /&gt;
* Humans&lt;br /&gt;
* Male&lt;br /&gt;
* Membrane Potentials&lt;br /&gt;
* Middle Aged&lt;br /&gt;
* Myocytes, Cardiac&lt;br /&gt;
* Patch-Clamp Techniques&lt;br /&gt;
* Potassium Channels, Inwardly Rectifying&lt;br /&gt;
* Protein Isoforms&lt;br /&gt;
* Reverse Transcriptase Polymerase Chain Reaction&lt;br /&gt;
* Young Adult&lt;br /&gt;
&lt;br /&gt;
|full-text-url=https://sci-hub.do/10.1139/cjpp-2012-0413&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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