Редактирование: DLG1

Disks large homolog 1 (Synapse-associated protein 97) (SAP-97) (SAP97) (hDlg)

==Publications==

{{medline-entry
|title=Altered expression of genes for Kir ion channels in dilated cardiomyopathy.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23889090
|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.
|mesh-terms=* Adolescent
* Adult
* Aging
* Blotting, Western
* Cardiomyopathy, Dilated
* Female
* Gene Expression
* Heart Ventricles
* Humans
* Male
* Membrane Potentials
* Middle Aged
* Myocytes, Cardiac
* Patch-Clamp Techniques
* Potassium Channels, Inwardly Rectifying
* Protein Isoforms
* Reverse Transcriptase Polymerase Chain Reaction
* Young Adult

|full-text-url=https://sci-hub.do/10.1139/cjpp-2012-0413
}}