Inhibition of c-Src Tyrosine Kinase Prevents Angiotensin II-Mediated Connexin-43 Remodeling and Sudden Cardiac Death.

02:31 EDT 8th July 2015 | BioPortfolio

Summary of "Inhibition of c-Src Tyrosine Kinase Prevents Angiotensin II-Mediated Connexin-43 Remodeling and Sudden Cardiac Death."

The aim of this study was to test whether c-Src tyrosine kinase mediates connexin-43 (Cx43) reduction and sudden cardiac death in a transgenic mouse model of cardiac-restricted overexpression of angiotensin-converting enzyme (ACE8/8 mice).

Affiliation

Section of Cardiology and Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, Illinois.

Journal Details

This article was published in the following journal.

Name: Journal of the American College of Cardiology
ISSN: 1558-3597
Pages: 2332-9

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Medical and Biotech [MESH] Definitions

A 43-kDa peptide which is a member of the connexin family of gap junction proteins. Connexin 43 is a product of a gene in the alpha class of connexin genes (the alpha-1 gene). It was first isolated from mammalian heart, but is widespread in the body including the brain.

This enzyme is a lymphoid-specific src family tyrosine kinase that is critical for T-cell development and activation. Lck is associated with the cytoplasmic domains of CD4, CD8 and the beta-chain of the IL-2 receptor, and is thought to be involved in the earliest steps of TCR-mediated T-cell activation.

The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activa

A protein kinase C subtype that was originally characterized as a CALCIUM-independent, serine-threonine kinase that is activated by PHORBOL ESTERS and DIACYLGLYCEROLS. It is targeted to specific cellular compartments in response to extracellular signals that activate G-PROTEIN-COUPLED RECEPTORS; TYROSINE KINASE RECEPTORS; and intracellular protein tyrosine kinase.

An eph family receptor found primarily in BRAIN and THYMUS. The EphB6 receptor is unusual in that its tyrosine kinase domain shares little homology with other members of this class. The unusual tyrosine kinase domain of this receptor appears to result in its lack of tyrosine kinase activity.


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