Deletion of the last five C-terminal amino acid residues of connexin43 leads to lethal ventricular arrhythmias in mice without affecting coupling via gap junction channels.

doi:10.1007/s00395-013-0348-y

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Deletion of the last five C-terminal amino acid residues of connexin43 leads to lethal ventricular arrhythmias in mice without affecting coupling via gap junction channels.

Basic research in cardiology - 1 May 2013

Lübkemeier Indra, Requardt Robert Pascal, Lin Xianming, Sasse Philipp, Andrié René, Schrickel Jan Wilko, Chkourko Halina, Bukauskas Feliksas F, Kim Jung-Sun, Frank Marina, Malan Daniela, Zhang Jiong, Wirth Angela, Dobrowolski Radoslaw, Mohler Peter J, Offermanns Stefan, Fleischmann Bernd K, Delmar Mario, Willecke Klaus

Abstract excerpt

The cardiac intercalated disc harbors mechanical and electrical junctions as well as ion channel complexes mediating propagation of electrical impulses. Cardiac connexin43 (Cx43) co-localizes and interacts with several of the proteins located at intercalated discs in the ventricular myocardium. We have generated conditional Cx43D378stop mice lacking the last five C-terminal amino acid residues, representing a...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Action Potentials

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Arrhythmias, Cardiac

Share to Connexin 43

Share to Electrocardiography, Ambulatory

Share to Gap Junctions

Share to Myocytes, Cardiac

Share to NAV1.5 Voltage-Gated Sodium Channel

Share to Zonula Occludens-1 Protein

Source

Open in PubMed Open full text

Identifiers

PMID: 23558439
DOI: 10.1007/s00395-013-0348-y
PMCID: PMC3678986

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Deletion of the last five C-terminal amino acid residues of connexin43 leads to lethal ventricular arrhythmias in mice without affecting coupling via gap junction channels.PMID 23558439Read ↗

Gap junctions and the connexin protein family.Semantic proximity Read ↗

Research progress of connexin 43 in cardiovascular diseasesSemantic proximity Read ↗

Slow ventricular conduction in mice heterozygous for a connexin43 null mutation.Semantic proximity Read ↗

Remodelling of gap junctions and connexin expression in diseased myocardium.Semantic proximity Read ↗

Conduction slowing and sudden arrhythmic death in mice with cardiac-restricted inactivation of connexin43.Semantic proximity Read ↗

Refining the molecular organization of the cardiac intercalated disc.Semantic proximity Read ↗

Gap junction alterations in human cardiac diseaseSemantic proximity Read ↗

Multilayered regulation of cardiac ion channels.Semantic proximity Read ↗

Arrhythmogenic cardiomyopathy and Brugada syndrome: Diseases of the connexomeSemantic proximity Read ↗

Diverse functions of vertebrate gap junctions.Semantic proximity Read ↗

HSPB7 prevents cardiac conduction system defect through maintaining intercalated disc integritySemantic proximity Read ↗

Functional role of connexin43 gap junction channels in adult mouse heart assessed by inducible gene deletion.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.