Overexpression of CaMKIIδc in RyR2R4496C+/- knock-in mice leads to altered intracellular Ca2+ handling and increased mortality.

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

We investigated whether increased Ca(2+)/calmodulin-dependent kinase II (CaMKII) activity aggravates defective excitation-contraction coupling and proarrhythmic activity in mice expressing R4496C mutated cardiac ryanodine receptors (RyR2).

Related collections

Author and article information

Journal

Journal ID (iso-abbrev): J Am Coll Cardiol

Title: Journal of the American College of Cardiology

Publisher: Elsevier BV

ISSN (Electronic): 1558-3597

ISSN (Print): 0735-1097

Publication date (Electronic): Jan 25 2011

Volume: 57

Issue: 4

Affiliations

[1 ] Department of Cardiology and Pneumology, Georg-August-University Göttingen, Göttingen, Germany.

Article

Publisher Item ID: S0735-1097(10)04487-6

DOI: 10.1016/j.jacc.2010.08.639

PubMed ID: 21251589

SO-VID: 1d14af24-b48a-4a7b-ac36-fe89370bd53f

History

Data availability:

Comments

Comment on this article

scite_

Smart Citations

Citing PublicationsSupportingMentioningContrasting

View Citations

See how this article has been cited at scite.ai

scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.