Ontology highlight
ABSTRACT: Rationale
Voltage-gated Na+ channel ( INa) function is critical for normal cardiac excitability. However, the Na+ channel late component ( INa,L) is directly associated with potentially fatal forms of congenital and acquired human arrhythmia. CaMKII (Ca2+/calmodulin-dependent kinase II) enhances INa,L in response to increased adrenergic tone. However, the pathways that negatively regulate the CaMKII/Nav1.5 axis are unknown and essential for the design of new therapies to regulate the pathogenic INa,L.Objective
To define phosphatase pathways that regulate INa,L in vivo.Methods and results
A mouse model lacking a key regulatory subunit (B56α) of the PP (protein phosphata
SUBMITTER: El Refaey M
PROVIDER: S-EPMC6395500 | biostudies-literature | 2019 Mar
REPOSITORIES: biostudies-literature