Discover Community Create You

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

Article

Molecular alteration of Ca(v)1.2 calcium channel in chronic myocardial infarction.

Pflugers Archiv : European journal of physiology - 1 Aug 2009

Liao Ping, Li Guang, Yu De Jie, Yong Tan Fong, Wang Jue Jin, Wang Jing, Soong Tuck Wah

Abstract excerpt

Ca(v)1.2 channels are important for excitation-contraction coupling of cardiac muscles. Alternative splicing of Ca(v)1.2 channels could produce extensive phenotypic variations of channel properties. In a rat model of chronic myocardial infarction, we investigated whether Ca(v)1.2 channels may alter the use of alternatively spliced exons to generate functional variants. A myocardial infarction model on rat was...

Read the complete abstract on PubMed

Topics

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

Share to Adaptation, Physiological
Share to Calcium Channels, L-Type

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chronic Disease

Share to Mutation

Share to Myocardial Infarction

Share to Rats, Wistar

Source

Identifiers

PMID: 19263075
DOI: 10.1007/s00424-009-0652-4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Molecular alteration of Ca(v)1.2 calcium channel in chronic myocardial infarction.PMID 19263075Read ↗

Exclusion of alternative exon 33 of Ca V 1.2 calcium channels in heart is proarrhythmogenicSemantic proximity Read ↗

Alternative Splicing of L-type CaV1.2 Calcium Channels: Implications in Cardiovascular DiseasesSemantic proximity Read ↗

Pathophysiological Significance of T-type Ca2+ Channels: Expression of T-type Ca2+ Channels in Fetal and Diseased HeartSemantic proximity Read ↗

Overexpression of Kir2.1 channel in embryonic stem cell-derived cardiomyocytes attenuates posttransplantation proarrhythmic risk in myocardial infarction.Semantic proximity Read ↗

Tissue distribution of a human Ca v 1.2 alpha1 subunit splice variant with a 75 bp insertion.Semantic proximity Read ↗

Disruption of NOX2-dependent Oxidative Injury with a Targeted Gene-Therapy Approach Prevents Atrial Fibrillation in a Canine ModelSemantic proximity Read ↗

Molecular heterogeneity of calcium channel beta-subunits in canine and human heart: evidence for differential subcellular localization.Semantic proximity Read ↗

Splicing for alternative structures of Cav1.2 Ca2+ channels in cardiac and smooth muscles.Semantic proximity Read ↗

Splice variants’ role in mediating different disease states in tissue requiring ion transduction through calcium channel for functionSemantic proximity Read ↗

Alternative splicing of voltage-gated calcium channels: from molecular biology to disease.Semantic proximity Read ↗

The E23K variant of the Kir6.2 subunit of the ATP-sensitive potassium channel increases susceptibility to ventricular arrhythmia in response to ischemia in rats.Semantic proximity Read ↗

Transcript scanning reveals novel and extensive splice variations in human l-type voltage-gated calcium channel, Cav1.2 alpha1 subunit.Semantic proximity Read ↗

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