Dataset Information

RyR2 phosphorylation profile in PKP2cKO mice

ABSTRACT: The project aimed to investigate whether there are alterations in the phosphorylation status of the Ryanodine receptor 2 (RyR2) in the left atria of mice with a cardiac-specific knockout of PKP2, compared to wild-type mice.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

SUBMITTER: Sergio D'Anna

LAB HEAD: Alicia Lundby

PROVIDER: PXD052074 | Pride | 2025-10-27

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	2024-02-15-decoys-contam-sp_mouse_2024_02_15.fasta.fas	Fasta
	20240119_TIMS6_EVO4_PRI_X1423_P0299_R1069_44min_DDA_S01_S2-A1_1_7172.pepXML	Pepxml
	20240119_TIMS6_EVO4_PRI_X1423_P0299_R1069_44min_DDA_S02_S2-A2_1_7173.pepXML	Pepxml
	20240119_TIMS6_EVO4_PRI_X1423_P0299_R1069_44min_DDA_S03_S2-A3_1_7174.pepXML	Pepxml
	20240119_TIMS6_EVO4_PRI_X1423_P0299_R1069_44min_DDA_S04_S2-A4_1_7175.pepXML	Pepxml

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Publications

Atrial cardiomyopathy resulting from loss of plakophilin-2 expression: Response to adrenergic stimulation and implications for the exercise response.

Phadke Kavya K D'Anna Sergio S Torres Vega Estefania E Xiao Junhua J Lin Xianming X Zhang Mingliang M Sall Joseph J Liang Feng-Xia FX Park David S DS Cerrone Marina M Lundby Alicia A Delmar Mario M van Opbergen Chantal J M CJM

The Journal of physiology 20241024 18

Atrial arrhythmias occur in 20-40% of patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) and are associated with an increased risk of sustained ventricular arrhythmias and inappropriate implantable cardioverter-defibrillator shocks. The pathophysiology of atrial arrhythmias in ARVC remains unclear. Most cases of gene-positive ARVC are linked to pathogenic variants in the desmosomal gene plakophilin-2 (PKP2). Here, we test the hypothesis that loss of PKP2 expression leads to pro ...[more]

PMID: 39446303

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Project description:Expression level, control and intercoordination of 66 selected heart rhythm determinant (HRD) genes were compared in atria and ventricles of 4 male and 4 female adult mice. We found that genes encoding various adrenergic receptors, ankyrins, ion channels and transporters, connexins and other components of the intercalated discs form a complex network that is chamber dependent and differs between the two sexes. In addition, most HRD genes in atria had higher expression in males than in females, while in ventricles expression levels were mostly higher in females than in males. Moreover, significant chamber-differences were observed between the sexes, with higher expression in atria than ventricles for males and higher expression in ventricles than atria for females. We have ranked the selected genes according to their prominence in controlling the HRD gene web through expression coordination with the other web genes and protecting the web though their own expression stability. Interestingly, the prominence hierarchy was substantially different between the two sexes. Taken together these findings indicate that the organizational principles of the heart rhythm transcriptome are sex-dependent, with the newly introduced prominence analysis allowing identification of genes that are pivotal for the sexual dichotomy. Four adult male (M) and 4 adult female (F) mice were decapitated, the hearts removed and atria (A) and ventricles (V) collected in separate tubes. 20 Âµg total RNA extracted in Trizol from each of the 16 samples was reverse transcribed in the presence of fluorescent Alexa FluorÂ®_647 and Alexa FluorÂ®_555-aha-dUTPs (Invitrogen, CA) to obtain labeled cDNAs Red and green-labeled samples of biological replicas were then co-hybridized (âmultiple yellowâ strategy) overnight at 50Â°C with mouse MO36k oligonucleotide arrays printed by Duke University (http://microarray.genome.duke.edu/spotted-arrays) with Operon Mouse Oligo Set, version 4.0. After washing (0.1% SDS and 1% SSC) to remove the non-hybridized cDNA, each array was scanned with GenePix 4000B scanner (MDS, Toronto, Canada) and images were primarily analyzed with GenePixPro 6.0 (Axon Instruments, CA).