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Journal: JACC: Basic to Translational Science
Article Title: JP2 and JCN Crosstalk Abrogate MURF1-Mediated JCN Ubiquitination and Degradation in Cardiomyocytes
doi: 10.1016/j.jacbts.2026.101534
Figure Lengend Snippet: Ca 2+ Handling in Adult Mouse Cardiomyocytes (A to C) Adult mouse cardiomyocytes were infected with Ad-JP2 or Ad-HA and exposed to palmitate or oleate. RyR2 Ca 2+ leak (F/F0), caffeine-induced peak (F/F0), and Tau-SERCA were measured. (D to F) Adult mouse cardiomyocytes were infected with Ad-JCN or Ad-HA and exposed to palmitate or oleate. RyR2 Ca 2+ leak (F/F0), Caffeine-induced peak (F/F0), and Tau-SERCA were detected. (G to I) Adult mouse cardiomyocytes were infected with Ad-shJP2 or Ad-HA. RyR2 Ca 2+ leak (F/F0), caffeine-induced peak (F/F0), and Tau-SERCA were detected. (J to L) Adult mouse cardiomyocytes were infected with Ad-AsJCN or Ad-HA. RyR2 Ca 2+ leak (F/F0), caffeine-induced peak (F/F0), and Tau-SERCA were determined. Data are mean ± SD, n = 9-11 different adult mouse cardiomyocytes in each group. Two-way analysis of variance followed by Newman-Keuls post hoc test was performed for multiple pairwise comparisons. Student's t -test was used for comparison between 2 groups. ∗ P < 0.05 vs Ad-HA or oleate + Ad-HA, and † P < 0.05 vs palmitate + Ad-HA. ∗ and †: P < 0.05; ∗∗ and ††: P < 0.01; ∗∗∗ and †††: P < 0.001. Abbreviations as in .
Article Snippet: Then, sarcoplasmic reticulum (SR) Ca 2+ leak via RyRs was estimated in 0
Techniques: Infection, Comparison
Journal: JACC: Basic to Translational Science
Article Title: JP2 and JCN Crosstalk Abrogate MURF1-Mediated JCN Ubiquitination and Degradation in Cardiomyocytes
doi: 10.1016/j.jacbts.2026.101534
Figure Lengend Snippet: Schematic Mechanism In normal conditions, JP2 binds to JCN and blocks the MURF1-JCN interaction, thereby preventing MURF1-mediated ubiquitination and proteasome-dependent degradation of JCN. However, the protein level of JP2 is reduced under stress, enabling MURF1 to bind to JCN and promoting MURF1-mediated ubiquitination and degradation of JCN. JCN reduction triggers the excessive opening and Ca 2+ release from RyR2, leading to cardiomyocyte injury. In contrast, overexpression of JP2 or JCN protects intracellular Ca 2+ homeostasis and prevents cell death under stress.
Article Snippet: Then, sarcoplasmic reticulum (SR) Ca 2+ leak via RyRs was estimated in 0
Techniques: Ubiquitin Proteomics, Over Expression