Recombinant mouse Ppp2r5a is typically produced in heterologous systems with the following specifications :
Studies using PPP2R5A knockout (KO) mice reveal:
Prolonged QT intervals and increased ventricular tachyarrhythmia under catecholaminergic stress
Dysregulated Ca²⁺ handling: KO cardiomyocytes exhibit spontaneous Ca²⁺ transients, promoting arrhythmogenic activity
Pathway linkage: PP2A-B56α deficiency reduces association with RyR2, increasing phosphorylation at serine-2814 and SR Ca²⁺ leak
Recombinant B56α is pivotal in cancer studies:
Hepatocellular carcinoma (HCC): Overexpression inhibits HCC cell proliferation (↓c-Myc, ↓Bcl-2) and metastasis via MAPK/AKT/WNT pathway suppression
HBV interaction: HBV infection downregulates PPP2R5A, facilitating HCC progression by evading phosphatase-mediated tumor suppression
Clinical correlation: Low PPP2R5A expression in Chinese HCC patients correlates with poor prognosis (p < 0.001)
Lentiviral infections: Accelerate PPP2R5A degradation to enhance viral replication
HBV: Modulates PP2A-B56α localization to disrupt host cell cycle checkpoints
Post-translational modifications: Recombinant proteins may lack native phosphorylation states
Species specificity: Mouse PP2R5A antibodies show cross-reactivity with human samples but require validation
Functional redundancy: B56β/γ subunits may compensate in knockout models, necessitating multi-isoform analyses