A dataset of VP4 regulates PINK1/Parkin-mediated mitophagy and ubiquitinates p62 for degradation

This dataset spans from March 2024 to March 2025 and originates from a mechanistic study on the outer capsid protein VP4 of type II Grass Carp Reovirus (GCRV Ⅱ). The research focuses on how VP4 enhances viral replication by promoting PINK1/Parkin‑mediated mitophagy. Over this 13‑month period, multiple rounds of proteomic, molecular, and cellular biology experiments were conducted. The dataset includes both time‑series and cross‑sectional data, as follows:1. Protein‑protein interaction data: Co‑immunoprecipitation and mass spectrometry records identifying the interaction between VP4 and p62, as well as quantitative measurements of VP4‑induced p62 degradation via the ubiquitin‑proteasome and autolysosomal pathways.2. Ubiquitination modification data: Characterization of VP4‑induced p62 ubiquitination chain types (K27‑ and K29‑linked ubiquitin chains) and identification of specific ubiquitination sites (lysine residues K6, K223, K468, and K473) collected at various time points from March 2024 to March 2025.3. Subcellular colocalization data: Confocal microscopy images and quantitative analyses showing the dynamic colocalization of VP4 with p62 and Parkin in the cytoplasm over time.4. Gene knockdown and truncation mutant data: Changes in p62 ubiquitination and degradation levels upon Parkin knockdown; effects of VP4 truncation mutants (targeting the PB1 and UBA domains of p62) on mitophagy and viral replication.5. Viral replication indicators: Time‑series measurements of GCRV Ⅱ replication titers, viral protein expression, and cell death levels under different conditions (e.g., VP4 overexpression, autophagy pathway inhibition).Data were collected at weekly or per‑experiment‑batch frequency, with a minimum of three biological replicates per condition. All raw data have undergone normalization, outlier removal, and standardized archiving. The dataset is formatted for time‑series analysis, differential expression statistics, and pathway enrichment analysis. It is suitable for further studies on how viral proteins hijack host autophagy machinery, modeling virus‑host interactions, and screening anti‑GCRV drug targets.