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Biomedical subjects

Baofeng Wang

Publications and source records attributed to Baofeng Wang.

2 recordsLinked to original sources

Alternative oxidase pathway inhibits PuWRKY7-PuHDAC15 complex to promote ester aroma synthesis in Nanguo pear.

Volatile esters are key contributors to the characteristic aroma in fruit, and their accumulation directly dictates fruit quality and consumer acceptance. The alternative oxidase pathway is known for its role in regulating fruit quality, but its molecular mechanism in ester aroma accumulation remains unclear. Here, we demonstrated that the alternative oxidase pathway acts as the dominant respiratory pathway in Nanguo pear (Pyrus ussuriensis) during ripening and promotes ester aroma accumulation by increasing histone acetylation levels of PuAAT1 (alcohol acetyltransferase 1), the key gene governing ester synthesis. Further, we identified PuHDAC15 as a critical histone deacetylase that modulates acetylation levels and interacts with the transcription factor PuWRKY7. Mechanistically, PuWRKY7 directly binds to the W-box elements in the PuAAT1 promoter. The PuHDAC15-PuWRKY7 complex acts synergistically to repress PuAAT1 transcription, thereby decreasing its histone acetylation levels and gene expression, and consequently inhibiting ester aroma accumulation in Nanguo pear. This study reveals how the alternative oxidase pathway integrates into fruit aroma formation via epigenetic regulation and gene expression, thereby providing a scientific basis for targeted improvement of fruit quality.

Plant Proteins

Analysis of the molecular mechanism underlying di(2-ethylhexyl) phthalate-induced bladder carcinogenesis via network toxicology and molecular docking approaches: An observational study.

This study aims to investigate the toxicity of di(2-ethylhexyl) phthalate (DEHP) and the potential molecular mechanisms of DEHP-induced bladder cancer (BLCA) using network toxicology and molecular docking strategies. The toxicity of DEHP was assessed using Prox-II software, and potential targets for DEHP-induced BLCA were identified by integrating data from ChEMBL database, Search Tool for Interactions of Chemicals, SwissTargetPrediction, GeneCards, Therapeutic Target Database, Online Mendelian Inheritance in Man, and The Cancer Genome Atlas. STRING database and Cytoscape were employed to construct target networks and determine core targets. The expression levels of core targets were analyzed using R. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed on potential and core targets. Molecular docking was carried out using CB-Dock 2 to verify the interactions between DEHP and core targets. A total of 105 potential targets related to DEHP-induced BLCA were identified, from which 7 core targets were selected: cyclin-dependent kinase 1, interleukin 6, cyclin-dependent kinase 2, cyclin B1, Erb-B2 receptor tyrosine kinase 2, cyclin B2, and B-cell lymphoma 2. IL-6 and B-cell lymphoma 2 showed downregulated expression in tumor tissues, while cyclin-dependent kinase 1, cyclin-dependent kinase 2, cyclin B1, Erb-B2 receptor tyrosine kinase 2, and cyclin B2 were upregulated. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses indicated that these targets were enriched in cell signaling and cancer-related pathways. Molecular docking confirmed that DEHP interacts with these core targets. DEHP may promote the development of BLCA by interacting with key proteins and signaling pathways. This study provides a theoretical basis for understanding the molecular mechanisms of DEHP-induced BLCA and offers references for future prevention and treatment strategies.

Diethylhexyl Phthalate