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MI2026 – FenXiang Shang
Fengxiang ShangMaster’s Student, Department of Anatomy, Histology and Embryology Yanbian University China |
Title:
Abstract: In vitro, EB could bind to DEK. RNF149 and RNF170 were identified as regulatory factors of DEK, poly ubiquitinating the K349 site in the DEK coding DNA sequence region 270–350 through K48 linkages and leading to its degradation. RNA sequencing showed that DEK overexpression upregulated the expression of genes such as RIPK1, FADD, and Caspase 8. Treatment with DEK siRNA or EB reduced the activation of the RIPK1-PANoptosis pathway in BEAS-2B-DEK cells. In vivo, EB significantly reduced the levels of DEK in house dust mite-induced mice and alleviated pulmonary inflammatory cell infiltration, goblet cell hyperplasia, collagen fiber deposition, and eosinophil proportion in BALF. Knocking out the DEK gene reduced RIPK1-induced PANoptosis, and inhibited airway inflammation and cell apoptosis. EB promotes the degradation of DEK by RNF149 and RNF170, inhibits the RIPK1-PANoptosis pathway, and may effectively suppress asthma. EB may become a potential drug for treating airway inflammation in asthma.
Biography: |

Fengxiang Shang