Related Experiment Video
Updated: Jul 17, 2026

Identification and Characterization of Immunogenic RNA Species in HDM Allergens that Modulate Eosinophilic Lung Inflammation
Published on: May 30, 2020
DHRS9 generates crotonyl-CoA from butyryl-CoA to epigenetically regulate STING transcription and potentiate immune
Yuling Zhang1,2, Fei Qin1,2, Jiajia Zhang1,2
1State Key Laboratory of Reproductive Medicine and Offspring Health, State Key Laboratory of Microbial Technology, Shandong Key Laboratory of Infection Immunity and Disease Intervention & Key Laboratory for Experimental Teratology of Ministry of Education, Shandong University, Jinan, Shandong, China.
Abstract:
The stimulator of interferon genes (STING) pathway is a cornerstone of innate immunity and a promising therapeutic target for autoimmune diseases, inflammation, and cancer treatment. Lysine crotonylation, a recently discovered post-translational modification, regulates various cellular processes; however, its role in STING activation remains unclear. Here, we identified dehydrogenase/reductase (SDR family) member 9 (DHRS9) as a critical metabolic regulator of the STING signaling pathway. DHRS9 deficiency impaired activation of the cGAS-STING pathway, suppressed antiviral immunity against HSV-1, and exacerbated viral replication. Mechanistically, DHRS9 converts butyryl-CoA into crotonyl-CoA, thereby enhancing histone crotonylation (H3K14cr and H3K18cr) at the STING promoter to drive its transcription. AAV-mediated DHRS9 delivery significantly enhances antiviral and antitumor immunity, demonstrating its robust therapeutic potential. This study reveals a metabolic-epigenetic axis that regulates STING expression, offering new therapeutic strategies for immune-related diseases.
More Related Videos
Related Concept Videos
Exon Recombination
Exon shuffling follows “splice frame rules.” Each exon has three reading...
Co-activators and Co-repressors
Master Transcription Regulators
Master Transcription Regulators
Cooperative Binding of Transcription Regulators

