Activation of the stress-activated protein kinase JNK in response to herpes simplex virus-1 infection coordinates transition of BRD4 from chromosome association to transcription elongation.

ABSTRACT: The c-Jun N-terminal kinase (JNK) signaling pathway is required for herpes simplex virus 1 lytic infection and reactivation from latency. JNK signaling regulates cellular processes in response to stress through transcriptional regulation. However, the mechanisms by which JNK regulates HSV-1 infection are less defined. We show here that HSV-1 infection triggers BRD4 transition from chromosome association to transcriptional regulation for viral infection. Specifically, HSV-1 infection induces JNK activation which mediates redistribution of BRD4, an epigenetic reader protein, from chromatin-targeting to association with proteins of transcriptional regulation. BRD4 transitions to viral infection regulation by complexing with P-TEFb, a positive transcription elongation factor, and association w

SUBMITTER: Sun W 

PROVIDER: S-EPMC12450640 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature