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. 2022 Sep 25;23(19):11308. doi: 10.3390/ijms231911308

Table 2.

Acetylation of host proteins during viral infection.

Protein Acetylation Site Function Reference
RIG-I K909 Deacetylation is critical for RIG-I activation in vivo and the production of IFN-β and pro-inflammatory cytokines [28,29]
OTUD3 K129 Hydrolyzes Lys63-linked poly-ubiquitination of MAVS to antagonize RLR signaling and shuts off innate antiviral immune response [32]
TBK1 K241 Deacetylation of TBK1 activates the phosphorylation of TBK1, enhances its kinase activity, and leads to an increased induction of type I IFNs [33]
IRF3 Prompts the DNA-binding activity of IRF3 homodimer [34]
IRF7 K92 Negatively modulates IRF7 DNA binding [35]
cGAS N-terminal domain Has a higher affinity to viral DNA and initiates a MITA/STING-dependent innate immune response to DNA viruses [36]
IFI16 K99, K128 Regulates subcellular localization and determines the initiation of pro-inflammatory responses and innate immune signaling when infected with DNA viruses, limiting viral replication and transmission [37]
P65 K218, K221, K310 Regulates different NF-kB functions [38]
IFNAR K399 Recruits IRF9, STAT1, and STAT2 [40]
K685 Regulates STAT3 dimerization and promotes nuclear accumulation of STAT3 and transcriptional activation following cytokine-induced signaling [41]
ISG15 C-terminal LRLRGG Deacetylation promotes the recycling of ISG15, targets selective autophagic degradation, and inhibits viral transmission [42,43,44]
α-tublin Enhances microtubule stability [45,46]
HSP90 K294 Reduces nuclear accumulation of viral polymerases and attenuates viral replication [48]
p53 K379 Trans-activates pro-apoptotic and IFN-stimulated genes to promote virus-induced apoptosis and activates the interferon pathway to enhance the antiviral effect [49]
LMNB1 K134 A molecular toggle that controls nuclear periphery stability, cell cycle progression, and DNA repair;
prevents lamina disruptions to inhibit virus production
[50]
NEDD4 K667 Essential for activating VP40 ubiquitination and virus budding [51]
H3K9 Plays an important role in BoDV-1-induced memory impairment [52]
Histone H3, H4 subunits Activates the transcription process [54]