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Table 1 The pathophysiologic processes modulated by USP4

From: USP4 function and multifaceted roles in cancer: a possible and potential therapeutic target

Authors, year Pathophysiologic processes Deubiquitinated targets Effects to the deubiquitinated targets Detailed mechanisms Refs.
Zhu et al., 2018 Liver fibrosis TβRI Stabilization HSC and EMT activation; liver fibrosis enhancement [51]
Zhao et al., 2018 NAFLD pathogenesis TAK1 Inactivation Alleviation NAFLD progression through inactivation of NF-κB and JNK signaling pathways [53]
Zhou et al., 2019 Hepatic I/R injury TAK1 Inactivation Alleviation hepatic I/R injury by inhibiting inflammatory caused by NF-κB signaling pathway [54]
Zhou et al., 2012 Innate immune response and immune homeostasis TRAF6 Inactivation Inhibition of the immunoinflammatory response caused by TLR/IL-1R-induced NF-κB activation [56]
Yang et al., 2015 Th17 cell function RORγt Stabilization IL-17 expression upregulation [57]
Lin et al., 2017 Treg cell function IRF8 Stabilization Enhancement of IL-10, TGF-β expression to promote Treg cell function [60]
Guo et al., 2017 Th2 cell function IRF4 Stabilization Enhancement of IL-4 expression to promote Th2 cell function [61]
Jiang et al., 2017 Spinal cord injury TRAF6 Inactivation Inhibition of secondary spinal cord injury through NF-κB inactivation [63]
Wang et al., 2013 Antiviral response RIG-I Stabilization Activation of RIG-I-induced IFN-β signaling pathway and VSV replication inhibition [70]
Xu et al., 2018 Antiviral response TRAF6 Stabilization Activation of TRAF6-mediated NF-κB signaling pathway and EV 71 replication inhibition [71]
Wijinhoven et al., 2015 DNA breaks repairment USP4 Stabilization DNA repairment enhancement [73]
Zhou et al., 2016 Osteoblast differentiation Dvl Inactivation Inhibition of Wnt/β-catenin signaling pathway mediated osteoblast differentiation [80]
Yun et al., 2017 Myogenesis HDAC1 and 4 Stabilization Enhancement of MyoD to inhibit myogenesis [82]
He et al., 2016 Pathological cardiac hypertrophy TAK1 Inactivation Inactivation of TAK1/JNK1/2/p38 to inhibit pathological cardiac hypertrophy [83]