Induction of Herpud1 expression by ER stress is regulated by Nrf1

Ho, Daniel V.; Chan, Jefferson Y.

doi:10.1016/j.febslet.2015.01.026

Cited by 42 publications

(35 citation statements)

References 39 publications

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“…HERPUD1 is a key component of the ER‐associated degradation multiprotein complex that helps to stabilize the complex and facilitate efficient degradation of unfolded proteins . EIF2AK3 is a UPR sensor protein while CREB3L2 is an ER stress transducer . These genes act downstream of ER stress and their upregulation thus supports the promotion of ER stress in the NP treatment group.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of titanium dioxide nanoparticle‐induced oxidative stress and modulation of plasma glucose in mice

Fan

Yao

et al. 2019

Environmental Toxicology

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Titanium dioxide nanoparticles (TiO2 NPs) are reported to increase plasma glucose levels in mice at specific doses. The production and accumulation of reactive oxygen species (ROS) is potentially the most important factor underlying the biological toxicity of TiO2 NPs but the underlying mechanisms are unclear at present. Data from genome‐wide analyses showed that TiO2 NPs induce endoplasmic reticulum (ER) stress and ROS generation, leading to the inference that TiO2 NP‐induced ER stress contributes to enhancement of ROS in mice. Resveratrol (Res) effectively relieved TiO2 NP‐induced ER stress and ROS generation by ameliorating expression of a common set of activated genes for both processes, signifying that ER stress and ROS are closely related. TiO2 NP‐induced ER stress occurred earlier than ROS generation. Upon treatment with 4‐phenylbutyric acid to relieve ER stress, plasma glucose levels tended toward normal and TiO2 NP increased ROS production was inhibited. These results suggest that TiO2 NP‐induced ER stress promotes the generation of ROS, in turn, triggering increased plasma glucose levels in mice. In addition, Res that displays the ability to reduce ER stress presents a dietary polyphenol antioxidant that can effectively prevent the toxicological effects of TiO2 NPs on plasma glucose metabolism.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of titanium dioxide nanoparticle‐induced oxidative stress and modulation of plasma glucose in mice

Fan

Yao

et al. 2019

Environmental Toxicology

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“…Dnajb9 encodes a member of the J-domain heat-shock protein 40 (HSP40) family that acts as a molecular co-chaperone for HSPA5 (68). Herpud1 encodes a ubiquitin-like domain protein that is believed to function in the ER-associated degradation of misfolded proteins (69). When combined with Xbp1 splicing above, these data by extension suggest that both the Ern1/Ire1a-Xbp1 and Atf6 branches of the UPR may also be activated in the Lop/+ lens, possibly, prior to the Eif2ak3/Perk-Atf4 branch.…”

Section: Discussionmentioning

confidence: 99%

Lens ER-stress response during cataract development in Mip-mutant mice

Zhou

Bennett

Shiels

2016

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Major intrinsic protein (MIP) is a functional water-channel (AQP0) that also plays a key role in establishing lens fiber cell architecture. Genetic variants of MIP have been associated with inherited and age-related forms of cataract; however, the underlying pathogenic mechanisms are unclear. Here we have used lens transcriptome profiling by microarray-hybridization and qPCR to identify pathogenic changes during cataract development in Mip-mutant (Lop/+) mice. In postnatal Lop/+ lenses (P7) 99 genes were up-regulated and 75 were down-regulated (>2-fold, p=<0.05) when compared with wild-type. A pathway analysis of up-regulated genes in the Lop/+ lens (P7) was consistent with endoplasmic reticulum (ER)-stress and activation of the unfolded protein response (UPR). The most up-regulated UPR genes (>4-fold) in the Lop/+ lens included Chac1 > Ddit3 > Atf3 > Trib3 > Xbp1 and the most down-regulated genes (>5-fold) included two anti-oxidant genes, Hspb1 and Hmox1. Lop/+ lenses were further characterized by abundant TUNEL-positive nuclei within central degenerating fiber cells, glutathione depletion, free-radical overproduction, and calpain hyper-activation. These data suggest that Lop/+ lenses undergo proteotoxic ER-stress induced cell-death resulting from prolonged activation of the Eif2ak3/Perk-Atf4-Ddit3-Chac1 branch of the UPR coupled with severe oxidative-stress.

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“…The full-length nature of all transcript variants has not been determined. HERPUD1 has an N -terminal ubiquitin-like domain that interacts with the ERAD system, and expression from the gene is induced by UPR through an ER stress response element in its promoter region [42]. HERPUD1 is a component of a larger ER-resident complex that includes HRD1 (an E3 ubiquitin ligase), DERL1, SELS/VIMP, and VCP/p97.…”

Section: Vzv-induced Erad Microarray Analysismentioning

confidence: 99%

Varicella-Zoster Virus Infectious Cycle: ER Stress, Autophagic Flux, and Amphisome-Mediated Trafficking

et al. 2016

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Varicella-zoster virus (VZV) induces abundant autophagy. Of the nine human herpesviruses, the VZV genome is the smallest (~124 kbp), lacking any known inhibitors of autophagy, such as the herpes simplex virus ICP34.5 neurovirulence gene. Therefore, this review assesses the evidence for VZV-induced cellular stress, endoplasmic-reticulum-associated degradation (ERAD), and autophagic flux during the VZV infectious cycle. Even though VZV is difficult to propagate in cell culture, the biosynthesis of the both N- and O-linked viral glycoproteins was found to be abundant. In turn, this biosynthesis provided evidence of endoplasmic reticulum (ER) stress, including a greatly enlarged ER and a greatly diminished production of cellular glycoproteins. Other signs of ER stress following VZV infection included detection of the alternatively spliced higher-molecular-weight form of XBP1 as well as CHOP. VZV infection in cultured cells leads to abundant autophagosome production, as was visualized by the detection of the microtubule-associated protein 1 light chain 3-II (LC3-II). The degree of autophagy induced by VZV infection is comparable to that induced in uninfected cells by serum starvation. The inhibition of autophagic flux by chemicals such as 3-methyladenine or ATG5 siRNA, followed by diminished virus spread and titers, has been observed. Since the latter observation pointed to the virus assembly/trafficking compartments, we purified VZ virions by ultracentrifugation and examined the virion fraction for components of the autophagy pathway. We detected LC3-II protein (an autophagy marker) as well as Rab11 protein, a component of the endosomal pathway. We also observed that the virion-containing vesicles were single-walled; thus, they are not autophagosomes. These results suggested that some VZ virions after secondary envelopment were transported to the outer cell membrane in a vesicle derived from both the autophagy and endosomal pathways, such as an amphisome. Thus, these results demonstrate that herpesvirus trafficking pathways can converge with the autophagy pathway.

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Induction of Herpud1 expression by ER stress is regulated by Nrf1

Cited by 42 publications

References 39 publications

Mechanisms of titanium dioxide nanoparticle‐induced oxidative stress and modulation of plasma glucose in mice

Mechanisms of titanium dioxide nanoparticle‐induced oxidative stress and modulation of plasma glucose in mice

Lens ER-stress response during cataract development in Mip-mutant mice

Varicella-Zoster Virus Infectious Cycle: ER Stress, Autophagic Flux, and Amphisome-Mediated Trafficking

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