ERp57/PDIA3: new insight

Chichiarelli, Silvia; Altieri, Fabio; Paglia, Giuliano; Rubini, Elisabetta; Minacori, Marco; Eufemi, Margherita

doi:10.1186/s11658-022-00315-x

Cited by 41 publications

(33 citation statements)

References 140 publications

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“…Interestingly, we found that several Lhx1os interactors correspond to proteins associated with the ER; among them, calreticulin, calnexin, and PDIA3 are known to transiently bind newly synthesized glycoproteins in the ER. 52 We were able to validate PDIA3, a member of the family of protein disulfide isomerases (PDIs) which controls protein folding through their ability to form and break disulfide bonds, 69 as a bona fide Lhx1os interactor. Notably, we show that the downregulation of either Lhx1os or PDIA3 affects the same set of ER stress-response genes, indicating that both components impinge on the same regulatory pathway.…”

Section: Discussionmentioning

confidence: 99%

A KO mouse model for the lncRNA Lhx1os produces motor neuron alterations and locomotor impairment

et al. 2023

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Section: Discussionmentioning

confidence: 99%

A KO mouse model for the lncRNA Lhx1os produces motor neuron alterations and locomotor impairment

et al. 2023

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“…Similarly, the PDIA3 membrane complex takes part in the rapid activation of WNT5A (Wnt family member 5A) by 1,25(OH) 2 D 3 -stimulated calcium influx and generation of secondary messengers, such as cAMP and/or IP3 [ 101 ]. Finally, some reports suggested nuclear localization of PDIA3 [ 114 , 125 ]. It is well established that PDIA3 has a noncanonic ER retention signal, Q/KEDL, but the presence of a Lys-rich nuclear localization signal was also suggested [ 111 ].…”

Section: Membrane-bound Receptor(s) and Targets For Vitamin Dmentioning

confidence: 99%

Nongenomic Activities of Vitamin D

Żmijewski

2022

Nutrients

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Vitamin D shows a variety of pleiotropic activities which cannot be fully explained by the stimulation of classic pathway- and vitamin D receptor (VDR)-dependent transcriptional modulation. Thus, existence of rapid and nongenomic responses to vitamin D was suggested. An active form of vitamin D (calcitriol, 1,25(OH)2D3) is an essential regulator of calcium–phosphate homeostasis, and this process is tightly regulated by VDR genomic activity. However, it seems that early in evolution, the production of secosteroids (vitamin-D-like steroids) and their subsequent photodegradation served as a protective mechanism against ultraviolet radiation and oxidative stress. Consequently, direct cell-protective activities of vitamin D were proven. Furthermore, calcitriol triggers rapid calcium influx through epithelia and its uptake by a variety of cells. Subsequently, protein disulfide-isomerase A3 (PDIA3) was described as a membrane vitamin D receptor responsible for rapid nongenomic responses. Vitamin D was also found to stimulate a release of secondary massagers and modulate several intracellular processes—including cell cycle, proliferation, or immune responses—through wingless (WNT), sonic hedgehog (SSH), STAT1-3, or NF-kappaB pathways. Megalin and its coreceptor, cubilin, facilitate the import of vitamin D complex with vitamin-D-binding protein (DBP), and its involvement in rapid membrane responses was suggested. Vitamin D also directly and indirectly influences mitochondrial function, including fusion–fission, energy production, mitochondrial membrane potential, activity of ion channels, and apoptosis. Although mechanisms of the nongenomic responses to vitamin D are still not fully understood, in this review, their impact on physiology, pathology, and potential clinical applications will be discussed.

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“…The most studied PDI is PDIA3 (ERp57/ Grp58), which is comprised of the canonical four thioredoxin domain structure of the a-b-b-a domain organisation. In general, the a-domains of PDIs contain the catalytic CXXC active site motif, which can exhibit thiol-sulphate reductase, oxidase or isomerase activity (Darby and Creighton, 1995;Chichiarelli et al, 2022). The b-domains bind substrates with high affinity to facilitate isomerization (Klappa et al, 1998).…”

Section: Protein Disulphide Isomerasesmentioning

confidence: 99%

Host cell stress response as a predictor of COVID-19 infectivity and disease progression

Caillet

Stofberg

Muleya

et al. 2022

Front. Mol. Biosci.

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The coronavirus disease (COVID-19) caused by a coronavirus identified in December 2019 has caused a global pandemic. COVID-19 was declared a pandemic in March 2020 and has led to more than 6.3 million deaths. The pandemic has disrupted world travel, economies, and lifestyles worldwide. Although vaccination has been an effective tool to reduce the severity and spread of the disease there is a need for more concerted approaches to fighting the disease. COVID-19 is characterised as a severe acute respiratory syndrome . The severity of the disease is associated with a battery of comorbidities such as cardiovascular diseases, cancer, chronic lung disease, and renal disease. These underlying diseases are associated with general cellular stress. Thus, COVID-19 exacerbates outcomes of the underlying conditions. Consequently, coronavirus infection and the various underlying conditions converge to present a combined strain on the cellular response. While the host response to the stress is primarily intended to be of benefit, the outcomes are occasionally unpredictable because the cellular stress response is a function of complex factors. This review discusses the role of the host stress response as a convergent point for COVID-19 and several non-communicable diseases. We further discuss the merits of targeting the host stress response to manage the clinical outcomes of COVID-19.

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ERp57/PDIA3: new insight

Cited by 41 publications

References 140 publications

A KO mouse model for the lncRNA Lhx1os produces motor neuron alterations and locomotor impairment

A KO mouse model for the lncRNA Lhx1os produces motor neuron alterations and locomotor impairment

Nongenomic Activities of Vitamin D

Host cell stress response as a predictor of COVID-19 infectivity and disease progression

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