Multi-level inhibition of coronavirus replication by chemical ER stress.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
20 09 2021
Historique:
received: 07 09 2020
accepted: 02 08 2021
entrez: 21 9 2021
pubmed: 22 9 2021
medline: 29 9 2021
Statut: epublish

Résumé

Coronaviruses (CoVs) are important human pathogens for which no specific treatment is available. Here, we provide evidence that pharmacological reprogramming of ER stress pathways can be exploited to suppress CoV replication. The ER stress inducer thapsigargin efficiently inhibits coronavirus (HCoV-229E, MERS-CoV, SARS-CoV-2) replication in different cell types including primary differentiated human bronchial epithelial cells, (partially) reverses the virus-induced translational shut-down, improves viability of infected cells and counteracts the CoV-mediated downregulation of IRE1α and the ER chaperone BiP. Proteome-wide analyses revealed specific pathways, protein networks and components that likely mediate the thapsigargin-induced antiviral state, including essential (HERPUD1) or novel (UBA6 and ZNF622) factors of ER quality control, and ER-associated protein degradation complexes. Additionally, thapsigargin blocks the CoV-induced selective autophagic flux involving p62/SQSTM1. The data show that thapsigargin hits several central mechanisms required for CoV replication, suggesting that this compound (or derivatives thereof) may be developed into broad-spectrum anti-CoV drugs.

Identifiants

pubmed: 34545074
doi: 10.1038/s41467-021-25551-1
pii: 10.1038/s41467-021-25551-1
pmc: PMC8452654
doi:

Substances chimiques

Cell Extracts 0
Endoplasmic Reticulum Chaperone BiP 0
Heat-Shock Proteins 0
Macrolides 0
Proteome 0
RNA, Messenger 0
Thapsigargin 67526-95-8
bafilomycin A1 88899-55-2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

5536

Subventions

Organisme : Deutsche Forschungsgemeinschaft (German Research Foundation)
ID : 284237345
Organisme : Deutsche Forschungsgemeinschaft (German Research Foundation)
ID : 268555672
Organisme : Deutsche Forschungsgemeinschaft (German Research Foundation)
ID : 197785619
Organisme : Deutsche Forschungsgemeinschaft (German Research Foundation)
ID : 416910386
Organisme : Deutsche Forschungsgemeinschaft (German Research Foundation)
ID : 390649896

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

© 2021. The Author(s).

Références

de Wit, E., van Doremalen, N., Falzarano, D. & Munster, V. J. S. A. R. S. and MERS: recent insights into emerging coronaviruses. Nat. Rev. Microbiol. 14, 523–534 (2016).
pubmed: 27344959 pmcid: 7097822 doi: 10.1038/nrmicro.2016.81
Gorbalenya, A. E. et al. The species Severe acute respiratory syndrome-related coronavirus: classifying 2019-nCoV and naming it SARS-CoV-2. Nat. Microbiol. 5, 536–544 (2020).
doi: 10.1038/s41564-020-0695-z
Gerna, G. et al. Genetic variability of human coronavirus OC43-, 229E-, and NL63-like strains and their association with lower respiratory tract infections of hospitalized infants and immunocompromised patients. J. Med. Virol. 78, 938–949 (2006).
pubmed: 16721849 pmcid: 7167039 doi: 10.1002/jmv.20645
Greenberg, S. B. Update on rhinovirus and coronavirus infections. Semin. Respir. Crit. Care Med. 32, 433–446 (2011).
pubmed: 21858748 doi: 10.1055/s-0031-1283283
Nicholson, K. G., Kent, J., Hammersley, V. & Cancio, E. Acute viral infections of upper respiratory tract in elderly people living in the community: comparative, prospective, population based study of disease burden. BMJ 315, 1060–1064 (1997).
pubmed: 9366736 pmcid: 2127683 doi: 10.1136/bmj.315.7115.1060
Jevsnik, M. et al. Coronavirus infections in hospitalized pediatric patients with acute respiratory tract disease. BMC Infect. Dis. 12, 365 (2012).
pubmed: 23256846 pmcid: 3557153 doi: 10.1186/1471-2334-12-365
Drosten, C. et al. Identification of a novel coronavirus in patients with severe acute respiratory syndrome. N. Engl. J. Med. 348, 1967–1976 (2003).
pubmed: 12690091 doi: 10.1056/NEJMoa030747
Rota, P. A. et al. Characterization of a novel coronavirus associated with severe acute respiratory syndrome. Science 300, 1394–1399 (2003).
pubmed: 12730500 doi: 10.1126/science.1085952
Guan, Y. et al. Molecular epidemiology of the novel coronavirus that causes severe acute respiratory syndrome. Lancet 363, 99–104 (2004).
pubmed: 14726162 pmcid: 7112497 doi: 10.1016/S0140-6736(03)15259-2
Zhu N. et al. A novel coronavirus from patients with pneumonia in China, 2019. N. Engl. J. Med. 382, 727−733 (2020).
Zhou, P. et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature 579, 270–273 (2020).
pubmed: 32015507 pmcid: 7095418 doi: 10.1038/s41586-020-2012-7
Zaki, A. M., van Boheemen, S., Bestebroer, T. M., Osterhaus, A. D. & Fouchier, R. A. Isolation of a novel coronavirus from a man with pneumonia in Saudi Arabia. N. Engl. J. Med. 367, 1814–1820 (2012).
pubmed: 23075143 doi: 10.1056/NEJMoa1211721
Fung, T. S. & Liu, D. X. Human coronavirus: host-pathogen interaction. Annu Rev. Microbiol. 73, 529–557 (2019).
pubmed: 31226023 doi: 10.1146/annurev-micro-020518-115759
de Wilde, A. H., Snijder, E. J., Kikkert, M. & van Hemert, M. J. Host factors in coronavirus replication. Curr. Top. Microbiol. Immunol. 419, 1–42 (2018).
pubmed: 28643204
Liao, Y., Wang, X., Huang, M., Tam, J. P. & Liu, D. X. Regulation of the p38 mitogen-activated protein kinase and dual-specificity phosphatase 1 feedback loop modulates the induction of interleukin 6 and 8 in cells infected with coronavirus infectious bronchitis virus. Virology 420, 106–116 (2011).
pubmed: 21959016 doi: 10.1016/j.virol.2011.09.003
Mizutani, T., Fukushi, S., Saijo, M., Kurane, I. & Morikawa, S. JNK and PI3k/Akt signaling pathways are required for establishing persistent SARS-CoV infection in Vero E6 cells. Biochim. Biophys. Acta 1741, 4–10 (2005).
pubmed: 15916886 pmcid: 7125767 doi: 10.1016/j.bbadis.2005.04.004
Poppe, M. et al. The NF-kappaB-dependent and -independent transcriptome and chromatin landscapes of human coronavirus 229E-infected cells. PLoS Pathog. 13, e1006286 (2017).
pubmed: 28355270 pmcid: 5386326 doi: 10.1371/journal.ppat.1006286
Snijder, E. J. et al. A unifying structural and functional model of the coronavirus replication organelle: tracking down RNA synthesis. PLoS Biol. 18, e3000715 (2020).
pubmed: 32511245 pmcid: 7302735 doi: 10.1371/journal.pbio.3000715
Romero-Brey, I. & Bartenschlager, R. Endoplasmic reticulum: the favorite intracellular niche for viral replication and assembly. Viruses 8, 160 (2016).
Wang, M. & Kaufman, R. J. Protein misfolding in the endoplasmic reticulum as a conduit to human disease. Nature 529, 326–335 (2016).
pubmed: 26791723 doi: 10.1038/nature17041
Karagoz, G. E., Acosta-Alvear, D. & Walter, P. The unfolded protein response: detecting and responding to fluctuations in the protein-folding capacity of the endoplasmic reticulum. Cold Spring Harb. Perspect. Biol. 11, a033886 (2019).
Hetz, C. & Papa, F. R. The unfolded protein response and cell fate control. Mol. Cell 69, 169–181 (2018).
pubmed: 29107536 doi: 10.1016/j.molcel.2017.06.017
Wu, H., Ng, B. S. & Thibault, G. Endoplasmic reticulum stress response in yeast and humans. Biosci. Rep. 34, e00118 (2014).
Pobre, K. F. R., Poet, G. J. & Hendershot, L. M. The endoplasmic reticulum (ER) chaperone BiP is a master regulator of ER functions: getting by with a little help from ERdj friends. J. Biol. Chem. 294, 2098–2108 (2019).
pubmed: 30563838 doi: 10.1074/jbc.REV118.002804
Bertolotti, A., Zhang, Y., Hendershot, L. M., Harding, H. P. & Ron, D. Dynamic interaction of BiP and ER stress transducers in the unfolded-protein response. Nat. Cell Biol. 2, 326–332 (2000).
pubmed: 10854322 doi: 10.1038/35014014
Cui, W., Li, J., Ron, D. & Sha, B. The structure of the PERK kinase domain suggests the mechanism for its activation. Acta Crystallogr D. Biol. Crystallogr. 67, 423–428 (2011).
pubmed: 21543844 pmcid: 3087621 doi: 10.1107/S0907444911006445
Carrara, M., Prischi, F., Nowak, P. R. & Ali, M. M. Crystal structures reveal transient PERK luminal domain tetramerization in endoplasmic reticulum stress signaling. EMBO J. 34, 1589–1600 (2015).
pubmed: 25925385 pmcid: 4474532 doi: 10.15252/embj.201489183
Kopp, M. C., Larburu, N., Durairaj, V., Adams, C. J. & Ali, M. M. U. UPR proteins IRE1 and PERK switch BiP from chaperone to ER stress sensor. Nat. Struct. Mol. Biol. 26, 1053–1062 (2019).
pubmed: 31695187 pmcid: 6858872 doi: 10.1038/s41594-019-0324-9
Han, J. et al. ER-stress-induced transcriptional regulation increases protein synthesis leading to cell death. Nat. Cell Biol. 15, 481–490 (2013).
pubmed: 23624402 pmcid: 3692270 doi: 10.1038/ncb2738
Urra, H. & Hetz, C. Fine-tuning PERK signaling to control cell fate under stress. Nat. Struct. Mol. Biol. 24, 789–790 (2017).
pubmed: 28981072 doi: 10.1038/nsmb.3478
Chen, Y. & Brandizzi, F. IRE1: ER stress sensor and cell fate executor. Trends Cell Biol. 23, 547–555 (2013).
pubmed: 23880584 doi: 10.1016/j.tcb.2013.06.005
Mungrue, I. N., Pagnon, J., Kohannim, O., Gargalovic, P. S. & Lusis, A. J. CHAC1/MGC4504 is a novel proapoptotic component of the unfolded protein response, downstream of the ATF4-ATF3-CHOP cascade. J. Immunol. 182, 466–476 (2009).
pubmed: 19109178 doi: 10.4049/jimmunol.182.1.466
Grootjans, J., Kaser, A., Kaufman, R. J. & Blumberg, R. S. The unfolded protein response in immunity and inflammation. Nat. Rev. Immunol. 16, 469–484 (2016).
pubmed: 27346803 pmcid: 5310224 doi: 10.1038/nri.2016.62
Hilton, A., Mizzen, L., MacIntyre, G., Cheley, S. & Anderson, R. Translational control in murine hepatitis virus infection. J. Gen. Virol. 67, 923–932 (1986).
pubmed: 3009691 doi: 10.1099/0022-1317-67-5-923
Oslowski, C. M., Urano, F. & Measuring, E. R. stress and the unfolded protein response using mammalian tissue culture system. Methods Enzymol. 490, 71–92 (2011).
pubmed: 21266244 pmcid: 3701721 doi: 10.1016/B978-0-12-385114-7.00004-0
Snijder, E. J., Decroly, E. & Ziebuhr, J. The nonstructural proteins directing coronavirus RNA synthesis and processing. Adv. Virus Res. 96, 59–126 (2016).
pubmed: 27712628 pmcid: 7112286 doi: 10.1016/bs.aivir.2016.08.008
Tombal, B., Weeraratna, A. T., Denmeade, S. R. & Isaacs, J. T. Thapsigargin induces a calmodulin/calcineurin-dependent apoptotic cascade responsible for the death of prostatic cancer cells. Prostate 43, 303–317 (2000).
pubmed: 10861750 doi: 10.1002/1097-0045(20000601)43:4<303::AID-PROS10>3.0.CO;2-V
Sehgal, P. et al. Inhibition of the sarco/endoplasmic reticulum (ER) Ca(2+)-ATPase by thapsigargin analogs induces cell death via ER Ca(2+) depletion and the unfolded protein response. J. Biol. Chem. 292, 19656–19673 (2017).
pubmed: 28972171 pmcid: 5712609 doi: 10.1074/jbc.M117.796920
Kokic, G. et al. Mechanism of SARS-CoV-2 polymerase stalling by remdesivir. Nat. Commun. 12, 279 (2021).
pubmed: 33436624 pmcid: 7804290 doi: 10.1038/s41467-020-20542-0
Sheahan, T. P. et al. Comparative therapeutic efficacy of remdesivir and combination lopinavir, ritonavir, and interferon beta against MERS-CoV. Nat. Commun. 11, 222 (2020).
pubmed: 31924756 pmcid: 6954302 doi: 10.1038/s41467-019-13940-6
Ogando, N. S. et al. SARS-coronavirus-2 replication in Vero E6 cells: replication kinetics, rapid adaptation and cytopathology. J. Gen. Virol. 101, 925–940 (2020).
pubmed: 32568027 pmcid: 7654748 doi: 10.1099/jgv.0.001453
Brown, A. J. et al. Broad spectrum antiviral remdesivir inhibits human endemic and zoonotic deltacoronaviruses with a highly divergent RNA dependent RNA polymerase. Antivir. Res. 169, 104541 (2019).
pubmed: 31233808 doi: 10.1016/j.antiviral.2019.104541
Jonsdottir, H. R. & Dijkman, R. Coronaviruses and the human airway: a universal system for virus-host interaction studies. Virol. J. 13, 24 (2016).
pubmed: 26852031 pmcid: 4744394 doi: 10.1186/s12985-016-0479-5
Zhou, Y. et al. Metascape provides a biologist-oriented resource for the analysis of systems-level datasets. Nat. Commun. 10, 1523 (2019).
pubmed: 30944313 pmcid: 6447622 doi: 10.1038/s41467-019-09234-6
Oikonomou, C. & Hendershot, L. M. Disposing of misfolded ER proteins: A troubled substrate’s way out of the ER. Mol. Cell Endocrinol. 500, 110630 (2020).
pubmed: 31669350 doi: 10.1016/j.mce.2019.110630
Mizushima, N. A brief history of autophagy from cell biology to physiology and disease. Nat. Cell Biol. 20, 521–527 (2018).
pubmed: 29686264 doi: 10.1038/s41556-018-0092-5
Leitman, J. et al. Herp coordinates compartmentalization and recruitment of HRD1 and misfolded proteins for ERAD. Mol. Biol. Cell 25, 1050–1060 (2014).
pubmed: 24478453 pmcid: 3967970 doi: 10.1091/mbc.e13-06-0350
Okuda-Shimizu, Y. & Hendershot, L. M. Characterization of an ERAD pathway for nonglycosylated BiP substrates, which require Herp. Mol. Cell 28, 544–554 (2007).
pubmed: 18042451 pmcid: 2149893 doi: 10.1016/j.molcel.2007.09.012
Behnke, J., Feige, M. J. & Hendershot, L. M. BiP and its nucleotide exchange factors Grp170 and Sil1: mechanisms of action and biological functions. J. Mol. Biol. 427, 1589–1608 (2015).
pubmed: 25698114 pmcid: 4356644 doi: 10.1016/j.jmb.2015.02.011
Leto, D. E. et al. Genome-wide CRISPR analysis identifies substrate-specific conjugation modules in ER-associated degradation. Mol. Cell 73, 377–389 e311 (2019).
pubmed: 30581143 doi: 10.1016/j.molcel.2018.11.015
Mun, K. & Punga, T. Cellular zinc finger protein 622 hinders human adenovirus lytic growth and limits binding of the viral pVII protein to virus DNA. J Virol. 93, e01628−18 (2019).
Jia, R. & Bonifacino, J. S. Regulation of LC3B levels by ubiquitination and proteasomal degradation. Autophagy 16, 382–384 (2020).
pubmed: 31880195 pmcid: 6984611 doi: 10.1080/15548627.2019.1709766
Katsuragi, Y., Ichimura, Y. & Komatsu, M. p62/SQSTM1 functions as a signaling hub and an autophagy adaptor. Febs J. 282, 4672–4678 (2015).
pubmed: 26432171 doi: 10.1111/febs.13540
Gorshkov, K. et al. The SARS-CoV-2 cytopathic effect is blocked by lysosome alkalizing small molecules. ACS Infect. Dis. 7, 1389−1408 (2020).
Yoshii, S. R. & Mizushima, N. Monitoring and measuring autophagy. Int. J. Mol. Sci. 18, 1865 (2017).
Lee, Z. W., Low, Y. L., Huang, S., Wang, T. & Deng, L. W. The cystathionine gamma-lyase/hydrogen sulfide system maintains cellular glutathione status. Biochem J. 460, 425–435 (2014).
pubmed: 24707893 doi: 10.1042/BJ20131434
Kokame, K., Agarwala, K. L. & Kato, H. Miyata T. Herp, a new ubiquitin-like membrane protein induced by endoplasmic reticulum stress. J. Biol. Chem. 275, 32846–32853 (2000).
pubmed: 10922362 doi: 10.1074/jbc.M002063200
Li, W. W., Alexandre, S., Cao, X. & Lee, A. S. Transactivation of the grp78 promoter by Ca2+ depletion. A comparative analysis with A23187 and the endoplasmic reticulum Ca(2+)-ATPase inhibitor thapsigargin. J. Biol. Chem. 268, 12003–12009 (1993).
pubmed: 8505325 doi: 10.1016/S0021-9258(19)50300-3
Ma, Y. J. & Hendershot, L. M. Herp is dually regulated by both the endoplasmic reticulum stress-specific branch of the unfolded protein response and a branch that is shared with other cellular stress pathways. J. Biol. Chem. 279, 13792–13799 (2004).
pubmed: 14742429 doi: 10.1074/jbc.M313724200
Sun, S. et al. IRE1alpha is an endogenous substrate of endoplasmic-reticulum-associated degradation. Nat. Cell Biol. 17, 1546–1555 (2015).
pubmed: 26551274 pmcid: 4670240 doi: 10.1038/ncb3266
Wang, J., Lee, J., Liem, D. & Ping, P. HSPA5 Gene encoding Hsp70 chaperone BiP in the endoplasmic reticulum. Gene 618, 14–23 (2017).
pubmed: 28286085 pmcid: 5632570 doi: 10.1016/j.gene.2017.03.005
Zhu, G. Y. & Lee, A. S. Role of the unfolded protein response, GRP78 and GRP94 in organ homeostasis. J. Cell Physiol. 230, 1413–1420 (2015).
pubmed: 25546813 pmcid: 4725317 doi: 10.1002/jcp.24923
Hsu, C. L., Prasad, R., Blackman, C. & Ng, D. T. Endoplasmic reticulum stress regulation of the Kar2p/BiP chaperone alleviates proteotoxicity via dual degradation pathways. Mol. Biol. Cell 23, 630–641 (2012).
pubmed: 22190740 pmcid: 3279391 doi: 10.1091/mbc.e11-04-0297
Halbleib, K. et al. Activation of the unfolded protein response by lipid bilayer stress. Mol. Cell 67, 673–684 e678 (2017).
pubmed: 28689662 doi: 10.1016/j.molcel.2017.06.012
Chang, T. K. et al. Coordination between two branches of the unfolded protein response determines apoptotic cell fate. Mol. Cell 71, 629–636 e625 (2018).
pubmed: 30118681 doi: 10.1016/j.molcel.2018.06.038
Sepulveda, D. et al. Interactome screening identifies the ER luminal chaperone Hsp47 as a regulator of the unfolded protein response transducer IRE1alpha. Mol. Cell 69, 238–252 e237 (2018).
pubmed: 29351844 doi: 10.1016/j.molcel.2017.12.028
Brodsky, J. L. Cleaning Up: ER-associated degradation to the rescue. Cell 151, 1163–1167 (2012).
pubmed: 23217703 pmcid: 3521611 doi: 10.1016/j.cell.2012.11.012
Christianson, J. C. et al. Defining human ERAD networks through an integrative mapping strategy. Nat. Cell Biol. 14, 93–U176 (2012).
doi: 10.1038/ncb2383
Noack, J., Bernasconi, R. & Molinari, M. How viruses hijack the ERAD tuning machinery. J. Virol. 88, 10272–10275 (2014).
pubmed: 24990995 pmcid: 4178841 doi: 10.1128/JVI.00801-14
Byun, H., Gou, Y. Q., Zook, A., Lozano, M. M. & Dudley, J. P. ERAD and how viruses exploit it. Front. Microbiol. 5, 330 (2014).
Miller K. et al. Coronavirus interactions with the cellular autophagy machinery. Autophagy 16, 1−9 (2020).
Quiroga, C. et al. Herp depletion protects from protein aggregation by up-regulating autophagy. Biochim. Biophys. Acta 1833, 3295–3305 (2013).
pubmed: 24120520 doi: 10.1016/j.bbamcr.2013.09.006
Fecchi, K. et al. Coronavirus interplay with lipid rafts and autophagy unveils promising therapeutic targets. Front. Microbiol. 11, 1821 (2020).
pubmed: 32849425 pmcid: 7431668 doi: 10.3389/fmicb.2020.01821
Ji, C. H. et al. The N-degron pathway mediates ER-phagy. Mol. Cell 75, 1058–1072 e1059 (2019).
pubmed: 31375263 doi: 10.1016/j.molcel.2019.06.028
Chino, H. & Mizushima, N. ER-Phagy: quality control and turnover of endoplasmic reticulum. Trends Cell Biol. 30, 384–398 (2020).
pubmed: 32302550 doi: 10.1016/j.tcb.2020.02.001
Wilkinson, S. ER-phagy: shaping up and destressing the endoplasmic reticulum. Febs J. 286, 2645–2663 (2019).
pubmed: 31116513 pmcid: 6772018
Ganley, I. G., Wong, P. M. & Jiang, X. Thapsigargin distinguishes membrane fusion in the late stages of endocytosis and autophagy. Autophagy 7, 1397–1399 (2011).
pubmed: 21921693 doi: 10.4161/auto.7.11.17651
Mauvezin, C., Nagy, P., Juhasz, G. & Neufeld, T. P. Autophagosome-lysosome fusion is independent of V-ATPase-mediated acidification. Nat. Commun. 6, 7007 (2015).
Toyoshima, C., Nakasako, M., Nomura, H. & Ogawa, H. Crystal structure of the calcium pump of sarcoplasmic reticulum at 2.6 A resolution. Nature 405, 647–655 (2000).
pubmed: 10864315 doi: 10.1038/35015017
Terracciano, R. et al Mapping the SARS-CoV-2-host protein-protein interactome by affinity purification mass spectrometry and proximity-dependent biotin labeling: a rational and straightforward route to discover host-directed anti-SARS-CoV-2 therapeutics. Int. J. Mol. Sci. 22, 532 (2021).
Samavarchi-Tehrani, P. et al. A SARS-C`oV-2-host proximity interactome. Preprint at bioRxiv https://doi.org/10.1101/2020.09.03.282103 (2020).
Stukalov, A. et al. Multi-level proteomics reveals host-perturbation strategies of SARS-CoV-2 and SARS-CoV. Nature 594, 246–252 (2021)
pubmed: 33845483 doi: 10.1038/s41586-021-03493-4
Bojkova, D. et al. Proteomics of SARS-CoV-2-infected host cells reveals therapy targets. Nature 583, 469–472 (2020).
pubmed: 32408336 doi: 10.1038/s41586-020-2332-7
Grenga, L. et al. Shotgun proteomics analysis of SARS-CoV-2-infected cells and how it can optimize whole viral particle antigen production for vaccines. Emerg. Microbes Infect. 9, 1712–1721 (2020).
pubmed: 32619390 pmcid: 7473198 doi: 10.1080/22221751.2020.1791737
Bouhaddou, M. et al. The global phosphorylation landscape of SARS-CoV-2 infection. Cell 182, 685–712 e619 (2020).
pubmed: 32645325 pmcid: 7321036 doi: 10.1016/j.cell.2020.06.034
Patkar, S. A., Rasmussen, U. & Diamant, B. On the mechanism of histamine release induced by thapsigargin from Thapsia garganica L. Agents Actions 9, 53–57 (1979).
pubmed: 88885 doi: 10.1007/BF02024109
Andersen, T. B., Lopez, C. Q., Manczak, T., Martinez, K. & Simonsen, H. T. Thapsigargin–from Thapsia L. to mipsagargin. Molecules 20, 6113–6127 (2015).
pubmed: 25856061 pmcid: 6272310 doi: 10.3390/molecules20046113
Chu, H., Dunstl, G., Felding, J. & Baran, P. S. Divergent synthesis of thapsigargin analogs. Bioorg. Med. Chem. Lett. 28, 2705–2707 (2018).
pubmed: 29636219 pmcid: 6119632 doi: 10.1016/j.bmcl.2018.03.065
Chu, H., Smith, J. M., Felding, J. & Baran, P. S. Scalable synthesis of (-)-thapsigargin. ACS Cent. Sci. 3, 47–51 (2017).
pubmed: 28149952 doi: 10.1021/acscentsci.6b00313
Lopez, C. Q. et al. Use of a temporary immersion bioreactor system for the sustainable production of thapsigargin in shoot cultures of Thapsia garganica. Plant Methods 14, 79 (2018).
pubmed: 30202426 pmcid: 6128993 doi: 10.1186/s13007-018-0346-z
Doan, N. T. et al. Targeting thapsigargin towards tumors. Steroids 97, 2–7 (2015).
pubmed: 25065587 doi: 10.1016/j.steroids.2014.07.009
Mahalingam, D. et al. A phase II, multicenter, single-arm study of mipsagargin (G-202) as a second-line therapy following sorafenib for adult patients with progressive advanced hepatocellular carcinoma. Cancers 11, 833 (2019).
Mahalingam, D. et al. Mipsagargin, a novel thapsigargin-based PSMA-activated prodrug: results of a first-in-man phase I clinical trial in patients with refractory, advanced or metastatic solid tumours. Br. J. Cancer 114, 986–994 (2016).
pubmed: 27115568 pmcid: 4984914 doi: 10.1038/bjc.2016.72
Marder, W. & McCune, W. J. Advances in immunosuppressive therapy. Semin. Respir. Crit. Care Med. 28, 398–417 (2007).
pubmed: 17764058 doi: 10.1055/s-2007-985612
Mehta, P. et al. COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet 395, 1033–1034 (2020).
pubmed: 32192578 pmcid: 7270045 doi: 10.1016/S0140-6736(20)30628-0
Wei, Y. et al. Pharmacological preconditioning with the cellular stress inducer thapsigargin protects against experimental sepsis. Pharm. Res. 141, 114–122 (2019).
doi: 10.1016/j.phrs.2018.12.017
Nakabayashi, H., Taketa, K., Miyano, K., Yamane, T. & Sato, J. Growth of human hepatoma cells lines with differentiated functions in chemically defined medium. Cancer Res. 42, 3858–3863 (1982).
pubmed: 6286115
Ziebuhr, J. & Siddell, S. G. Processing of the human coronavirus 229E replicase polyproteins by the virus-encoded 3C-like proteinase: identification of proteolytic products and cleavage sites common to pp1a and pp1ab. J. Virol. 73, 177–185 (1999).
pubmed: 9847320 pmcid: 103821 doi: 10.1128/JVI.73.1.177-185.1999
Spiegel, M. et al. Inhibition of beta interferon induction by severe acute respiratory syndrome coronavirus suggests a two-step model for activation of interferon regulatory factor 3. J. Virol. 79, 2079–2086 (2005).
pubmed: 15681410 pmcid: 546554 doi: 10.1128/JVI.79.4.2079-2086.2005
Iwasaki, S. & Ingolia, N. T. The growing toolbox for protein synthesis studies. Trends Biochem. Sci. 42, 612–624 (2017).
pubmed: 28566214 pmcid: 5533619 doi: 10.1016/j.tibs.2017.05.004
Chen, S., Zhou, Y., Chen, Y. & Gu, J. fastp: an ultra-fast all-in-one FASTQ preprocessor. Bioinformatics 34, i884–i890 (2018).
pubmed: 30423086 pmcid: 6129281 doi: 10.1093/bioinformatics/bty560
Dobin, A. et al. STAR: ultrafast universal RNA-seq aligner. Bioinformatics 29, 15–21 (2013).
pubmed: 23104886 doi: 10.1093/bioinformatics/bts635
Liao, Y., Smyth, G. K. & Shi, W. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. Bioinformatics 30, 923–930 (2014).
pubmed: 24227677 doi: 10.1093/bioinformatics/btt656
Love, M. I., Huber, W. & Anders, S. Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2. Genome Biol. 15, 550 (2014).
pubmed: 25516281 pmcid: 4302049 doi: 10.1186/s13059-014-0550-8
Wisniewski, J. R. Filter-aided sample preparation for proteome analysis. Methods Mol. Biol. 1841, 3–10 (2018).
pubmed: 30259475 doi: 10.1007/978-1-4939-8695-8_1
Tyanova, S., Temu, T. & Cox, J. The MaxQuant computational platform for mass spectrometry-based shotgun proteomics. Nat. Protoc. 11, 2301–2319 (2016).
pubmed: 27809316 doi: 10.1038/nprot.2016.136
Tyanova, S. et al. The Perseus computational platform for comprehensive analysis of (prote)omics data. Nat. Methods 13, 731–740 (2016).
pubmed: 27348712 doi: 10.1038/nmeth.3901
Szklarczyk, D. et al. STRING v11: protein−protein association networks with increased coverage, supporting functional discovery in genome-wide experimental datasets. Nucleic Acids Res. 47, D607–D613 (2019).
pubmed: 30476243 doi: 10.1093/nar/gky1131
Cline, M. S. et al. Integration of biological networks and gene expression data using Cytoscape. Nat. Protoc. 2, 2366–2382 (2007).
pubmed: 17947979 pmcid: 3685583 doi: 10.1038/nprot.2007.324
Luo, W., Pant, G., Bhavnasi, Y. K., Blanchard, S. G. Jr. & Brouwer, C. Pathview Web: user friendly pathway visualization and data integration. Nucleic Acids Res. 45, W501–W508 (2017).
pubmed: 28482075 pmcid: 5570256 doi: 10.1093/nar/gkx372
Deutsch, E. W. et al. The ProteomeXchange consortium in 2020: enabling ‘big data’ approaches in proteomics. Nucleic Acids Res. 48, D1145–D1152 (2020).
pubmed: 31686107
Perez-Riverol, Y. et al. The PRIDE database and related tools and resources in 2019: improving support for quantification data. Nucleic Acids Res. 47, D442–D450 (2019).
pubmed: 30395289 doi: 10.1093/nar/gky1106

Auteurs

Mohammed Samer Shaban (MS)

Rudolf Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany.

Christin Müller (C)

Institute of Medical Virology, Justus Liebig University, Giessen, Germany.

Christin Mayr-Buro (C)

Rudolf Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany.

Hendrik Weiser (H)

Rudolf Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany.

Johanna Meier-Soelch (J)

Rudolf Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany.

Benadict Vincent Albert (BV)

Rudolf Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany.

Axel Weber (A)

Rudolf Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany.

Uwe Linne (U)

Mass spectrometry facility of the Department of Chemistry, Philipps University, Marburg, Germany.

Torsten Hain (T)

Institute of Medical Microbiology, Justus Liebig University, Giessen, Germany.
German Center for Infection Research (DZIF), partner site Giessen-Marburg-Langen, Giessen, Germany.

Ilya Babayev (I)

Rudolf Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany.

Nadja Karl (N)

Institute of Medical Virology, Justus Liebig University, Giessen, Germany.

Nina Hofmann (N)

Bioinformatics and Systems Biology, Justus Liebig University, Giessen, Germany.

Stephan Becker (S)

Institute of Virology, Philipps University, Marburg, Germany.

Susanne Herold (S)

Department of Internal Medicine II for Pulmonary and Critical Care Medicine and Infectious Diseases, Justus Liebig University, and Institute for Lung Health (ILH), Giessen, Germany.
German Center for Lung Research (DZL) and Universities of Giessen and Marburg Lung Center (UGMLC), Giessen, Germany.

M Lienhard Schmitz (ML)

German Center for Lung Research (DZL) and Universities of Giessen and Marburg Lung Center (UGMLC), Giessen, Germany.
Institute of Biochemistry, Justus Liebig University, Giessen, Germany.

John Ziebuhr (J)

Institute of Medical Virology, Justus Liebig University, Giessen, Germany. john.ziebuhr@viro.med.uni-giessen.de.
German Center for Infection Research (DZIF), partner site Giessen-Marburg-Langen, Giessen, Germany. john.ziebuhr@viro.med.uni-giessen.de.

Michael Kracht (M)

Rudolf Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany. michael.kracht@pharma.med.uni-giessen.de.
German Center for Lung Research (DZL) and Universities of Giessen and Marburg Lung Center (UGMLC), Giessen, Germany. michael.kracht@pharma.med.uni-giessen.de.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH