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cr uuu---uuuuu |
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231226s2022 xx |||||o 00| ||eng c |
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7 |
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|a 10.1016/j.clim.2022.109027
|2 doi
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|a pubmed25n1134.xml
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|a (DE-627)NLM340418885
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|a (NLM)35513305
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|a (PII)S1521-6616(22)00108-5
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Rivera, Edgardo Guzman
|e verfasserin
|4 aut
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| 245 |
1 |
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|a SARS-CoV-2/COVID-19 and its relationship with NOD2 and ubiquitination
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| 264 |
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|c 2022
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| 336 |
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 17.05.2022
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|a Date Revised 10.09.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2022 Elsevier Inc. All rights reserved.
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|a COVID-19 infection activates the immune system to cause autoimmune and autoinflammatory diseases. We provide a comprehensive review of the relationship between SARS-CoV-2, NOD2 and ubiquitination. COVID-19 infection partly results from host inborn errors and genetic factors and can lead to autoinflammatory disease. The interaction between defective NOD2 and viral infection may trigger NOD2-associated disease. SARS-CoV-2 can alter UBA1 and abnormal ubiquitination leading to VEXAS syndrome. Both NOD2 and ubiquitination play important roles in controlling inflammatory process. Receptor interacting protein kinase 2 is a key component of the NOD2 activation pathway and becomes ubiquitinated to recruit downstream effector proteins. NOD2 mutations result in loss of ubiquitin binding and increase ligand-stimulated NOD2 signaling. During viral infection, mutations of either NOD2 or UBA1 genes or in combination can facilitate autoinflammatory disease. COVID-19 infection can cause autoinflammatory disease. There are reciprocal interactions between SARS-CoV-2, NOD2 and ubiquitination
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| 650 |
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|a Journal Article
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| 650 |
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|a Review
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| 650 |
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|a Autoinflammatory disease
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| 650 |
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4 |
|a COVID-19
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| 650 |
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4 |
|a NOD2
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| 650 |
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4 |
|a SARS-CoV-2
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| 650 |
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4 |
|a Ubiquitination
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| 650 |
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4 |
|a VEXAS syndrome
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| 650 |
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4 |
|a Yao syndrome
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| 650 |
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7 |
|a NOD2 protein, human
|2 NLM
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| 650 |
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7 |
|a Nod2 Signaling Adaptor Protein
|2 NLM
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| 650 |
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7 |
|a Ubiquitin
|2 NLM
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| 700 |
1 |
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|a Patnaik, Asha
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Salvemini, Joann
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Jain, Sanjeev
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Lee, Katherine
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Lozeau, Daniel
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Yao, Qingping
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 238(2022) vom: 01. Mai, Seite 109027
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnas
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| 773 |
1 |
8 |
|g volume:238
|g year:2022
|g day:01
|g month:05
|g pages:109027
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| 856 |
4 |
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|u http://dx.doi.org/10.1016/j.clim.2022.109027
|3 Volltext
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| 912 |
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|a GBV_USEFLAG_A
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| 912 |
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|a SYSFLAG_A
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|a GBV_NLM
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|a GBV_ILN_11
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| 912 |
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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