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Article ; Online: K63-linked polyubiquitination of LGP2 by Riplet regulates RIG-I-dependent innate immune response.

Kouwaki, Takahisa / Nishimura, Tasuku / Wang, Guanming / Nakagawa, Reiko / Oshiumi, Hiroyuki

2022 Volume 24, Issue 2, Page(s) e54844

Abstract: Type I interferons (IFNs) exhibit strong antiviral activity and induce the expression of antiviral proteins. Since excessive expression of type I IFNs is harmful to the host, their expression should be turned off at the appropriate time. In this study, ... ...

Abstract	Type I interferons (IFNs) exhibit strong antiviral activity and induce the expression of antiviral proteins. Since excessive expression of type I IFNs is harmful to the host, their expression should be turned off at the appropriate time. In this study, we find that post-translational modification of LGP2, a member of the RIG-I-like receptor family, modulates antiviral innate immune responses. The LGP2 protein undergoes K63-linked polyubiquitination in response to cytoplasmic double-stranded RNAs or viral infection. Our mass spectrometry analysis reveals the K residues ubiquitinated by the Riplet ubiquitin ligase. LGP2 ubiquitination occurs with a delay compared to RIG-I ubiquitination. Interestingly, ubiquitination-defective LGP2 mutations increase the expression of type I IFN at a late phase, whereas the mutant proteins attenuate other antiviral proteins, such as SP100, PML, and ANKRD1. Our data indicate that delayed polyubiquitination of LGP2 fine-tunes RIG-I-dependent antiviral innate immune responses at a late phase of viral infection.
MeSH term(s)	Humans ; Antiviral Agents ; DEAD Box Protein 58/genetics ; DEAD Box Protein 58/metabolism ; DEAD-box RNA Helicases/genetics ; Immunity, Innate ; Interferon Type I/genetics ; Ubiquitin/metabolism ; Ubiquitination ; Virus Diseases
Chemical Substances	Antiviral Agents ; DEAD Box Protein 58 (EC 3.6.4.13) ; DEAD-box RNA Helicases (EC 3.6.4.13) ; Interferon Type I ; Ubiquitin ; RIGI protein, human (EC 3.6.1.-) ; DHX58 protein, human (EC 2.7.7.-)
Language	English
Publishing date	2022-12-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.15252/embr.202254844
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Article ; Online: RIG-I-Like Receptor-Mediated Recognition of Viral Genomic RNA of Severe Acute Respiratory Syndrome Coronavirus-2 and Viral Escape From the Host Innate Immune Responses.

Kouwaki, Takahisa / Nishimura, Tasuku / Wang, Guanming / Oshiumi, Hiroyuki

Frontiers in immunology

2021 Volume 12, Page(s) 700926

Abstract: RIG-I-like receptors (RLR), RIG-I and MDA5, are cytoplasmic viral RNA sensors that recognize viral double-stranded RNAs and trigger signals to induce antiviral responses, including type I interferon production. Severe acute respiratory syndrome ... ...

Abstract	RIG-I-like receptors (RLR), RIG-I and MDA5, are cytoplasmic viral RNA sensors that recognize viral double-stranded RNAs and trigger signals to induce antiviral responses, including type I interferon production. Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) caused the coronavirus disease 2019 pandemic. However, the RLR role in innate immune response to SARS-CoV-2 has not been fully elucidated. Here, we studied the roles of RLR in cytokine expression responding to SARS-CoV-2 and found that not only MDA5 but also RIG-I are involved in innate immune responses in some types of human cells. Transfection of total RNAs extracted from SARS-CoV-2-infected cells into epithelial cells induced IFN-β, IP-10, and Ccl5 mRNA expression. The cytokine expression was reduced by knockout of either RIG-I or MDA5, suggesting that both proteins are required for appropriate innate immune response to SARS-CoV-2. Two viral genomic RNA regions strongly induced type I IFN expression, and a 200-base fragment of viral RNA preferentially induced type I IFN in a RIG-I-dependent manner. In contrast, SARS-CoV-2 infectious particles hardly induced cytokine expression, suggesting viral escape from the host response. Viral 9b protein inhibited RIG-I and MAVS interaction, and viral 7a protein destabilized the TBK1 protein, leading to attenuated IRF-3 phosphorylation required for type I IFN expression. Our data elucidated the mechanism underlying RLR-mediated response to SARS-CoV-2 infection and viral escape from the host innate immune response.
MeSH term(s)	COVID-19/immunology ; Gene Knockdown Techniques ; HEK293 Cells ; Host-Pathogen Interactions ; Humans ; Immune Evasion ; Immunity, Innate ; Interferon Regulatory Factor-3/metabolism ; Interferon Type I/metabolism ; Interferon-Induced Helicase, IFIH1/genetics ; Interferon-Induced Helicase, IFIH1/metabolism ; Phosphorylation ; RNA, Viral/immunology ; Receptors, Retinoic Acid/genetics ; Receptors, Retinoic Acid/metabolism ; SARS-CoV-2/physiology ; Severe Acute Respiratory Syndrome/immunology ; Signal Transduction ; Viral Matrix Proteins/metabolism
Chemical Substances	IRF3 protein, human ; Interferon Regulatory Factor-3 ; Interferon Type I ; PLAAT4 protein, human ; RNA, Viral ; Receptors, Retinoic Acid ; Viral Matrix Proteins ; sars7a protein, SARS virus ; IFIH1 protein, human (EC 3.6.1.-) ; Interferon-Induced Helicase, IFIH1 (EC 3.6.4.13)
Language	English
Publishing date	2021-06-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.700926
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Article ; Online: Aging-Associated Extracellular Vesicles Contain Immune Regulatory microRNAs Alleviating Hyperinflammatory State and Immune Dysfunction in the Elderly.

Tsukamoto, Hirotake / Kouwaki, Takahisa / Oshiumi, Hiroyuki

iScience

2020 Volume 23, Issue 9, Page(s) 101520

Abstract: Aging-associated changes in the immune system often lead to immune dysfunction; however, the mechanisms that underlie this phenomenon have yet to be fully elucidated. This study found that the microRNA-192 (miR-192) is an aging-associated immune ... ...

Abstract	Aging-associated changes in the immune system often lead to immune dysfunction; however, the mechanisms that underlie this phenomenon have yet to be fully elucidated. This study found that the microRNA-192 (miR-192) is an aging-associated immune regulatory microRNA whose concentration was significantly increased in aged extracellular vesicles (EVs) due to the hyperinflammatory state of aged mice. Interestingly, EV miR-192 exhibited anti-inflammatory effects on macrophages. In our aged mouse model, aging was associated with prolonged inflammation in the lung upon stimulation with inactivated influenza whole virus particles (WVP), whereas EV miR-192 alleviated the prolonged inflammation associated with aging. The hyperinflammatory state of aged mice resulted in reduced production of specific antibodies and efficacy of vaccination with WVP; however, EV miR-192 attenuated this hyperinflammatory state and improved vaccination efficacy in aged mice. Our data indicate that aged EVs constitute a negative feedback loop that alleviates aging-associated immune dysfunction.
Language	English
Publishing date	2020-09-01
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2020.101520
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Article ; Online: HPV vaccines induce trained immunity and modulate pro-inflammatory cytokine expression in response to secondary Toll-like receptor stimulations.

Yamaguchi, Mako / Mtali, Yohana S / Sonokawa, Hitomi / Takashima, Ken / Fukushima, Yoshimi / Kouwaki, Takahisa / Oshiumi, Hiroyuki

Microbiology and immunology

2023 Volume 68, Issue 2, Page(s) 65–74

Abstract: Cervical cancer is caused mostly by human papillomavirus (HPV), and several HPV vaccines have been developed to prevent its onset. Vaccines include antigens as well as adjuvants, with adjuvants playing an important role in activating the innate immune ... ...

Abstract	Cervical cancer is caused mostly by human papillomavirus (HPV), and several HPV vaccines have been developed to prevent its onset. Vaccines include antigens as well as adjuvants, with adjuvants playing an important role in activating the innate immune responses necessary for inducing adaptive immunological responses. Recent research has shown the presence of trained immunity inside the innate immune system. However, trained immunity conferred by HPV vaccinations is not well understood. In this work, we explored the innate immune responses and trained immunity caused by two HPV vaccines, Cervarix and Gardasil. Cervarix includes monophosphoryl lipid A and an aluminum adjuvant, and it significantly increased the expression of IL-6 and IFN-β mRNAs in RAW264.7 cells. On the contrary, Gardasil, which only includes an aluminum adjuvant, exhibited little cytokine expression but increased the expression of TLRs. Furthermore, Cervarix significantly increased IL-1β secretion from mouse macrophages, while Gardasil only mildly induced IL-1β secretion. Interestingly, initial stimulation with Gardasil enhanced the expression of IL-6 and TNF-α mRNAs upon secondary stimulation with TLR ligands, indicating that Gardasil induced trained immunity in macrophages. Moreover, Gardasil injection into mice resulted in enhanced TNF-α production in sera following secondary TLR stimulation. Our findings suggest that HPV vaccinations have the ability to induce trained immunity that modulate TLR ligand responses.
MeSH term(s)	Humans ; Animals ; Mice ; Cytokines ; Human Papillomavirus Recombinant Vaccine Quadrivalent, Types 6, 11, 16, 18 ; Tumor Necrosis Factor-alpha ; Interleukin-6/genetics ; Trained Immunity ; Papillomavirus Infections/prevention & control ; Aluminum ; Papillomavirus Vaccines/genetics ; Adjuvants, Immunologic ; Toll-Like Receptors
Chemical Substances	Cytokines ; Human Papillomavirus Recombinant Vaccine Quadrivalent, Types 6, 11, 16, 18 ; Tumor Necrosis Factor-alpha ; Interleukin-6 ; Aluminum (CPD4NFA903) ; Papillomavirus Vaccines ; Adjuvants, Immunologic ; Toll-Like Receptors
Language	English
Publishing date	2023-12-17
Publishing country	Australia
Document type	Journal Article
ZDB-ID	224792-6
ISSN	1348-0421 ; 0385-5600
ISSN (online)	1348-0421
ISSN	0385-5600
DOI	10.1111/1348-0421.13108
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Ud II Zs.204: Show issues

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Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Aging-Associated Extracellular Vesicles Contain Immune Regulatory microRNAs Alleviating Hyperinflammatory State and Immune Dysfunction in the Elderly

Hirotake Tsukamoto / Takahisa Kouwaki / Hiroyuki Oshiumi

iScience, Vol 23, Iss 9, Pp 101520- (2020)

2020

Abstract: Summary: Aging-associated changes in the immune system often lead to immune dysfunction; however, the mechanisms that underlie this phenomenon have yet to be fully elucidated. This study found that the microRNA-192 (miR-192) is an aging-associated immune ...

Abstract	Summary: Aging-associated changes in the immune system often lead to immune dysfunction; however, the mechanisms that underlie this phenomenon have yet to be fully elucidated. This study found that the microRNA-192 (miR-192) is an aging-associated immune regulatory microRNA whose concentration was significantly increased in aged extracellular vesicles (EVs) due to the hyperinflammatory state of aged mice. Interestingly, EV miR-192 exhibited anti-inflammatory effects on macrophages. In our aged mouse model, aging was associated with prolonged inflammation in the lung upon stimulation with inactivated influenza whole virus particles (WVP), whereas EV miR-192 alleviated the prolonged inflammation associated with aging. The hyperinflammatory state of aged mice resulted in reduced production of specific antibodies and efficacy of vaccination with WVP; however, EV miR-192 attenuated this hyperinflammatory state and improved vaccination efficacy in aged mice. Our data indicate that aged EVs constitute a negative feedback loop that alleviates aging-associated immune dysfunction.
Keywords	Human Physiology ; Immunology ; Molecular Biology ; Molecular Physiology ; Science ; Q
Subject code	616
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Attenuation of the Innate Immune Response against Viral Infection Due to ZNF598-Promoted Binding of FAT10 to RIG-I.

Wang, Guanming / Kouwaki, Takahisa / Okamoto, Masaaki / Oshiumi, Hiroyuki

Cell reports

2019 Volume 28, Issue 8, Page(s) 1961–1970.e4

Abstract: Excessive innate immune response is harmful to the host, and aberrant activation of the cytoplasmic viral RNA sensors RIG-I and MDA5 leads to autoimmune disorders. ZNF598 is an E3 ubiquitin ligase involved in the ribosome quality control pathway. It is ... ...

Abstract	Excessive innate immune response is harmful to the host, and aberrant activation of the cytoplasmic viral RNA sensors RIG-I and MDA5 leads to autoimmune disorders. ZNF598 is an E3 ubiquitin ligase involved in the ribosome quality control pathway. It is also involved in the suppression of interferon (IFN)-stimulated gene (ISG) expression; however, its underlying mechanism is unclear. In this study, we show that ZNF598 is a negative regulator of the RIG-I-mediated signaling pathway, and endogenous ZNF598 protein binds to RIG-I. ZNF598 ubiquitin ligase activity is dispensable for the suppression of RIG-I signaling. Instead, ZNF598 delivers a ubiquitin-like protein FAT10 to the RIG-I protein, resulting in the inhibition of RIG-I polyubiquitination, which is required for triggering downstream signaling to produce type I IFN. Moreover, ZNF598-mediated suppression is abrogated by FAT10 knockout. Our data elucidate the mechanism by which ZNF598 inhibits RIG-I-mediated innate immune response.
MeSH term(s)	Carrier Proteins/metabolism ; Cell Line ; Cytokines/metabolism ; DEAD Box Protein 58/metabolism ; Humans ; Immunity, Innate ; Protein Binding ; Receptors, Immunologic ; Signal Transduction ; Ubiquitin/metabolism ; Ubiquitination ; Ubiquitins/metabolism ; Virus Diseases/immunology
Chemical Substances	Carrier Proteins ; Cytokines ; Receptors, Immunologic ; UBD protein, human ; Ubiquitin ; Ubiquitins ; ZNF598 protein, human ; RIGI protein, human (EC 3.6.1.-) ; DEAD Box Protein 58 (EC 3.6.4.13)
Language	English
Publishing date	2019-08-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2019.07.081
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: TICAM-1/TRIF associates with Act1 and suppresses IL-17 receptor-mediated inflammatory responses.

Miyashita, Yusuke / Kouwaki, Takahisa / Tsukamoto, Hirotake / Okamoto, Masaaki / Nakamura, Kimitoshi / Oshiumi, Hiroyuki

Life science alliance

2021 Volume 5, Issue 2

Abstract: TICAM-1 (also called TRIF) is the sole adaptor of TLR3 that recognizes double-stranded RNA. Here, we report that TICAM-1 is involved not only in TLR3 signaling but also in the cytokine receptor IL-17RA signaling. We found that TICAM-1 bound to IL-17R ... ...

Abstract	TICAM-1 (also called TRIF) is the sole adaptor of TLR3 that recognizes double-stranded RNA. Here, we report that TICAM-1 is involved not only in TLR3 signaling but also in the cytokine receptor IL-17RA signaling. We found that TICAM-1 bound to IL-17R adaptor Act1 to inhibit the interaction between IL-17RA and Act1. Interestingly,
MeSH term(s)	Adaptor Proteins, Vesicular Transport/genetics ; Adaptor Proteins, Vesicular Transport/metabolism ; Animals ; Autoimmune Diseases/etiology ; Autoimmune Diseases/metabolism ; Autoimmunity ; Biomarkers ; Connexin 43/metabolism ; Disease Susceptibility ; Gene Knockdown Techniques ; Inflammation/etiology ; Inflammation/metabolism ; Mice ; Peptide Fragments/metabolism ; Receptors, Interleukin/metabolism ; Signal Transduction
Chemical Substances	ACT1 protein ; Adaptor Proteins, Vesicular Transport ; Biomarkers ; Connexin 43 ; Peptide Fragments ; Receptors, Interleukin
Language	English
Publishing date	2021-11-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202101181
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Article ; Online: Circulating extracellular vesicle microRNAs associated with adverse reactions, proinflammatory cytokine, and antibody production after COVID-19 vaccination.

Miyashita, Yusuke / Yoshida, Takanobu / Takagi, Yuriko / Tsukamoto, Hirotake / Takashima, Ken / Kouwaki, Takahisa / Makino, Katsunari / Fukushima, Satoshi / Nakamura, Kimitoshi / Oshiumi, Hiroyuki

NPJ vaccines

2022 Volume 7, Issue 1, Page(s) 16

Abstract: mRNA-based vaccines have been used globally to eradicate the coronavirus-disease 2019 (COVID-19) pandemic. Vaccine efficacy and adverse reactions depend on immune responses, such as proinflammatory cytokine production and lymphocyte activation. We ... ...

Abstract	mRNA-based vaccines have been used globally to eradicate the coronavirus-disease 2019 (COVID-19) pandemic. Vaccine efficacy and adverse reactions depend on immune responses, such as proinflammatory cytokine production and lymphocyte activation. We conducted a prospective cohort study to investigate relationships among specific antibody titers, adverse reactions, proinflammatory cytokine production, and immune-regulatory microRNA (miRNA) levels in serum extracellular vesicles (EVs) after COVID-19 vaccination (BNT162b2). Local adverse reactions after the second dose, such as local pain and swelling, were less correlated with those of systemic symptoms, such as fever and muscle pain, whereas serum TNF-α levels were associated with systemic adverse reactions and with specific antibody titers. Interestingly, EV miR-92a-2-5p levels in sera were negatively correlated with degrees of adverse reactions, and EV miR-148a levels were associated with specific antibody titers. Our data suggest a potential of circulating EV miRNAs as biomarkers for vaccine efficacy and adverse reactions.
Language	English
Publishing date	2022-02-08
Publishing country	England
Document type	Journal Article
ISSN	2059-0105
ISSN (online)	2059-0105
DOI	10.1038/s41541-022-00439-3
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Article ; Online: Attenuation of the Innate Immune Response against Viral Infection Due to ZNF598-Promoted Binding of FAT10 to RIG-I

Guanming Wang / Takahisa Kouwaki / Masaaki Okamoto / Hiroyuki Oshiumi

Cell Reports, Vol 28, Iss 8, Pp 1961-1970.e

2019 Volume 4

Abstract: Summary: Excessive innate immune response is harmful to the host, and aberrant activation of the cytoplasmic viral RNA sensors RIG-I and MDA5 leads to autoimmune disorders. ZNF598 is an E3 ubiquitin ligase involved in the ribosome quality control pathway. ...

Abstract	Summary: Excessive innate immune response is harmful to the host, and aberrant activation of the cytoplasmic viral RNA sensors RIG-I and MDA5 leads to autoimmune disorders. ZNF598 is an E3 ubiquitin ligase involved in the ribosome quality control pathway. It is also involved in the suppression of interferon (IFN)-stimulated gene (ISG) expression; however, its underlying mechanism is unclear. In this study, we show that ZNF598 is a negative regulator of the RIG-I-mediated signaling pathway, and endogenous ZNF598 protein binds to RIG-I. ZNF598 ubiquitin ligase activity is dispensable for the suppression of RIG-I signaling. Instead, ZNF598 delivers a ubiquitin-like protein FAT10 to the RIG-I protein, resulting in the inhibition of RIG-I polyubiquitination, which is required for triggering downstream signaling to produce type I IFN. Moreover, ZNF598-mediated suppression is abrogated by FAT10 knockout. Our data elucidate the mechanism by which ZNF598 inhibits RIG-I-mediated innate immune response. : Wang et al. find that ZNF598 is a negative regulator of RIG-I and attenuates excessive cytokine and chemokine expression during viral infection. They show that ZNF598 delivers ubiquitin-like modifier FAT10 to RIG-I, thereby attenuating Riplet-mediated K63-linked polyubiquitination of RIG-I, which is essential for triggering antiviral responses. Keywords: RIG-I, innate immunity, virus, interferon, ubiquitin, ZNF598, FAT10
Keywords	Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2019-08-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Ubiquitin ligase RIPLET mediates polyubiquitination of RIG-I and LGP2 and regulates the innate immune responses to SARS-CoV-2 infection

Kouwaki, Takahisa / Nishimura, Tasuku / Wang, Guanming / Nakagawa, Reiko / Oshiumi, Hiroyuki

bioRxiv

Abstract: RIG-I, a cytoplasmic viral RNA sensor, is crucial for innate antiviral immune responses; however, there are controversies about the regulatory mechanism of RIG-I by several ubiquitin ligases and LGP2. This study revealed that the RIPLET ubiquitin ligase ... ...

Abstract	RIG-I, a cytoplasmic viral RNA sensor, is crucial for innate antiviral immune responses; however, there are controversies about the regulatory mechanism of RIG-I by several ubiquitin ligases and LGP2. This study revealed that the RIPLET ubiquitin ligase is a general activating factor for RIG-I signaling. In contrast, another ubiquitin ligase, TRIM25, activated RIG-I in a cell-type-specific manner. RIPLET and TRIM25 functions were modulated by accessory factors, such as ZCCH3C and NLRP12. Interestingly, we found an additional role of RIPLET in innate immune responses. RIPLET induced delayed polyubiquitination of LGP, resulting in the attenuation of excessive cytokine expression at the late phase. Moreover, RIPLET was involved in the innate immune responses against SARS-CoV-2 infection, a cause of the recent COVID-19 pandemic. Our data indicate that RIPLET fine-tunes innate immune responses via polyubiquitination of RIG-I and LGP2 against virus infection, including SARS-CoV-2.
Keywords	covid19
Language	English
Publishing date	2021-01-25
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2021.01.25.428042
Database	COVID19

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