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Article ; Online: What role for cellular metabolism in the control of hepatitis viruses?

Diaz, Olivier / Vidalain, Pierre-Olivier / Ramière, Christophe / Lotteau, Vincent / Perrin-Cocon, Laure

2022 Volume 13, Page(s) 1033314

Abstract: Hepatitis B, C and D viruses (HBV, HCV, HDV, respectively) specifically infect human hepatocytes and often establish chronic viral infections of the liver, thus escaping antiviral immunity for years. Like other viruses, hepatitis viruses rely on the ... ...

Abstract	Hepatitis B, C and D viruses (HBV, HCV, HDV, respectively) specifically infect human hepatocytes and often establish chronic viral infections of the liver, thus escaping antiviral immunity for years. Like other viruses, hepatitis viruses rely on the cellular machinery to meet their energy and metabolite requirements for replication. Although this was initially considered passive parasitism, studies have shown that hepatitis viruses actively rewire cellular metabolism through molecular interactions with specific enzymes such as glucokinase, the first rate-limiting enzyme of glycolysis. As part of research efforts in the field of immunometabolism, it has also been shown that metabolic changes induced by viruses could have a direct impact on the innate antiviral response. Conversely, detection of viral components by innate immunity receptors not only triggers the activation of the antiviral defense but also induces in-depth metabolic reprogramming that is essential to support immunological functions. Altogether, these complex triangular interactions between viral components, innate immunity and hepatocyte metabolism may explain why chronic hepatitis infections progressively lead to liver inflammation and progression to cirrhosis, fibrosis and hepatocellular carcinoma (HCC). In this manuscript, we first present a global overview of known connections between the innate antiviral response and cellular metabolism. We then report known molecular mechanisms by which hepatitis viruses interfere with cellular metabolism in hepatocytes and discuss potential consequences on the innate immune response. Finally, we present evidence that drugs targeting hepatocyte metabolism could be used as an innovative strategy not only to deprive viruses of key metabolites, but also to restore the innate antiviral response that is necessary to clear infection.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular ; Liver Neoplasms ; Hepatitis Viruses ; Hepatocytes ; Antiviral Agents/therapeutic use
Chemical Substances	Antiviral Agents
Language	English
Publishing date	2022-11-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1033314
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Article ; Online: Rôle du métabolisme cellulaire dans le contrôle des hépatites virales chroniques.

Diaz, Olivier / Legrand, Anne-Flore / El-Orch, Walid / Jacolin, Florentine / Lotteau, Vincent / Ramière, Christophe / Vidalain, Pierre-Olivier / Perrin-Cocon, Laure

Medecine sciences : M/S

2023 Volume 39, Issue 10, Page(s) 754–762

Abstract: Hepatitis viruses modify the cellular metabolism of hepatocytes by interacting with specific enzymes such as glucokinase. The metabolic changes induced by viruses can have a direct impact on the innate antiviral response. The complex interactions between ...

Title translation	Role of cellular metabolism in the control of chronic viral hepatitis.
Abstract	Hepatitis viruses modify the cellular metabolism of hepatocytes by interacting with specific enzymes such as glucokinase. The metabolic changes induced by viruses can have a direct impact on the innate antiviral response. The complex interactions between viral components, innate immunity, and hepatocyte metabolism explain why chronic hepatitis infections lead to liver inflammation, progressing to cirrhosis, fibrosis, and hepatocellular carcinoma. Metabolic regulators could be used in innovative therapies to deprive viruses of key metabolites and induce an antiviral defense.
MeSH term(s)	Humans ; Hepatitis, Chronic ; Carcinoma, Hepatocellular ; Liver Neoplasms ; Hepatitis, Viral, Human ; Antiviral Agents/therapeutic use
Chemical Substances	Antiviral Agents
Language	French
Publishing date	2023-11-09
Publishing country	France
Document type	English Abstract ; Journal Article
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2023125
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Article ; Online: Instability of the NS1 Glycoprotein from La Reunion 2018 Dengue 2 Virus (Cosmopolitan-1 Genotype) in Huh7 Cells Is Due to Lysine Residues on Positions 272 and 324.

Ogire, Eva / Diaz, Olivier / Vidalain, Pierre-Olivier / Lotteau, Vincent / Desprès, Philippe / Roche, Marjolaine

International journal of molecular sciences

2021 Volume 22, Issue 4

Abstract: La Reunion island in the South West Indian Ocean is now endemic for dengue following the introduction of dengue virus serotype 2 (DENV-2) cosmopolitan-I genotype in 2017. DENV-2 infection causes a wide spectrum of clinical manifestations ranging from flu- ...

Abstract	La Reunion island in the South West Indian Ocean is now endemic for dengue following the introduction of dengue virus serotype 2 (DENV-2) cosmopolitan-I genotype in 2017. DENV-2 infection causes a wide spectrum of clinical manifestations ranging from flu-like disease to severe dengue. The nonstructural glycoprotein 1 (NS1) has been identified as playing a key role in dengue disease severity. The intracellular NS1 exists as a homodimer, whereas a fraction is driven towards the plasma membrane or released as a soluble hexameric protein. Here, we characterized the NS1 glycoproteins from clinical isolates DES-14 and RUN-18 that were collected during the DENV-2 epidemics in Tanzania in 2014 and La Reunion island in 2018, respectively. In relation to hepatotropism of the DENV, expression of recombinant DES-14 NS1 and RUN-18 NS1 glycoproteins was compared in human hepatoma Huh7 cells. We observed that RUN-18 NS1 was poorly stable in Huh7 cells compared to DES-14 NS1. The instability of RUN-18 NS1 leading to a low level of NS1 secretion mostly relates to lysine residues on positions 272 and 324. Our data raise the issue of the consequences of a defect in NS1 stability in human hepatocytes in relation to the major role of NS1 in the pathogenesis of the DENV-2 infection.
MeSH term(s)	Amino Acid Substitution ; Antigens, Viral/chemistry ; Antigens, Viral/genetics ; Cell Line, Tumor ; Dengue/epidemiology ; Dengue/metabolism ; Dengue/virology ; Dengue Virus/metabolism ; Epidemics ; Genotype ; HEK293 Cells ; Hepatocytes/metabolism ; Hepatocytes/virology ; Humans ; Lysine/chemistry ; Protein Multimerization ; Protein Stability ; Recombinant Proteins/chemistry ; Reunion/epidemiology ; Serogroup ; Tanzania/epidemiology ; Transfection ; Viral Nonstructural Proteins/chemistry ; Viral Nonstructural Proteins/genetics
Chemical Substances	Antigens, Viral ; NS1 protein, Dengue virus type 2 ; Recombinant Proteins ; Viral Nonstructural Proteins ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2021-02-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22041951
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Article ; Online: Domain 2 of Hepatitis C Virus Protein NS5A Activates Glucokinase and Induces Lipogenesis in Hepatocytes.

Perrin-Cocon, Laure / Kundlacz, Cindy / Jacquemin, Clémence / Hanoulle, Xavier / Aublin-Gex, Anne / Figl, Marianne / Manteca, Jeremy / André, Patrice / Vidalain, Pierre-Olivier / Lotteau, Vincent / Diaz, Olivier

International journal of molecular sciences

2022 Volume 23, Issue 2

Abstract: Hepatitis C virus (HCV) relies on cellular lipid metabolism for its replication, and actively modulates lipogenesis and lipid trafficking in infected hepatocytes. This translates into an intracellular accumulation of triglycerides leading to liver ... ...

Abstract	Hepatitis C virus (HCV) relies on cellular lipid metabolism for its replication, and actively modulates lipogenesis and lipid trafficking in infected hepatocytes. This translates into an intracellular accumulation of triglycerides leading to liver steatosis, cirrhosis and hepatocellular carcinoma, which are hallmarks of HCV pathogenesis. While the interaction of HCV with hepatocyte metabolic pathways is patent, how viral proteins are able to redirect central carbon metabolism towards lipogenesis is unclear. Here, we report that the HCV protein NS5A activates the glucokinase (GCK) isoenzyme of hexokinases through its D2 domain (NS5A-D2). GCK is the first rate-limiting enzyme of glycolysis in normal hepatocytes whose expression is replaced by the hexokinase 2 (HK2) isoenzyme in hepatocellular carcinoma cell lines. We took advantage of a unique cellular model specifically engineered to re-express GCK instead of HK2 in the Huh7 cell line to evaluate the consequences of NS5A-D2 expression on central carbon and lipid metabolism. NS5A-D2 increased glucose consumption but decreased glycogen storage. This was accompanied by an altered mitochondrial respiration, an accumulation of intracellular triglycerides and an increased production of very-low density lipoproteins. Altogether, our results show that NS5A-D2 can reprogram central carbon metabolism towards a more energetic and glycolytic phenotype compatible with HCV needs for replication.
MeSH term(s)	Cell Line, Tumor ; Gene Knockdown Techniques ; Glucokinase/metabolism ; Glycogen/metabolism ; Glycolysis ; Hepacivirus/physiology ; Hepatitis C/metabolism ; Hepatitis C/virology ; Hepatocytes/metabolism ; Hepatocytes/virology ; Host-Pathogen Interactions ; Humans ; Lipid Metabolism ; Lipogenesis ; Mitochondria/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; RNA-Dependent RNA Polymerase/chemistry ; RNA-Dependent RNA Polymerase/metabolism ; Viral Nonstructural Proteins/chemistry ; Viral Nonstructural Proteins/metabolism
Chemical Substances	Viral Nonstructural Proteins ; Glycogen (9005-79-2) ; Glucokinase (EC 2.7.1.2) ; NS-5 protein, hepatitis C virus (EC 2.7.7.48) ; RNA-Dependent RNA Polymerase (EC 2.7.7.48)
Language	English
Publishing date	2022-01-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23020919
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Article ; Online: The current landscape of coronavirus-host protein-protein interactions.

Perrin-Cocon, Laure / Diaz, Olivier / Jacquemin, Clémence / Barthel, Valentine / Ogire, Eva / Ramière, Christophe / André, Patrice / Lotteau, Vincent / Vidalain, Pierre-Olivier

Journal of translational medicine

2020 Volume 18, Issue 1, Page(s) 319

Abstract: In less than 20 years, three deadly coronaviruses, SARS-CoV, MERS-CoV and SARS-CoV-2, have emerged in human population causing hundreds to hundreds of thousands of deaths. Other coronaviruses are causing epizootic representing a significant threat for ... ...

Abstract	In less than 20 years, three deadly coronaviruses, SARS-CoV, MERS-CoV and SARS-CoV-2, have emerged in human population causing hundreds to hundreds of thousands of deaths. Other coronaviruses are causing epizootic representing a significant threat for both domestic and wild animals. Members of this viral family have the longest genome of all RNA viruses, and express up to 29 proteins establishing complex interactions with the host proteome. Deciphering these interactions is essential to identify cellular pathways hijacked by these viruses to replicate and escape innate immunity. Virus-host interactions also provide key information to select targets for antiviral drug development. Here, we have manually curated the literature to assemble a unique dataset of 1311 coronavirus-host protein-protein interactions. Functional enrichment and network-based analyses showed coronavirus connections to RNA processing and translation, DNA damage and pathogen sensing, interferon production, and metabolic pathways. In particular, this global analysis pinpointed overlooked interactions with translation modulators (GIGYF2-EIF4E2), components of the nuclear pore, proteins involved in mitochondria homeostasis (PHB, PHB2, STOML2), and methylation pathways (MAT2A/B). Finally, interactome data provided a rational for the antiviral activity of some drugs inhibiting coronaviruses replication. Altogether, this work describing the current landscape of coronavirus-host interactions provides valuable hints for understanding the pathophysiology of coronavirus infections and developing effective antiviral therapies.
MeSH term(s)	Animals ; Betacoronavirus/physiology ; COVID-19 ; Coronavirus/chemistry ; Coronavirus/metabolism ; Coronavirus Infections/metabolism ; Coronavirus Infections/virology ; Databases, Protein ; Host-Pathogen Interactions/physiology ; Humans ; Mitochondrial Proteins/metabolism ; Pandemics ; Pneumonia, Viral/metabolism ; Pneumonia, Viral/virology ; Protein Interaction Maps ; SARS-CoV-2 ; Transcription Factors/metabolism ; Viral Proteins/metabolism ; Virus Replication/genetics
Chemical Substances	Mitochondrial Proteins ; Transcription Factors ; Viral Proteins
Keywords	covid19
Language	English
Publishing date	2020-08-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1479-5876
ISSN (online)	1479-5876
DOI	10.1186/s12967-020-02480-z
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Article ; Online: Toll-like Receptor 4-Induced Glycolytic Burst in Human Monocyte-Derived Dendritic Cells Results from p38-Dependent Stabilization of HIF-1α and Increased Hexokinase II Expression.

Perrin-Cocon, Laure / Aublin-Gex, Anne / Diaz, Olivier / Ramière, Christophe / Peri, Francesco / André, Patrice / Lotteau, Vincent

Journal of immunology (Baltimore, Md. : 1950)

2018 Volume 201, Issue 5, Page(s) 1510–1521

Abstract: Cell metabolism now appears as an essential regulator of immune cells activation. In particular, TLR stimulation triggers metabolic reprogramming of dendritic cells (DCs) with an increased glycolytic flux, whereas inhibition of glycolysis alters their ... ...

Abstract	Cell metabolism now appears as an essential regulator of immune cells activation. In particular, TLR stimulation triggers metabolic reprogramming of dendritic cells (DCs) with an increased glycolytic flux, whereas inhibition of glycolysis alters their functional activation. The molecular mechanisms involved in the control of glycolysis upon TLR stimulation are poorly understood for human DCs. TLR4 activation of human monocyte-derived DCs (MoDCs) stimulated glycolysis with an increased glucose consumption and lactate production. Global hexokinase (HK) activity, controlling the initial rate-limiting step of glycolysis, was also increased. TLR4-induced glycolytic burst correlated with a differential modulation of HK isoenzymes. LPS strongly enhanced the expression of HK2, whereas HK3 was reduced, HK1 remained unchanged, and HK4 was not expressed. Expression of the other rate-limiting glycolytic enzymes was not significantly increased. Exploring the signaling pathways involved in LPS-induced glycolysis with various specific inhibitors, we observed that only the inhibitors of p38-MAPK (SB203580) and of HIF-1α DNA binding (echinomycin) reduced both the glycolytic activity and production of cytokines triggered by TLR4 stimulation. In addition, LPS-induced HK2 expression required p38-MAPK-dependent HIF-1α accumulation and transcriptional activity. TLR1/2 and TLR2/6 stimulation increased glucose consumption by MoDCs through alternate mechanisms that are independent of p38-MAPK activation. TBK1 contributed to glycolysis regulation when DCs were stimulated via TLR2/6. Therefore, our results indicate that TLR4-dependent upregulation of glycolysis in human MoDCs involves a p38-MAPK-dependent HIF-1α accumulation, leading to an increased HK activity supported by enhanced HK2 expression.
MeSH term(s)	Cells, Cultured ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Gene Expression Regulation, Enzymologic/drug effects ; Gene Expression Regulation, Enzymologic/immunology ; Hexokinase/immunology ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/immunology ; Lipopolysaccharides/toxicity ; Monocytes/immunology ; Monocytes/pathology ; Protein Stability ; Toll-Like Receptor 4/agonists ; Toll-Like Receptor 4/immunology ; p38 Mitogen-Activated Protein Kinases/immunology
Chemical Substances	HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Lipopolysaccharides ; TLR4 protein, human ; Toll-Like Receptor 4 ; lipopolysaccharide, Escherichia coli O111 B4 ; HK2 protein, human (EC 2.7.1.1) ; Hexokinase (EC 2.7.1.1) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2018-07-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1701522
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Article ; Online: A hexokinase isoenzyme switch in human liver cancer cells promotes lipogenesis and enhances innate immunity.

Perrin-Cocon, Laure / Vidalain, Pierre-Olivier / Jacquemin, Clémence / Aublin-Gex, Anne / Olmstead, Keedrian / Panthu, Baptiste / Rautureau, Gilles Jeans Philippe / André, Patrice / Nyczka, Piotr / Hütt, Marc-Thorsten / Amoedo, Nivea / Rossignol, Rodrigue / Filipp, Fabian Volker / Lotteau, Vincent / Diaz, Olivier

Communications biology

2021 Volume 4, Issue 1, Page(s) 217

Abstract: During the cancerous transformation of normal hepatocytes into hepatocellular carcinoma (HCC), the enzyme catalyzing the first rate-limiting step of glycolysis, namely the glucokinase (GCK), is replaced by the higher affinity isoenzyme, hexokinase 2 (HK2) ...

Abstract	During the cancerous transformation of normal hepatocytes into hepatocellular carcinoma (HCC), the enzyme catalyzing the first rate-limiting step of glycolysis, namely the glucokinase (GCK), is replaced by the higher affinity isoenzyme, hexokinase 2 (HK2). Here, we show that in HCC tumors the highest expression level of HK2 is inversely correlated to GCK expression, and is associated to poor prognosis for patient survival. To further explore functional consequences of the GCK-to-HK2 isoenzyme switch occurring during carcinogenesis, HK2 was knocked-out in the HCC cell line Huh7 and replaced by GCK, to generate the Huh7-GCK
MeSH term(s)	Cell Line, Tumor ; Energy Metabolism ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; Glucokinase/genetics ; Glucokinase/metabolism ; Hexokinase/genetics ; Hexokinase/metabolism ; Humans ; Immunity, Innate ; Isoenzymes ; Lipogenesis ; Liver Neoplasms/enzymology ; Liver Neoplasms/genetics ; Liver Neoplasms/immunology ; Signal Transduction
Chemical Substances	Isoenzymes ; HK2 protein, human (EC 2.7.1.1) ; Hexokinase (EC 2.7.1.1) ; Glucokinase (EC 2.7.1.2)
Language	English
Publishing date	2021-02-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-021-01749-3
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Article ; Online: Modified lipoproteins provide lipids that modulate dendritic cell immune function.

Perrin-Cocon, Laure / Diaz, Olivier / André, Patrice / Lotteau, Vincent

Biochimie

2013 Volume 95, Issue 1, Page(s) 103–108

Abstract: Both physiological and pathological situations can result in biochemical changes of low-density lipoproteins (LDL). Because they can deliver signals to dendritic cells (DC), these modified lipoproteins now appear as regulators of the immune response. ... ...

Abstract	Both physiological and pathological situations can result in biochemical changes of low-density lipoproteins (LDL). Because they can deliver signals to dendritic cells (DC), these modified lipoproteins now appear as regulators of the immune response. Among these modified lipoproteins, oxidized LDL (oxLDL) that accumulate during inflammatory conditions have been extensively studied. Numerous studies have shown that oxLDL induce the maturation of DC, enhancing their ability to activate IFNγ secretion by T cells. LDL treated by secreted phospholipase A(2) also promote DC maturation. Among the bioactive lipids generated by oxidation or phospholipase treatment of LDL, lysophosphatidylcholine (LPC) and some saturated fatty acids induce DC maturation whereas some unsaturated fatty acids or oxidized derivatives have opposite effects. Among other factors, the nuclear receptor peroxisome-proliferator activated receptor γ (PPARγ) plays a crucial role in this regulation. Non-modified lipoproteins also contribute to the regulation of DC function, suggesting that the balance between native and modified lipoproteins, as well as the biochemical nature of the LDL modifications, can regulate the activation threshold of DC. Here we discuss two pathological situations in which the impact of LDL modifications on inflammation and immunity could play an important role. During atherosclerosis, modified LDL accumulating in the arterial intima may interfere with DC maturation and function, promoting a Th1 immune response and a local inflammation favoring the development of the pathology. In patients chronically infected, the hepatitis C virus (HCV) interferes with lipoprotein metabolism resulting in the production of infectious modified lipoproteins. These lipo-viral-particles (LVP) are modified low-density lipoproteins containing viral material that can alter DC maturation and affect specific toll-like receptor signaling. In conclusion, lipoprotein modifications play an important role in the regulation of immunity by delivering signals of danger to DC and modulating their function.
MeSH term(s)	Atherosclerosis/immunology ; Atherosclerosis/pathology ; Cell Differentiation ; Dendritic Cells/chemistry ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Hepacivirus/immunology ; Hepacivirus/pathogenicity ; Hepatitis C/immunology ; Hepatitis C/pathology ; Hepatitis C/virology ; Humans ; Immunity, Cellular ; Inflammation/immunology ; Inflammation/metabolism ; Lipoproteins, LDL/chemistry ; Lipoproteins, LDL/metabolism ; Lysophosphatidylcholines/immunology ; Lysophosphatidylcholines/metabolism ; Membrane Lipids/chemistry ; Membrane Lipids/immunology ; Membrane Lipids/metabolism ; Signal Transduction/immunology
Chemical Substances	Lipoproteins, LDL ; Lysophosphatidylcholines ; Membrane Lipids ; oxidized low density lipoprotein
Language	English
Publishing date	2013-01
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	120345-9
ISSN	1638-6183 ; 0300-9084
ISSN (online)	1638-6183
ISSN	0300-9084
DOI	10.1016/j.biochi.2012.08.006
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Article: The current landscape of coronavirus-host protein-protein interactions

Perrin-Cocon, Laure / Diaz, Olivier / Jacquemin, Clémence / Barthel, Valentine / Ogire, Eva / Ramière, Christophe / André, Patrice / Lotteau, Vincent / Vidalain, Pierre-Olivier

J Transl Med

Abstract	In less than 20 years, three deadly coronaviruses, SARS-CoV, MERS-CoV and SARS-CoV-2, have emerged in human population causing hundreds to hundreds of thousands of deaths. Other coronaviruses are causing epizootic representing a significant threat for both domestic and wild animals. Members of this viral family have the longest genome of all RNA viruses, and express up to 29 proteins establishing complex interactions with the host proteome. Deciphering these interactions is essential to identify cellular pathways hijacked by these viruses to replicate and escape innate immunity. Virus-host interactions also provide key information to select targets for antiviral drug development. Here, we have manually curated the literature to assemble a unique dataset of 1311 coronavirus-host protein-protein interactions. Functional enrichment and network-based analyses showed coronavirus connections to RNA processing and translation, DNA damage and pathogen sensing, interferon production, and metabolic pathways. In particular, this global analysis pinpointed overlooked interactions with translation modulators (GIGYF2-EIF4E2), components of the nuclear pore, proteins involved in mitochondria homeostasis (PHB, PHB2, STOML2), and methylation pathways (MAT2A/B). Finally, interactome data provided a rational for the antiviral activity of some drugs inhibiting coronaviruses replication. Altogether, this work describing the current landscape of coronavirus-host interactions provides valuable hints for understanding the pathophysiology of coronavirus infections and developing effective antiviral therapies.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #720240
Database	COVID19

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Book ; Article ; Online: The current landscape of coronavirus-host protein-protein interactions

Perrin-Coccon, Laure / Diaz, Olivier / Jacquemin, Clémence / Barthel, Valentine / Ogire, Eva / Ramière, Christophe / André, Patrice / Lotteau, Vincent / Vidalain, Pierre-Olivier

https://hal.archives-ouvertes.fr/hal-02874650 ; 2020

2020

Abstract: In less than twenty years, three deadly coronaviruses, SARS-CoV, MERS-CoV and SARS-CoV-2, have emerged in human population causing hundreds to hundreds of thousands of deaths. Other coronaviruses are causing epizootic representing a significant threat ... ...

Abstract	In less than twenty years, three deadly coronaviruses, SARS-CoV, MERS-CoV and SARS-CoV-2, have emerged in human population causing hundreds to hundreds of thousands of deaths. Other coronaviruses are causing epizootic representing a significant threat for both domestic and wild animals. Members of this viral family have the longest genome of all RNA viruses, and express up to 29 proteins establishing complex interactions with the host proteome. Deciphering these interactions is essential to identify cellular pathways hijacked by these viruses to replicate and escape innate immunity. Virus-host interactions also provide key information to select targets for antiviral drug development. Here, we have manually curated the literature to assemble a unique dataset of 1311 coronavirus-host protein-protein interactions. Functional enrichment and network-based analyses showed coronavirus connections to RNA processing and translation, DNA damage and pathogen sensing, interferon production, and metabolic pathways. In particular, this global analysis pinpointed overlooked interactions with translation modulators (GIGYF2-EIF4E2), components of the nuclear pore, proteins involved in mitochondria homeostasis (PHB, PHB2, STOML2), and methylation pathways (MAT2A/B). Finally, interactome data provided a rational for the antiviral activity of some drugs inhibiting coronaviruses replication. Altogether, this work describing the current landscape of coronavirus-host interactions provides valuable hints for understanding the pathophysiology of coronavirus infections and developing effective antiviral therapies.
Keywords	[SDV]Life Sciences [q-bio] ; [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology ; [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology ; covid19
Subject code	612
Language	English
Publishing date	2020-06-19
Publisher	HAL CCSD
Publishing country	fr
Document type	Book ; Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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