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Article ; Online: Schlafens Can Put Viruses to Sleep.

Kim, Eui Tae / Weitzman, Matthew D

2022 Volume 14, Issue 2

Abstract: The Schlafen gene family encodes for proteins involved in various biological tasks, including cell proliferation, differentiation, and T cell development. Schlafens were initially discovered in mice, and have been studied in the context of cancer biology, ...

Abstract	The Schlafen gene family encodes for proteins involved in various biological tasks, including cell proliferation, differentiation, and T cell development. Schlafens were initially discovered in mice, and have been studied in the context of cancer biology, as well as their role in protecting cells during viral infection. This protein family provides antiviral barriers via direct and indirect effects on virus infection. Schlafens can inhibit the replication of viruses with both RNA and DNA genomes. In this review, we summarize the cellular functions and the emerging relationship between Schlafens and innate immunity. We also discuss the functions and distinctions of this emerging family of proteins as host restriction factors against viral infection. Further research into Schlafen protein function will provide insight into their mechanisms that contribute to intrinsic and innate host immunity.
MeSH term(s)	Animals ; Cell Cycle Proteins/immunology ; Endoribonucleases/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Immune Evasion ; Immunity, Innate ; Mice ; Virus Diseases/immunology
Chemical Substances	Cell Cycle Proteins ; Endoribonucleases (EC 3.1.-)
Language	English
Publishing date	2022-02-21
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14020442
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Phosphorylation regulates viral biomolecular condensates to promote infectious progeny production.

Grams, Nicholas / Charman, Matthew / Halko, Edwin / Lauman, Richard / Garcia, Benjamin A / Weitzman, Matthew D

The EMBO journal

2024 Volume 43, Issue 2, Page(s) 277–303

Abstract: Biomolecular condensates (BMCs) play important roles in diverse biological processes. Many viruses form BMCs which have been implicated in various functions critical for the productive infection of host cells. The adenovirus L1-52/55 kilodalton protein ( ... ...

Abstract	Biomolecular condensates (BMCs) play important roles in diverse biological processes. Many viruses form BMCs which have been implicated in various functions critical for the productive infection of host cells. The adenovirus L1-52/55 kilodalton protein (52K) was recently shown to form viral BMCs that coordinate viral genome packaging and capsid assembly. Although critical for packaging, we do not know how viral condensates are regulated during adenovirus infection. Here we show that phosphorylation of serine residues 28 and 75 within the N-terminal intrinsically disordered region of 52K modulates viral condensates in vitro and in cells, promoting liquid-like properties. Furthermore, we demonstrate that phosphorylation of 52K promotes viral genome packaging and the production of infectious progeny particles. Collectively, our findings provide insights into how viral condensate properties are regulated and maintained in a state conducive to their function in viral progeny production. In addition, our findings have implications for antiviral strategies aimed at targeting the regulation of viral BMCs to limit viral multiplication.
MeSH term(s)	Phosphorylation ; Biomolecular Condensates ; Viral Proteins/genetics ; Viral Proteins/metabolism ; Virus Replication ; Viruses
Chemical Substances	Viral Proteins
Language	English
Publishing date	2024-01-02
Publishing country	England
Document type	Journal Article
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.1038/s44318-023-00021-0
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Zs.A 1808: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Schlafens Can Put Viruses to Sleep

Kim, Eui Tae / Weitzman, Matthew D.

Viruses. 2022 Feb. 21, v. 14, no. 2

2022

Abstract	The Schlafen gene family encodes for proteins involved in various biological tasks, including cell proliferation, differentiation, and T cell development. Schlafens were initially discovered in mice, and have been studied in the context of cancer biology, as well as their role in protecting cells during viral infection. This protein family provides antiviral barriers via direct and indirect effects on virus infection. Schlafens can inhibit the replication of viruses with both RNA and DNA genomes. In this review, we summarize the cellular functions and the emerging relationship between Schlafens and innate immunity. We also discuss the functions and distinctions of this emerging family of proteins as host restriction factors against viral infection. Further research into Schlafen protein function will provide insight into their mechanisms that contribute to intrinsic and innate host immunity.
Keywords	DNA ; RNA ; T-lymphocytes ; cell proliferation ; genes ; innate immunity ; viruses
Language	English
Dates of publication	2022-0221
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v14020442
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Replication Compartments of DNA Viruses in the Nucleus: Location, Location, Location.

Charman, Matthew / Weitzman, Matthew D

Viruses

2020 Volume 12, Issue 2

Abstract: DNA viruses that replicate in the nucleus encompass a range of ubiquitous and clinically important viruses, from acute pathogens to persistent tumor viruses. These viruses must co-opt nuclear processes for the benefit of the virus, whilst evading host ... ...

Abstract	DNA viruses that replicate in the nucleus encompass a range of ubiquitous and clinically important viruses, from acute pathogens to persistent tumor viruses. These viruses must co-opt nuclear processes for the benefit of the virus, whilst evading host processes that would otherwise attenuate viral replication. Accordingly, DNA viruses induce the formation of membraneless assemblies termed viral replication compartments (VRCs). These compartments facilitate the spatial organization of viral processes and regulate virus-host interactions. Here, we review advances in our understanding of VRCs. We cover their initiation and formation, their function as the sites of viral processes, and aspects of their composition and organization. In doing so, we highlight ongoing and emerging areas of research highly pertinent to our understanding of nuclear-replicating DNA viruses.
MeSH term(s)	Cell Nucleus/virology ; DNA Viruses/physiology ; Host Microbial Interactions ; Humans ; Viral Proteins/genetics ; Viral Replication Compartments ; Virus Replication
Chemical Substances	Viral Proteins
Keywords	covid19
Language	English
Publishing date	2020-01-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v12020151
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Adeno-Associated Virus Genome Interactions Important for Vector Production and Transduction.

Maurer, Anna C / Weitzman, Matthew D

Human gene therapy

2020 Volume 31, Issue 9-10, Page(s) 499–511

Abstract: Recombinant adeno-associated virus has emerged as one of the most promising gene therapy delivery vectors. Development of these vectors took advantage of key features of the wild-type adeno-associated virus (AAV), enabled by basic studies of the ... ...

Abstract	Recombinant adeno-associated virus has emerged as one of the most promising gene therapy delivery vectors. Development of these vectors took advantage of key features of the wild-type adeno-associated virus (AAV), enabled by basic studies of the underlying biology and requirements for transcription, replication, and packaging of the viral genome. Each step in generating and utilizing viral vectors involves numerous molecular interactions that together determine the efficiency of vector production and gene delivery. Once delivered into the cell, interactions with host proteins will determine the fate of the viral genome, and these will impact the intended goal of gene delivery. Here, we provide an overview of known interactions of the AAV genome with viral and cellular proteins involved in its amplification, packaging, and expression. Further appreciation of how the AAV genome interacts with host factors will enhance how this simple virus can be harnessed for an array of vector purposes that benefit human health.
MeSH term(s)	Animals ; Dependovirus/genetics ; Gene Transfer Techniques ; Genetic Therapy ; Genetic Vectors ; Genome, Viral ; Helper Viruses/physiology ; Host Microbial Interactions ; Humans ; Transduction, Genetic ; Virus Replication
Language	English
Publishing date	2020-04-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1028152-6
ISSN	1557-7422 ; 1043-0342
ISSN (online)	1557-7422
ISSN	1043-0342
DOI	10.1089/hum.2020.069
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Zs.A 2988: Show issues

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Article ; Online: Addressing the benefits of inhibiting APOBEC3-dependent mutagenesis in cancer.

Petljak, Mia / Green, Abby M / Maciejowski, John / Weitzman, Matthew D

Nature genetics

2022 Volume 54, Issue 11, Page(s) 1599–1608

Abstract: Mutational signatures associated with apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC)3 cytosine deaminase activity have been found in over half of cancer types, including some therapy-resistant and metastatic tumors. Driver ... ...

Abstract	Mutational signatures associated with apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC)3 cytosine deaminase activity have been found in over half of cancer types, including some therapy-resistant and metastatic tumors. Driver mutations can occur in APOBEC3-favored sequence contexts, suggesting that mutagenesis by APOBEC3 enzymes may drive cancer evolution. The APOBEC3-mediated signatures are often detected in subclonal branches of tumor phylogenies and are acquired in cancer cell lines over long periods of time, indicating that APOBEC3 mutagenesis can be ongoing in cancer. Collectively, these and other observations have led to the proposal that APOBEC3 mutagenesis represents a disease-modifying process that could be inhibited to limit tumor heterogeneity, metastasis and drug resistance. However, critical aspects of APOBEC3 biology in cancer and in healthy tissues have not been clearly defined, limiting well-grounded predictions regarding the benefits of inhibiting APOBEC3 mutagenesis in different settings in cancer. We discuss the relevant mechanistic gaps and strategies to address them to investigate whether inhibiting APOBEC3 mutagenesis may confer clinical benefits in cancer.
MeSH term(s)	Humans ; Mutagenesis/genetics ; Neoplasms/genetics ; Neoplasms/pathology ; APOBEC-1 Deaminase/genetics ; Mutation ; Cytidine Deaminase/genetics ; APOBEC Deaminases/genetics
Chemical Substances	APOBEC-1 Deaminase (EC 3.5.4.36) ; Cytidine Deaminase (EC 3.5.4.5) ; APOBEC3 proteins, human (EC 3.5.4.5) ; APOBEC Deaminases (EC 3.5.4.5)
Language	English
Publishing date	2022-10-24
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-022-01196-8
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Zs.A 3613: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 46: Show issues

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Article ; Online: Herpes simplex virus replication compartments: From naked release to recombining together.

Kobiler, Oren / Weitzman, Matthew D

PLoS pathogens

2019 Volume 15, Issue 6, Page(s) e1007714

MeSH term(s)	Animals ; Gene Expression Regulation, Viral/physiology ; Herpesvirus 1, Human/physiology ; Humans ; Virus Release/physiology ; Virus Replication/physiology
Language	English
Publishing date	2019-06-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7366
ISSN (online)	1553-7374
ISSN	1553-7366
DOI	10.1371/journal.ppat.1007714
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The spectrum of APOBEC3 activity: From anti-viral agents to anti-cancer opportunities.

Green, Abby M / Weitzman, Matthew D

DNA repair

2019 Volume 83, Page(s) 102700

Abstract: The APOBEC3 family of cytosine deaminases are part of the innate immune response to viral infection, but also have the capacity to damage cellular DNA. Detection of mutational signatures consistent with APOBEC3 activity, together with elevated APOBEC3 ... ...

Abstract	The APOBEC3 family of cytosine deaminases are part of the innate immune response to viral infection, but also have the capacity to damage cellular DNA. Detection of mutational signatures consistent with APOBEC3 activity, together with elevated APOBEC3 expression in cancer cells, has raised the possibility that these enzymes contribute to oncogenesis. Genome deamination by APOBEC3 enzymes also elicits DNA damage response signaling and presents therapeutic vulnerabilities for cancer cells. Here, we discuss implications of APOBEC3 activity in cancer and the potential to exploit their mutagenic activity for targeted cancer therapies.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antiviral Agents/pharmacology ; Cytidine Deaminase/genetics ; Cytidine Deaminase/metabolism ; Humans ; Molecular Targeted Therapy/methods ; Mutation ; Neoplasms/drug therapy ; Neoplasms/enzymology ; Neoplasms/genetics
Chemical Substances	Antineoplastic Agents ; Antiviral Agents ; Cytidine Deaminase (EC 3.5.4.5)
Language	English
Publishing date	2019-09-13
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2071608-4
ISSN	1568-7856 ; 1568-7864
ISSN (online)	1568-7856
ISSN	1568-7864
DOI	10.1016/j.dnarep.2019.102700
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 5555: Show issues

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Article ; Online: Serotype-specific restriction of wild-type adenoviruses by the cellular Mre11-Rad50-Nbs1 complex.

Pancholi, Neha J / Weitzman, Matthew D

Virology

2018 Volume 518, Page(s) 221–231

Abstract: During viral replication in the nucleus, the DNA genomes of adenoviruses are accessible to cellular DNA-binding proteins. Human adenovirus type 5 (Ad5) targets the cellular Mre11-Rad50-Nbs1 complex (MRN) to evade detection by the DNA damage response (DDR) ...

Abstract	During viral replication in the nucleus, the DNA genomes of adenoviruses are accessible to cellular DNA-binding proteins. Human adenovirus type 5 (Ad5) targets the cellular Mre11-Rad50-Nbs1 complex (MRN) to evade detection by the DNA damage response (DDR). Ad5 mutants that cannot target MRN have reduced viral propagation. Previous studies showed that diverse adenovirus serotypes interact differently with MRN. While these studies revealed diverse MRN interactions among serotypes, it remains unclear how these differences influence viral replication. Here, we examined effects of the DDR on several adenovirus serotypes. We demonstrate that wild-type Ad9 and Ad12 do not overcome MRN impairment. We also examined viral proteins involved in targeting MRN and found that unlike Ad5-E4orf3, expression of Ad9-E4orf3 is not sufficient for MRN mislocalization observed during infection. We conclude that adenovirus serotypes target MRN in distinct ways, and the MRN complex can impair DNA replication of wild-type viruses across the adenovirus family.
MeSH term(s)	Acid Anhydride Hydrolases ; Adenoviruses, Human/immunology ; Adenoviruses, Human/physiology ; Cell Cycle Proteins/metabolism ; Cell Line ; DNA Repair Enzymes/metabolism ; DNA-Binding Proteins/metabolism ; Host-Pathogen Interactions ; Humans ; MRE11 Homologue Protein/metabolism ; Nuclear Proteins/metabolism ; Serogroup ; Virus Replication
Chemical Substances	Cell Cycle Proteins ; DNA-Binding Proteins ; MRE11 protein, human ; NBN protein, human ; Nuclear Proteins ; MRE11 Homologue Protein (EC 3.1.-) ; Acid Anhydride Hydrolases (EC 3.6.-) ; RAD50 protein, human (EC 3.6.-) ; DNA Repair Enzymes (EC 6.5.1.-)
Language	English
Publishing date	2018-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2018.02.023
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Ud II Zs.172: Show issues

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Article: Double-Strand Break Repair Pathways Differentially Affect Processing and Transduction by Dual AAV Vectors.

Maurer, Anna C / Benyamini, Brian / Fan, Vinson B / Whitney, Oscar N / Dailey, Gina M / Darzacq, Xavier / Weitzman, Matthew D / Tjian, Robert

bioRxiv : the preprint server for biology

2023

Abstract: Recombinant adeno-associated viral vectors (rAAV) are a powerful tool for gene delivery but have a limited DNA carrying capacity. Efforts to expand this genetic payload have focused on engineering the vector components, such as dual trans-splicing ... ...

Abstract	Recombinant adeno-associated viral vectors (rAAV) are a powerful tool for gene delivery but have a limited DNA carrying capacity. Efforts to expand this genetic payload have focused on engineering the vector components, such as dual trans-splicing vectors which double the delivery size by exploiting the natural concatenation of rAAV genomes in host nuclei. We hypothesized that inefficient dual vector transduction could be improved by modulating host factors which affect concatenation. Since factors mediating concatenation are not well defined, we performed a genome-wide screen to identify host cell regulators. We discovered that Homologous Recombination (HR) is inhibitory to dual vector transduction. We demonstrate that depletion or inhibition of HR factors BRCA1 and Rad51 significantly increase reconstitution of a large split transgene by increasing both concatenation and expression from rAAVs. Our results define new roles for DNA damage repair in rAAV transduction and highlight the potential for pharmacological intervention to increase genetic payload of rAAV vectors.
Language	English
Publishing date	2023-09-19
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.09.19.558438
Database	MEDical Literature Analysis and Retrieval System OnLINE

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