LIVIVO - Search results -

Search results

Result 1 - 10 of total 35

Search options

Article ; Online: Keeping viruses in Chk: DNA damage signaling puts the brakes on transformation.

Lilley, Caroline E / Weitzman, Matthew D

2010 Volume 8, Issue 6, Page(s) 464–466

Abstract: Oncogenic viruses infect many cells but rarely lead to tumorigenesis. In this issue of Cell Host & Microbe, Nikitin et al. describe how a protective DNA damage response acts to suppress transformation in the majority of cells latently infected with ... ...

Abstract	Oncogenic viruses infect many cells but rarely lead to tumorigenesis. In this issue of Cell Host & Microbe, Nikitin et al. describe how a protective DNA damage response acts to suppress transformation in the majority of cells latently infected with Epstein-Barr virus (EBV).
Language	English
Publishing date	2010-12-13
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2010.11.010
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6578: Show issues

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

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Changing the ubiquitin landscape during viral manipulation of the DNA damage response.

Weitzman, Matthew D / Lilley, Caroline E / Chaurushiya, Mira S

FEBS letters

2011 Volume 585, Issue 18, Page(s) 2897–2906

Abstract: Viruses often induce signaling through the same cellular cascades that are activated by damage to the cellular genome. Signaling triggered by viral proteins or exogenous DNA delivered by viruses can be beneficial or detrimental to viral infection. ... ...

Abstract	Viruses often induce signaling through the same cellular cascades that are activated by damage to the cellular genome. Signaling triggered by viral proteins or exogenous DNA delivered by viruses can be beneficial or detrimental to viral infection. Viruses have therefore evolved to dissect the cellular DNA damage response pathway during infection, often marking key cellular regulators with ubiquitin to induce their degradation or change their function. Signaling controlled by ubiquitin or ubiquitin-like proteins has recently emerged as key regulator of the cellular DNA damage response. Situated at the interface between DNA damage signaling and the ubiquitin system, viruses can reveal key convergence points in this important cellular pathway. In this review, we examine how viruses harness the diversity of the cellular ubiquitin system to modulate the DNA damage signaling pathway. We discuss the implications of viral infiltration of this pathway for both the transcriptional program of the virus and for the cellular response to DNA damage.
MeSH term(s)	DNA Damage ; DNA Repair ; Host-Pathogen Interactions ; Humans ; Signal Transduction ; Ubiquitin/metabolism ; Viral Proteins/metabolism ; Viral Proteins/physiology ; Virus Diseases/genetics ; Virus Diseases/physiopathology ; Virus Diseases/virology ; Viruses/metabolism
Chemical Substances	Ubiquitin ; Viral Proteins
Language	English
Publishing date	2011-05-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2011.04.049
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.B 282: Show issues

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

Order via subito

Details ▾

Article ; Online: Genomes in conflict: maintaining genome integrity during virus infection.

Weitzman, Matthew D / Lilley, Caroline E / Chaurushiya, Mira S

Annual review of microbiology

2010 Volume 64, Page(s) 61–81

Abstract: The cellular surveillance network for sensing and repairing damaged DNA prevents an array of human diseases, and when compromised it can lead to genomic instability and cancer. The carefully maintained cellular response to DNA damage is challenged during ...

Abstract	The cellular surveillance network for sensing and repairing damaged DNA prevents an array of human diseases, and when compromised it can lead to genomic instability and cancer. The carefully maintained cellular response to DNA damage is challenged during viral infection, when foreign DNA is introduced into the cell. The battle between virus and host generates a genomic conflict. The host attempts to limit viral infection and protect its genome, while the virus deploys tactics to eliminate, evade, or exploit aspects of the cellular defense. Studying this conflict has revealed that the cellular DNA damage response machinery comprises part of the intrinsic cellular defense against viral infection. In this review we examine recent advances in this emerging field. We identify common themes used by viruses in their attempts to commandeer or circumvent the host cell's DNA repair machinery, and highlight potential outcomes of the conflict for both virus and host.
MeSH term(s)	Animals ; DNA Damage ; DNA Repair ; Genomic Instability ; Humans ; Models, Biological ; Neoplasms/genetics ; Neoplasms/virology ; Virus Diseases/pathology ; Viruses/pathogenicity
Language	English
Publishing date	2010
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	207931-8
ISSN	1545-3251 ; 0066-4227
ISSN (online)	1545-3251
ISSN	0066-4227
DOI	10.1146/annurev.micro.112408.134016
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Se 30: Show issues

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

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Critical analysis of an oncolytic herpesvirus encoding granulocyte-macrophage colony stimulating factor for the treatment of malignant melanoma.

Hughes, Tasha / Coffin, Robert S / Lilley, Caroline E / Ponce, Rafael / Kaufman, Howard L

Oncolytic virotherapy

2014 Volume 3, Page(s) 11–20

Abstract: Oncolytic viruses that selectively lyse tumor cells with minimal damage to normal cells are a new area of therapeutic development in oncology. An attenuated herpesvirus encoding the granulocyte-macrophage colony stimulating factor (GM-CSF), known as ... ...

Abstract	Oncolytic viruses that selectively lyse tumor cells with minimal damage to normal cells are a new area of therapeutic development in oncology. An attenuated herpesvirus encoding the granulocyte-macrophage colony stimulating factor (GM-CSF), known as talimogene laherparepvec (T-VEC), has been identified as an attractive oncolytic virus for cancer therapy based on preclinical tumor studies and results from early-phase clinical trials and a large randomized Phase III study in melanoma. In this review, we discuss the basic biology of T-VEC, describe the role of GM-CSF as an immune adjuvant, summarize the preclinical data, and report the outcomes of published clinical trials using T-VEC. The emerging data suggest that T-VEC is a safe and potentially effective antitumor therapy in malignant melanoma and represents the first oncolytic virus to demonstrate therapeutic activity against human cancer in a randomized, controlled Phase III study.
Language	English
Publishing date	2014-01-15
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	2799361-9
ISSN	2253-1572
ISSN	2253-1572
DOI	10.2147/OV.S36701
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Chromatin at the intersection of viral infection and DNA damage.

Lilley, Caroline E / Chaurushiya, Mira S / Weitzman, Matthew D

Biochimica et biophysica acta

2009 Volume 1799, Issue 3-4, Page(s) 319–327

Abstract: During infection, viruses cause global disruption to nuclear architecture in their attempt to take over the cell. In turn, the host responds with various defenses, which include chromatin-mediated silencing of the viral genome and activation of DNA ... ...

Abstract	During infection, viruses cause global disruption to nuclear architecture in their attempt to take over the cell. In turn, the host responds with various defenses, which include chromatin-mediated silencing of the viral genome and activation of DNA damage signaling pathways. Dynamic exchanges at chromatin, and specific post-translational modifications on histones have recently emerged as master controllers of DNA damage signaling and repair. Studying viral control of chromatin modifications is identifying histones as important players in the battle between host and virus for control of cell cycle and gene expression. These studies are revealing new complexities of the virus-host interaction, uncovering the potential of chromatin as an anti-viral defense mechanism, and also providing unique insights into the role of chromatin in DNA repair.
MeSH term(s)	Animals ; Cell Cycle/genetics ; Chromatin/physiology ; DNA Damage/genetics ; Histones/metabolism ; Humans ; Virus Diseases/genetics ; Viruses/pathogenicity
Chemical Substances	Chromatin ; Histones
Language	English
Publishing date	2009-07-17
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbagrm.2009.06.007
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.247: Show issues

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

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Stat3-mediated alterations in lysosomal membrane protein composition.

Lloyd-Lewis, Bethan / Krueger, Caroline C / Sargeant, Timothy J / D'Angelo, Michael E / Deery, Michael J / Feret, Renata / Howard, Julie A / Lilley, Kathryn S / Watson, Christine J

The Journal of biological chemistry

2018 Volume 293, Issue 12, Page(s) 4244–4261

Abstract: Lysosome function is essential in cellular homeostasis. In addition to its recycling role, the lysosome has recently been recognized as a cellular signaling hub. We have shown in mammary epithelial cells, ... ...

Abstract	Lysosome function is essential in cellular homeostasis. In addition to its recycling role, the lysosome has recently been recognized as a cellular signaling hub. We have shown in mammary epithelial cells, both
MeSH term(s)	Animals ; Cell Death ; Cells, Cultured ; Epithelial Cells/cytology ; Epithelial Cells/metabolism ; Female ; Intracellular Membranes/metabolism ; Lysosomal Membrane Proteins/metabolism ; Lysosomes/metabolism ; Mammary Glands, Animal/cytology ; Mammary Glands, Animal/metabolism ; Proteome/metabolism ; Proteomics ; STAT3 Transcription Factor/metabolism ; Signal Transduction
Chemical Substances	Lysosomal Membrane Proteins ; Proteome ; STAT3 Transcription Factor ; Stat3 protein, mouse
Language	English
Publishing date	2018-01-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA118.001777
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.108: Show issues

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

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Construction of multiply disabled herpes simplex viral vectors for gene delivery to the nervous system.

Lilley, Caroline E / Coffin, Robert S

Methods in molecular medicine

2003 Volume 76, Page(s) 33–49

MeSH term(s)	Animals ; Cell Line ; Central Nervous System/virology ; DNA, Viral/genetics ; DNA, Viral/metabolism ; Ganglia, Spinal/cytology ; Ganglia, Spinal/metabolism ; Ganglia, Spinal/virology ; Gene Expression Regulation, Viral ; Gene Transfer Techniques ; Genes, Viral ; Genetic Therapy ; Genetic Vectors ; Genome, Viral ; Herpesvirus 1, Human/genetics ; Herpesvirus 1, Human/physiology ; Humans ; Neurons/cytology ; Neurons/physiology ; Promoter Regions, Genetic ; Rats ; Transgenes
Chemical Substances	DNA, Viral
Language	English
Publishing date	2003-04-01
Publishing country	United States
Document type	Journal Article
ISSN	1543-1894
ISSN	1543-1894
DOI	10.1385/1-59259-304-6:33
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Using or abusing: viruses and the cellular DNA damage response.

Lilley, Caroline E / Schwartz, Rachel A / Weitzman, Matthew D

Trends in microbiology

2007 Volume 15, Issue 3, Page(s) 119–126

Abstract: During infection, viruses attempt to hijack the cell while the host responds with various defense systems. Traditional defenses include the interferon response and apoptosis, but recent work suggests that this antiviral arsenal also includes the cellular ...

Abstract	During infection, viruses attempt to hijack the cell while the host responds with various defense systems. Traditional defenses include the interferon response and apoptosis, but recent work suggests that this antiviral arsenal also includes the cellular DNA damage response machinery. The observation of interactions between viruses and cellular DNA repair proteins has not only uncovered new complexities of the virus-host interaction but is also reinforcing the view that viruses can reveal key regulators of cellular pathways through the proteins they target.
MeSH term(s)	Animals ; DNA Damage ; DNA Repair ; Humans ; Proteins/metabolism ; Signal Transduction ; Viral Proteins/metabolism ; Viruses/metabolism
Chemical Substances	Proteins ; Viral Proteins
Language	English
Publishing date	2007-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1158963-2
ISSN	1878-4380 ; 0966-842X
ISSN (online)	1878-4380
ISSN	0966-842X
DOI	10.1016/j.tim.2007.01.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3738: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: The intrinsic antiviral defense to incoming HSV-1 genomes includes specific DNA repair proteins and is counteracted by the viral protein ICP0.

Lilley, Caroline E / Chaurushiya, Mira S / Boutell, Chris / Everett, Roger D / Weitzman, Matthew D

PLoS pathogens

2011 Volume 7, Issue 6, Page(s) e1002084

Abstract: Cellular restriction factors responding to herpesvirus infection include the ND10 components PML, Sp100 and hDaxx. During the initial stages of HSV-1 infection, novel sub-nuclear structures containing these ND10 proteins form in association with incoming ...

Abstract	Cellular restriction factors responding to herpesvirus infection include the ND10 components PML, Sp100 and hDaxx. During the initial stages of HSV-1 infection, novel sub-nuclear structures containing these ND10 proteins form in association with incoming viral genomes. We report that several cellular DNA damage response proteins also relocate to sites associated with incoming viral genomes where they contribute to the cellular front line defense. We show that recruitment of DNA repair proteins to these sites is independent of ND10 components, and instead is coordinated by the cellular ubiquitin ligases RNF8 and RNF168. The viral protein ICP0 targets RNF8 and RNF168 for degradation, thereby preventing the deposition of repressive ubiquitin marks and counteracting this repair protein recruitment. This study highlights important parallels between recognition of cellular DNA damage and recognition of viral genomes, and adds RNF8 and RNF168 to the list of factors contributing to the intrinsic antiviral defense against herpesvirus infection.
MeSH term(s)	Animals ; Cells, Cultured ; Chlorocebus aethiops ; DNA Repair Enzymes/genetics ; DNA Repair Enzymes/metabolism ; DNA Repair Enzymes/physiology ; DNA-Binding Proteins/metabolism ; DNA-Binding Proteins/physiology ; Genome, Viral/immunology ; Herpesvirus 1, Human/genetics ; Herpesvirus 1, Human/immunology ; Humans ; Immediate-Early Proteins/genetics ; Immediate-Early Proteins/metabolism ; Immediate-Early Proteins/physiology ; Immune Evasion/genetics ; Immune Evasion/physiology ; Immunity, Innate/genetics ; Immunity, Innate/physiology ; Mice ; Mice, Knockout ; Models, Biological ; Protein Processing, Post-Translational ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitin-Protein Ligases/physiology ; Vero Cells ; Viruses/immunology
Chemical Substances	DNA-Binding Proteins ; Immediate-Early Proteins ; RNF8 protein, human ; RNF168 protein, human (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Vmw110 protein, Human herpesvirus 1 (EC 2.3.2.27) ; DNA Repair Enzymes (EC 6.5.1.-)
Language	English
Publishing date	2011-06-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1002084
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The intrinsic antiviral defense to incoming HSV-1 genomes includes specific DNA repair proteins and is counteracted by the viral protein ICP0.

Caroline E Lilley / Mira S Chaurushiya / Chris Boutell / Roger D Everett / Matthew D Weitzman

PLoS Pathogens, Vol 7, Iss 6, p e

2011 Volume 1002084

Abstract	Cellular restriction factors responding to herpesvirus infection include the ND10 components PML, Sp100 and hDaxx. During the initial stages of HSV-1 infection, novel sub-nuclear structures containing these ND10 proteins form in association with incoming viral genomes. We report that several cellular DNA damage response proteins also relocate to sites associated with incoming viral genomes where they contribute to the cellular front line defense. We show that recruitment of DNA repair proteins to these sites is independent of ND10 components, and instead is coordinated by the cellular ubiquitin ligases RNF8 and RNF168. The viral protein ICP0 targets RNF8 and RNF168 for degradation, thereby preventing the deposition of repressive ubiquitin marks and counteracting this repair protein recruitment. This study highlights important parallels between recognition of cellular DNA damage and recognition of viral genomes, and adds RNF8 and RNF168 to the list of factors contributing to the intrinsic antiviral defense against herpesvirus infection.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	572
Language	English
Publishing date	2011-06-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED