Matches in SemOpenAlex for { <https://semopenalex.org/work/W2346310044> ?p ?o ?g. }
- W2346310044 abstract "Human herpes simplex virus (HSV) is a ubiquitous human pathogen that establishes a lifelong latent infection and is associated with mucocutaneous lesions. In multicellular organisms, cell death is a crucial host defense mechanism that eliminates pathogen-infected cells. Apoptosis is a well-defined form of programmed cell death executed by a group of cysteine proteases, called caspases. Studies have shown that HSV has evolved strategies to counteract caspase activation and apoptosis by encoding anti-apoptotic viral proteins such as gD, gJ, Us3, LAT, and the ribonucleotide reductase large subunit (R1). Recently, necroptosis has been identified as a regulated form of necrosis that can be invoked in the absence of caspase activity. Receptor-interacting kinase 3 (RIP3 or RIPK3) has emerged as a central signaling molecule in necroptosis; it is activated via interaction with other RIP homotypic interaction motif (RHIM)-containing proteins such as RIP1 (or RIPK1). There is increasing evidence that HSV R1 manipulates necroptosis via the RHIM-dependent inactivation or activation ofRIP3 in a species-specific manner. This review summarizes the current understanding of the interplay between HSV infection and cell death pathways, with an emphasis on apoptosis and necroptosis." @default.
- W2346310044 created "2016-06-24" @default.
- W2346310044 creator A5025033434 @default.
- W2346310044 creator A5036621543 @default.
- W2346310044 date "2016-05-06" @default.
- W2346310044 modified "2023-10-12" @default.
- W2346310044 title "The interplay between human herpes simplex virus infection and the apoptosis and necroptosis cell death pathways" @default.
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- W2346310044 doi "https://doi.org/10.1186/s12985-016-0528-0" @default.
- W2346310044 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4859980" @default.
- W2346310044 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27154074" @default.
- W2346310044 hasPublicationYear "2016" @default.
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