ArticleJournal of virology2002
Cation-independent mannose 6-phosphate receptor blocks apoptosis induced by herpes simplex virus 1 mutants lacking glycoprotein D and is likely the target of antiapoptotic activity of the glycoprotein.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026Review
- Mannose-6-Phosphate-Tagged Liposomes Exhibit Increased Transcytosis Across Human Blood-Brain Barrier Model.Pharmaceutics · 2026Article
- Peroxisomes exhibit compromised structure and matrix protein content in SARS-CoV-2-infected cells.Molecular biology of the cell · 2021Article
- Relief of Cadmium-Induced Intestinal Motility Disorder in Mice byFrontiers in immunology · 2020Article
- Overexpression of the Insulin-Like Growth Factor II Receptor Increases β-Amyloid Production and Affects Cell Viability.Molecular and cellular biology · 2015Article
- Increased activity and altered subcellular distribution of lysosomal enzymes determine neuronal vulnerability in Niemann-Pick type C1-deficient mice.The American journal of pathology · 2009Article
- Apoptosis and antigen receptor function in T and B cells following exposure to herpes simplex virus.Virology · 2007Article
- Separation of receptor-binding and profusogenic domains of glycoprotein D of herpes simplex virus 1 into distinct interacting proteins.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Up-regulation of cation-independent mannose 6-phosphate receptor and endosomal-lysosomal markers in surviving neurons after 192-IgG-saporin administrations into the adult rat brain.The American journal of pathology · 2006Article
- Herpes simplex virus type 1 enters human epidermal keratinocytes, but not neurons, via a pH-dependent endocytic pathway.Journal of virology · 2005Article
- Identification of cell surface and secreted proteins essential for tumor cell survival using a genetic suppressor element screen.Oncogene · 2004Article
- Conserved cysteine-rich domain of paramyxovirus simian virus 5 V protein plays an important role in blocking apoptosis.Journal of virology · 2004Article
- The domains of glycoprotein D required to block apoptosis induced by herpes simplex virus 1 are largely distinct from those involved in cell-cell fusion and binding to nectin1.Journal of virology · 2003Article
- Induction of apoptosis by paramyxovirus simian virus 5 lacking a small hydrophobic gene.Journal of virology · 2003Article
- Engineered herpes simplex virus 1 is dependent on IL13Ralpha 2 receptor for cell entry and independent of glycoprotein D receptor interaction.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Truncated forms of glycoprotein D of herpes simplex virus 1 capable of blocking apoptosis and of low-efficiency entry into cells form a heterodimer dependent on the presence of a cysteine located in the shared transmembrane domains.Journal of virology · 2002Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Herpes simplex virus 1 mutants lacking the gene encoding glycoprotein D (gD) and the gD normally present in the envelope of the virus (gD(-/-) stocks) or mutants lacking the gD gene but containing trans-induced gD in their envelopes (gD(-/+)) cause apoptosis in human SK-N-SH cells. The gD(-/-) virions are taken up by endocytosis and are degraded, whereas gD(-/+) viruses replicate but produce gD(-/-) virus. Apoptosis is blocked by delivery of the gD gene in trans. Studies designed to test several hypotheses concerning the role of gD in apoptosis revealed the following. (i) gD(-/-) and gD(-/+) stocks induce fragmentation of cellular DNA in SK-N-SH, HEp-2, HeLa, and Vero cell lines. (ii) Chloroquine blocks apoptosis induced by gD(-/-) stocks but not by gD(-/+) stocks. The drug also rescues gD(-/-) from degradation. (iii) Cells transduced with cation-independent mannose 6-phosphate receptor (CI-MPR) block apoptosis induced by either gD(-/-) or gD(-/+) virus. (iv) Expression of sequences antisense to the cloned CI-MPR gene induced apoptosis by themselves. Wild-type virus but not gD(-/-) or gD(-/+) stocks of mutant virus blocked apoptosis induced by the expression of CI-MPR antisense sequences. These results exclude the possibility that to block apoptosis, gD must interact with its HveA receptor, a member of the tumor necrosis factor alpha receptor family. Instead, the data suggest that gD blocks the influx of lysosomal enzymes into the endosomal compartment by binding to CI-MPR. This conclusion is consistent with published reports that phosphorylated gD interacts with CI-MPR.
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