ArticleProceedings of the National Academy of Sciences of the United States of America1995
Human immunodeficiency virus 1 envelope-initiated G2-phase programmed cell death.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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
12 citing papers in PubMed, 44 citations in OpenAlex.
- HIV-1 gp120 and morphine induced oxidative stress: role in cell cycle regulation.Frontiers in microbiology · 2015Article
- The HIV-1 gp120/V3 modifies the response of uninfected CD4 T cells to antigen presentation: mapping of the specific transcriptional signature.Journal of translational medicine · 2011Article
- Mechanisms of HIV-associated lymphocyte apoptosis: 2010.Cell death & disease · 2010Review
- Human immunodeficiency virus type 1 Vpr induces DNA replication stress in vitro and in vivo.Journal of virology · 2006Article
- Sequential involvement of Cdk1, mTOR and p53 in apoptosis induced by the HIV-1 envelope.The EMBO journal · 2002Article
- Cytopathic killing of peripheral blood CD4(+) T lymphocytes by human immunodeficiency virus type 1 appears necrotic rather than apoptotic and does not require env.Journal of virology · 2002Article
- HIV-1 Vpr enhances viral burden by facilitating infection of tissue macrophages but not nondividing CD4+ T cells.The Journal of experimental medicine · 2001Article
- Human immunodeficiency virus type 1 (HIV-1) Vpr functions as an immediate-early protein during HIV-1 infection.Journal of virology · 1999Article
- Human immunodeficiency virus type 1 induction mediated by genistein is linked to cell cycle arrest in G2.Journal of virology · 1998Article
- Vpr stimulates viral expression and induces cell killing in human immunodeficiency virus type 1-infected dividing Jurkat T cells.Journal of virology · 1998Article
- A major human immunodeficiency virus type 1-initiated killing pathway distinct from apoptosis.Journal of virology · 1997Article
- Apoptosis: A Current Molecular Analysis.Pathology oncology research : POR · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite intensive investigation, no clearly defined mechanism explaining human immunodeficiency virus (HIV)-induced cell killing has emerged. HIV-1 infection is initiated through a high-affinity interaction between the HIV-1 external envelope glycoprotein (gp120) and the CD4 receptor on T cells. Cell killing is a later event intimately linked by in vitro genetic analyses with the fusogenic properties of the HIV envelope glycoprotein gp120 and transmembrane glycoprotein gp41. In this report, we describe aberrancies in cell cycle regulatory proteins initiated by cell-cell contact between T cells expressing HIV-1 envelope glycoproteins and other T cells expressing CD4 receptors. Cells rapidly accumulate cyclin B protein and tyrosine-hyperphosphorylated p34cdc2 (cdk1) kinase, indicative of cell cycle arrest at G2 phase. Moreover, these cells continue to synthesize cyclin B protein, enlarge and display an abnormal ballooned morphology, and disappear from the cultures in a pattern previously described for cytotoxicity induced by DNA synthesis (S phase) inhibitors. Similar changes are observed in peripheral blood mononuclear cells infected in vitro with pathogenic primary isolates of HIV-1.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.