ArticleThe Journal of cell biology1994
HIV-1 transactivator protein Tat induces proliferation and TGF beta expression in human articular chondrocytes.
Article in The Journal of cell biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 78 citations in OpenAlex.
- HIV-1 Tat-induced disruption of epithelial junctions and epithelial-mesenchymal transition of oral and genital epithelial cells lead to increased invasiveness of neoplastic cells and the spread of herpes simplex virus and cytomegalovirus.Frontiers in immunology · 2025Review
- Viruses exploit growth factor mechanisms to achieve augmented pathogenicity and promote tumorigenesis.Archives of microbiology · 2024Review
- Effect of HIV-1 Tat on the formation of the mitotic spindle by interaction with ribosomal protein S3.Scientific reports · 2018Article
- Regulation of the Immune Response by TGF-β: From Conception to Autoimmunity and Infection.Cold Spring Harbor perspectives in biology · 2017Review
- HIV-1 Tat protein binds to TLR4-MD2 and signals to induce TNF-α and IL-10.Retrovirology · 2013Article
- HIV-1 Tat interacts with and regulates the localization and processing of amyloid precursor protein.PloS one · 2013Article
- GLI2 regulates TGF-β1 in human CD4+ T cells: implications in cancer and HIV pathogenesis.PloS one · 2012Article
- Effect of cocaine on human immunodeficiency virus-mediated pulmonary endothelial and smooth muscle dysfunction.American journal of respiratory cell and molecular biology · 2011Article
- Macrophage signaling in HIV-1 infection.Retrovirology · 2010Review
- HIV-Tat promotes cellular proliferation and inhibits NGF-induced differentiation through mechanisms involving Id1 regulation.Oncogene · 2004Article
- The active metabolite of leflunomide, A77 1726, increases the production of IL-1 receptor antagonist in human synovial fibroblasts and articular chondrocytes.Arthritis research & therapy · 2004Article
- Interferon beta stimulates interleukin 1 receptor antagonist production in human articular chondrocytes and synovial fibroblasts.Annals of the rheumatic diseases · 2004Article
- The expression of HIV-1 tat and nef genes induces cell-specific changes in growth properties and morphology of different types of rat cells.Cell proliferation · 2002Article
- Human immunodeficiency virus-1 tat induces hyperproliferation and dysregulation of renal glomerular epithelial cells.The American journal of pathology · 2002Article
- Production of interleukin-1 receptor antagonist by human articular chondrocytes.Arthritis research · 2002Article
- HIV-1 tat induced apoptosis of T-cells is not mediated by TGF-beta.Medical oncology (Northwood, London, England) · 2000Article
- Fibronectin modulates the effects of HIV-1 Tat on the growth of murine Kaposi's sarcoma-like cells through the down-regulation of tyrosine phosphorylation.The American journal of pathology · 1998Article
- Caprine arthritis encephalitis virus dysregulates the expression of cytokines in macrophages.Journal of virology · 1997Article
- Recombinant human immunodeficiency virus type 1 genomes with tat unconstrained by overlapping reading frames reveal residues in Tat important for replication in tissue culture.Journal of virology · 1996Article
- Activation of transcription factor NF-kappaB by the Tat protein of human immunodeficiency virus type 1.Journal of virology · 1996Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The human immunodeficiency virus-1 (HIV-1) protein Tat binds to cell surface antigens and can regulate cellular responses. Tat has similar immunosuppressive effects as transforming growth factor-beta (TGF beta) and both inhibit lymphocyte proliferation. TGF beta is expressed by primary human articular chondrocytes and is their most potent growth factor. The present study analyzed the interactions of TGF beta and HIV Tat in the regulation of human articular chondrocytes. Synthetic or recombinant full-length Tat (1-86) induced chondrocyte proliferation and this was of similar magnitude as the response to TGF beta. Tat peptides that did not contain the RGD motif had similar chondrocyte stimulatory activity as full-length Tat. Among a series of Tat peptides, peptide 38-62 which contains the basic domain was the only one active, suggesting that this region is responsible for the effects on chondrocyte proliferation. Full-length Tat and peptide 38-62 synergized with TGF beta and induced proliferative responses that were greater than those obtained with any combination of the known chondrocyte growth factors. Further characterization of the interactions between Tat and TGF beta showed that Tat increased synthesis and TGF beta activity and TGF beta 1 mRNA levels. The stimulatory effects of Tat and peptide 38-62 on chondrocyte proliferation were reduced by neutralizing antibodies to TGF beta and by TGF beta antisense oligonucleotides. These results identify a virally encoded protein and a synthetic peptide derived from it as novel and potent chondrocyte growth stimuli which act at least in part through the induction of TGF beta.
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