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https://doi.org/10.1186/1742-4690-10-101
Title: | Immune adaptor ADAP in T cells regulates HIV-1 transcription and cell-cell viral spread via different co-receptors | Authors: | Wei, B Han, L Abbink, T.E.M Groppelli, E Lim, D Thaker, Y.R Gao, W Zhai, R Wang, J Lever, A Jolly, C Wang, H Rudd, C.E |
Keywords: | adaptor protein adhesion and degranulation promoting adaptor protein CD28 antigen chemokine receptor CCR5 chemokine receptor CXCR4 glycoprotein immunoglobulin enhancer binding protein lymphocyte function associated antigen 1 protein SH2 small interfering RNA transcription factor NFAT unclassified drug article cell adhesion cell proliferation conjugation cooperation dendritic cell down regulation genetic transcription human human cell Human immunodeficiency virus 1 immunocompetent cell long terminal repeat nonhuman protein binding protein expression T lymphocyte virus transcription Human immunodeficiency virus 1 Adaptor Proteins, Signal Transducing Cell Adhesion HIV-1 Humans Lymphocyte Function-Associated Antigen-1 Phosphoproteins T-Lymphocytes Transcription, Genetic Virus Replication |
Issue Date: | 2013 | Citation: | Wei, B, Han, L, Abbink, T.E.M, Groppelli, E, Lim, D, Thaker, Y.R, Gao, W, Zhai, R, Wang, J, Lever, A, Jolly, C, Wang, H, Rudd, C.E (2013). Immune adaptor ADAP in T cells regulates HIV-1 transcription and cell-cell viral spread via different co-receptors. Retrovirology 10 (1) : 101. ScholarBank@NUS Repository. https://doi.org/10.1186/1742-4690-10-101 | Rights: | Attribution 4.0 International | Abstract: | Background: Immune cell adaptor protein ADAP (adhesion and degranulation-promoting adaptor protein) mediates aspects of T-cell adhesion and proliferation. Despite this, a connection between ADAP and infection by the HIV-1 (human immunodeficiency virus-1) has not been explored.Results: In this paper, we show for the first time that ADAP and its binding to SLP-76 (SH2 domain-containing leukocyte protein of 76 kDa) regulate HIV-1 infection via two distinct mechanisms and co-receptors. siRNA down-regulation of ADAP, or expression of a mutant that is defective in associating to its binding partner SLP-76 (termed M12), inhibited the propagation of HIV-1 in T-cell lines and primary human T-cells. In one step, ADAP and its binding to SLP-76 were needed for the activation of NF-?B and its transcription of the HIV-1 long terminal repeat (LTR) in cooperation with ligation of co-receptor CD28, but not LFA-1. In a second step, the ADAP-SLP-76 module cooperated with LFA-1 to regulate conjugate formation between T-cells and dendritic cells or other T-cells as well as the development of the virological synapse (VS) and viral spread between immune cells.Conclusions: These findings indicate that ADAP regulates two steps of HIV-1 infection cooperatively with two distinct receptors, and as such, serves as a new potential target in the blockade of HIV-1 infection. © 2013 Wei et al.; licensee BioMed Central Ltd. | Source Title: | Retrovirology | URI: | https://scholarbank.nus.edu.sg/handle/10635/181802 | ISSN: | 17424690 | DOI: | 10.1186/1742-4690-10-101 | Rights: | Attribution 4.0 International |
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