ArticleJournal of immunology (Baltimore, Md. : 1950)2012
The adaptor protein SLP-76 regulates HIV-1 release and cell-to-cell transmission in T cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Dynamic response landscape of immune cells identified immune dysfunction which predicts disease progression in COVID-19 infected patients.International journal of biological sciences · 2022Article
- Proteo-Transcriptomic Dynamics of Cellular Response to HIV-1 Infection.Scientific reports · 2019Article
- Immune adaptor ADAP in T cells regulates HIV-1 transcription and cell-cell viral spread via different co-receptors.Retrovirology · 2013Article
- N-terminal Slit2 inhibits HIV-1 replication by regulating the actin cytoskeleton.Retrovirology · 2013Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
HIV-1 infection in T cells is regulated by TCR activation. However, the cellular proteins of the TCR pathway that regulate HIV-1 infection are poorly characterized. In this study, in HIV-1 infection, we observed a significant reduction of HIV-1 virus production in Src homology 2 domain-containing leukocyte protein of 76 kDa (SLP-76)-deficient Jurkat T cells compared with wild-type and SLP-76-reconstituted Jurkat T cells. We further confirmed the role of SLP-76 in HIV-1 infection by small interfering RNA-mediated knockdown in MT4 cells and PBMCs. Structural-functional analysis revealed that the N-terminal domain of SLP-76 was important for regulating HIV-1 infection. Further mechanistic studies revealed that lack of SLP-76 impaired virus release, but did not affect viral entry, integration, and transcription. We also showed that SLP-76 plays a critical role in cell-to-cell transmission of HIV-1. Signaling studies revealed that SLP-76 associated with viral negative regulatory factor protein and multiple signaling molecules during HIV-1 infection. Furthermore, SLP-76 facilitated the association of negative regulatory factor and F-actin, suggesting that SLP-76 mediates the formation of a signaling complex that may regulate viral release via cytoskeletal changes. Taken together, our studies demonstrate a novel role for the adaptor molecule SLP-76 in regulating HIV-1 infection in T cells with the potential to develop innovative strategies against HIV-1.
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