Abstract:
:Human immunodeficiency virus (HIV)-infected cells actively release the transcriptional activator (Tat) viral protein that is required for efficient HIV gene transcription. Extracellular Tat is able to enter uninfected cells. We recently reported that internalized Tat escapes endosomes to reach the cytosol and is then recruited to the plasma membrane by phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2). As a consequence, Tat strongly impairs different critical cellular functions in several cell types. Here we will review recent evidences showing that Tat, by affecting the interaction of key cellular effectors with PtdIns(4,5)P2, blocks exocytosis from neuroendocrine cells, perturbs the synaptic vesicle exo-endocytosis cycle, prevents efficient phagocytosis by macrophages, and alters potassium channel activity in cardiac cells. Potential mechanistic aspects of Tat effects on these cellular processes will be discussed.
journal_name
Biochimiejournal_title
Biochimieauthors
Beaumelle B,Tóth P,Malak OA,Chopard C,Loussouarn G,Vitale Ndoi
10.1016/j.biochi.2017.05.014subject
Has Abstractpub_date
2017-10-01 00:00:00pages
80-85eissn
0300-9084issn
1638-6183pii
S0300-9084(17)30125-6journal_volume
141pub_type
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