Benzolactam-related compounds promote apoptosis of HIV-infected human cells via protein kinase C–induced HIV latency reversal - Matsuda, Kouki; Kobayakawa, Takuya; Tsuchiya, Kiyoto; Hattori, Shin-ichiro; Nomura, Wataru; Gatanaga, Hiroyuki; Yoshimura, Kazuhisa; Oka, Shinichi; Endo, Yasuyuki; Tamamura, Hirokazu; Mitsuya, Hiroaki; Maeda, Kenji (The Journal of biological chemistry, 2019)
Keywords: antiviral agent; apoptosis; Apoptosis - drug effects; Benzodiazepinones - pharmacology; benzolactam; Caspase 3 - biosynthesis; Caspase 3 - genetics; CD4-Positive T-Lymphocytes - metabolism; CD4-Positive T-Lymphocytes - pathology; CD4-Positive T-Lymphocytes - virology; Cell Cycle Proteins; Developmental Biology; Female; Gene Expression Regulation, Enzymologic - drug effects; HIV cure; HIV Infections - genetics; HIV Infections - metabolism; HIV Infections - pathology; HIV-1 - physiology; human immunodeficiency virus (HIV); Humans; latency-reversing agents; latent infection; Male; Nuclear Proteins - antagonists & inhibitors; Nuclear Proteins - genetics; Nuclear Proteins - metabolism; PKC activator; protein kinase C (PKC); Protein Kinase C - genetics; Protein Kinase C - metabolism; retrovirus; Transcription Factors - antagonists & inhibitors; Transcription Factors - genetics; Transcription Factors - metabolism; Virus Latency - drug effects; retrovirus; benzolactam; human immunodeficiency virus (HIV); protein kinase C (PKC); PKC activator; apoptosis; antiviral agent; latency-reversing agents; latent infection; HIV cure