Initiation of transcription and translation elongation at the HIV-1 LTR (WP3414)
Following cellular activation or drug treatment, NFAT and NF-kB translocate to the nucleus and bind sites at the HIV-1 LTR. NFAT and NF-kB recruit p300/CBP to the LTR, resulting in acetylation of histone tails and transcriptional activation. In the case of NF-kB, proteosomal degradation of IkBa permits NF-kB translocation and displacement of the p50 homodimers. This is followed by Tat- dependent elongation in which Tat recruits the P-TEFb complex to TAR. Cdk9 phosphorylates the CTD of RNA Pol II, resulting in increased processivity. P-TEFb phosphorylates DSIF and NELF, resulting in removal of NELF from Pol II and converting DSIF into a positive elongation factor, thereby promoting productive elongation. Data nodes in blue represent HIV proteins. Proteins on this pathway have targeted assays available via the [https://assays.cancer.gov/available_assays?wp_id=WP3414 CPTAC Assay Portal]
AuthorsKristina Hanspers and Andika Tan
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Disease Ontologyhuman immunodeficiency virus infectious disease
- An integrated overview of HIV-1 latency. Ruelas DS, Greene WC. Cell. 2013 Oct 24;155(3):519–29. PubMed Europe PMC Scholia