Initiation of transcription and translation elongation at the HIV-1 LTR (Homo sapiens)

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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.