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Figure 2 | Retrovirology

Figure 2

From: A Cyclin T1 point mutation that abolishes positive transcription elongation factor (P-TEFb) binding to Hexim1 and HIV tat

Figure 2

Positioning of Cyclin T1 mutations on the 3D structure of P-TEFb. (A), (B), (C) and (D) Cyclin T1 mutations were localised on P-TEFb.ATP (pdb3blq) and (E) and (F) on Tat.P-TEFb.ATP (pdb3MIA) 3D structures. The N-terminal cyclin fold is in pale yellow, the C-terminal one is in pale cyan and Tat is in pink. Mutations are coloured according to their 2-hybrid interaction phenotype (Figure 1B); in red [Cdk9(+++); Hexim1(−)], orange [Cdk9(+++); Hexim1(+)], brown [Cdk9(+); Hexim1(−)] and black [Cdk9(−); Hexim1(−)]. Targeted mutagenesis of K168 and D169 provided [Cdk9(+++); Hexim1(−)] interaction phenotypes. (G) Aromatic residues in the funnel formed by helices in N-terminal and C-terminal Cyclin folds. Position of Cyclin T1 mutations on helices H1 (yellow), H2 (green), H1′ (cyan) and H2′ (marine) of P-TEFb.ATP (pdb3blq) structure; (H) and (I) H-bond network linking the cyclin fold helices to Y175 in P-TEFb.ATP (pdb3blq) and Tat.P-TEFb.ATP (pdb3MIA), respectively.

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