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1.
Figure 2

Figure 2. From: Potent and Selective Photo-inactivation of Proteins With Peptoid-Ruthenium Conjugates.

A hyper-potent CALI inhibitor of VEGFR2. (a) Chemical structure of RuGU40C4. The modified Ru(II) (bpy) 2+3 complex and GU40C4 peptoid are shown in red and blue, respectively. (b) Dose-dependent inhibition of VEGF-induced autophosphorylation of VEGFR2 on PAE/KDR cells by RuGU40C4 with irradiation (10 min).

Jiyong Lee, et al. Nat Chem Biol. ;6(4):258-260.
2.
Figure 3

Figure 3. From: Potent and Selective Photo-inactivation of Proteins With Peptoid-Ruthenium Conjugates.

Visible light-triggered inactivation of the 26S proteasome by a ruthenium-peptoid conjugate. (a) Illustration of the 26S proteasome and gate opening of the 20S proteasome. (b) Chemical structure of RuRIP1. The modified Ru(II) (bpy) 2+3 complex and RIP1 peptoid are shown in red and blue, respectively. (c) Chymotrypsin-like peptidase activity of purified, yeast 26S proteasome was measured in the presence of RuRIP1 with or without irradiation by monitoring the cleavage of fluorogenic substrate, Suc-LLVY-AMC. (d) The effect of RuRIP1 on chymotrypsin-like activity of the 26S proteasome in HeLa cells with or without irradiation (30 min) was assessed by measuring luminescence generated by substrate (Suc-LLVY-aminoluciferin) cleavage.

Jiyong Lee, et al. Nat Chem Biol. ;6(4):258-260.
3.
Figure 1

Figure 1. From: Potent and Selective Photo-inactivation of Proteins With Peptoid-Ruthenium Conjugates.

Visible light-triggered inactivation of the Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) by a ruthenium-peptoid conjugate. (a) Chemical structure of RuGU40C. The modified Ru(II)(bpy)32+ complex and the GU40C peptoid are shown in red and blue, respectively. (b) Western blots showing the level of phospho-VEGFR2 (the active form of the receptor) and total VEGFR2 after receptor-expressing cells (PAE/KDR) were incubated under the conditions indicated. The duration of irradiation was 10 minutes. FGU40C = fluorescein-conjugated GU40C (see Supplementary Fig. 2). RuCON = a Ru(II)(bpy)32+-conjugated control peptoid that does not bind VEGFR2 (see Supplementary Fig. 2). (c) Dose-dependence of the inhibition of autophosphorylation of VEGFR2 by RuGU40C with or without irradiation. (d) Effect of ruthenium-peptoid conjugates on the VEGF-induced formation of tubes by human umbilical vascular endothelial cells (HUVECs). HUVECs on Matrigel-coated plates were incubated under the conditions indicated and irradiated (10 min). 16hr after the addition of VEGF, degree of tube formation was evaluated by quantitative analysis (AngioQuant software) of images obtained using a light microscope (see Fig S3 for representative images). (e) Analysis of the specificity of RuGU40C-mediated inhibition of VEGFR2. The effect of the ruthenium-peptoid conjugate on hormone-mediated autophosphorylation (activation) of VEGFR2 or EGFR was examined by western blot in the presence or absence of irradiation (10 min) in cells that express both receptors (H441) and evaluated by quantitative analysis (Image J). Note that there is a basal level of phosph-VEGFR2 present even in the absence of VEGF treatment.

Jiyong Lee, et al. Nat Chem Biol. ;6(4):258-260.

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