By Marek Los, Henning Walczak
The amount bargains perception into the main learn issues that contain caspases. major specialists from numerous components of biology and drugs have compiled this quantity in order that either the beginner and the pro will use this because the major reference for caspases for years yet to come. The reader will know about the function of caspases in apoptosis signaling, irritation and melanoma treatment whereas being up-to-date at the technique used to review caspases and the efforts of pharmaceutical study in concentrating on caspases.
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Extra info for Caspases: Their Role in Cell Death and Cell Survival (Molecular Biology Intelligence Unit)
Nature 1992; 356:768-774. 5. Ellis HM, Horvitz HR. Genetic control of programmed cell death in the nematode C. elegans. Cell 1986; 44:817-29. 6. Yuan J, Shaham S, Ledoux S et al. The C. elegans cell death gene ced-3 encodes a protein similar to mammalian interleukin-1 beta-converting enzyme. Cell 1993; 75:641-652. 7. Adams JM, Cory S. Life-or-death decisions by the Bcl-2 protein family. Trends Biochem Sci 2001; 26:61-66. 8. Fernandes-Alnemri T, Litwack G, Alnemri ES. Mch2, a new member of the apoptotic Ced-3/Ice cysteine protease gene family.
The catalytic mechanism occurs in steps (Fig. 6). First, His237 in the catalytic diad acts as the general base attracting a proton from Cys285 and thus enhances the nucleophilic property of the latter (Fig. 6A). Then, Cys285 attacks the P1 amide bond of the substrate thereby inducing formation of the tetrahedral intermediate. At this stage the substrate is covalently attached to the catalytic cysteine that has lost its nucleophilic property (Fig. 6B). Next, the C-terminal peptide of the substrate is released from the complex, while the peptide N-terminal of the scissile bond and the enzyme form an acyl-enzyme complex (Fig.
165,166 By replacing the tetrapeptide pseudosubstrate LVAD in CrmA with the substrate recognition site DQMD from the promiscuous caspase inhibitor baculovirus p35 (see below), it became clear that this tetrapeptide, by large, determines the specificity of CrmA for its target caspase. 167-169 Interfering with both apoptosis and inflammation can be considered beneficial for the virus. 176 The activity of most caspases, including mammalian caspases and CED-3, can be blocked by p35 with Ki values as low as 100 pM (Table 7).