Sandbox Reserved 1122: Difference between revisions
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=== IP3R inhibition === | === IP3R inhibition === | ||
Bcl-2 localized at the ER membrane participates in the control of Ca2+ content and release. The inositol 1,4,5-trisphosphate receptor (IP3R) is the Ca2+ release channel localized in the ER. Its pro-apoptotic activity can be directly inhibited by Bcl-2, its homology domain 4 (BH4) being essential for this effect. <scene name='71/719863/Scenelucas/1'>BH4</scene> comprises 20 amino acids organized in alpha-helical structure which is required to inhibit IP3R. Residues K17, H20, Y21 and R26 participate in the inhibition of IP3R because they are very accessible and proximal in the secondary structure. <ref> [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3795776/ Alpha-Helical Destabilization of the Bcl-2-BH4-Domain Peptide Abolishes Its Ability to Inhibit the IP3 Receptor]</ref> | Bcl-2 localized at the ER membrane participates in the control of Ca2+ content and release. The inositol 1,4,5-trisphosphate receptor (IP3R) is the Ca2+ release channel localized in the ER. Its pro-apoptotic activity can be directly inhibited by Bcl-2, its homology domain 4 (BH4) being essential for this effect. <scene name='71/719863/Scenelucas/1'>BH4</scene> comprises 20 amino acids organized in alpha-helical structure which is required to inhibit IP3R. Residues <scene name='71/719863/Sceneip3inter/1'>K17, H20, Y21 and R26'</scene> participate in the inhibition of IP3R because they are very accessible and proximal in the secondary structure. <ref> [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3795776/ Alpha-Helical Destabilization of the Bcl-2-BH4-Domain Peptide Abolishes Its Ability to Inhibit the IP3 Receptor]</ref> | ||
=== Regulation of the mitochondrial pathway of apoptosis === | === Regulation of the mitochondrial pathway of apoptosis === | ||
