Sandbox Reserved 1122: Difference between revisions
From Proteopedia
Jump to navigationJump to search
No edit summary |
No edit summary |
||
| Line 13: | Line 13: | ||
=== IP3R inhibition === | === IP3R inhibition === | ||
Bcl-2 localized at the endoplasmic reticulum (ER) membranes participates in the control of Ca2+ content and release. The inositol 1,4,5-trisphosphate receptor (IP3R) which is the primary Ca2+ release channel localized in the ER. Its pro-apoptotic activity can be directly inhibited by the Bcl-2, homology domain 4 (BH4) being essential and sufficient for this effect. BH4 comprises 20 amino acids (10-30) 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. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3795776/] | Bcl-2 localized at the endoplasmic reticulum (ER) membranes participates in the control of Ca2+ content and release. The inositol 1,4,5-trisphosphate receptor (IP3R) which is the primary Ca2+ release channel localized in the ER. Its pro-apoptotic activity can be directly inhibited by the Bcl-2, homology domain 4 (BH4) being essential and sufficient for this effect. BH4 comprises 20 amino acids (10-30) 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> | ||
=== Regulation of the mitochondrial pathway of apoptosis === | === Regulation of the mitochondrial pathway of apoptosis === | ||
