4pgs: Difference between revisions

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<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4pgs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4pgs OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4pgs RCSB], [http://www.ebi.ac.uk/pdbsum/4pgs PDBsum]</span></td></tr>
<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4pgs FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4pgs OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4pgs RCSB], [http://www.ebi.ac.uk/pdbsum/4pgs PDBsum]</span></td></tr>
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== Publication Abstract from PubMed ==
Calcium homeostasis balances passive calcium leak and active calcium uptake. Human Bax inhibitor-1 (hBI-1) is an antiapoptotic protein that mediates a calcium leak and is representative of a highly conserved and widely distributed family, the transmembrane Bax inhibitor motif (TMBIM) proteins. Here, we present crystal structures of a bacterial homolog and characterize its calcium leak activity. The structure has a seven-transmembrane-helix fold that features two triple-helix sandwiches wrapped around a central C-terminal helix. Structures obtained in closed and open conformations are reversibly interconvertible by change of pH. A hydrogen-bonded, pKa (where Ka is the acid dissociation constant)-perturbed pair of conserved aspartate residues explains the pH dependence of this transition, and biochemical studies show that pH regulates calcium influx in proteoliposomes. Homology models for hBI-1 provide insights into TMBIM-mediated calcium leak and cytoprotective activity.
Structural basis for a pH-sensitive calcium leak across membranes.,Chang Y, Bruni R, Kloss B, Assur Z, Kloppmann E, Rost B, Hendrickson WA, Liu Q Science. 2014 Jun 6;344(6188):1131-5. doi: 10.1126/science.1252043. PMID:24904158<ref>PMID:24904158</ref>
From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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== References ==
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