3f7b: Difference between revisions
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<StructureSection load='3f7b' size='340' side='right'caption='[[3f7b]], [[Resolution|resolution]] 2.05Å' scene=''> | <StructureSection load='3f7b' size='340' side='right'caption='[[3f7b]], [[Resolution|resolution]] 2.05Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[3f7b]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/ | <table><tr><td colspan='2'>[[3f7b]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3F7B OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3F7B FirstGlance]. <br> | ||
</td></tr><tr id=' | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.05Å</td></tr> | ||
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=AG5:N-(2-PHENYLETHYL)-2-(PHENYLSULFANYL)-5-SULFAMOYLPYRIDINE-3-CARBOXAMIDE'>AG5</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr> | |||
<tr id=' | |||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3f7b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3f7b OCA], [https://pdbe.org/3f7b PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3f7b RCSB], [https://www.ebi.ac.uk/pdbsum/3f7b PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3f7b ProSAT]</span></td></tr> | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3f7b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3f7b OCA], [https://pdbe.org/3f7b PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3f7b RCSB], [https://www.ebi.ac.uk/pdbsum/3f7b PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3f7b ProSAT]</span></td></tr> | ||
</table> | </table> | ||
== Disease == | == Disease == | ||
[https://www.uniprot.org/uniprot/CAH4_HUMAN CAH4_HUMAN] Defects in CA4 are the cause of retinitis pigmentosa type 17 (RP17) [MIM:[https://omim.org/entry/600852 600852]. RP leads to degeneration of retinal photoreceptor cells. Patients typically have night vision blindness and loss of midperipheral visual field. As their condition progresses, they lose their far peripheral visual field and eventually central vision as well. RP17 inheritance is autosomal dominant. Note=Defective acid overload removal from retina and retinal epithelium, due to mutant CA4, is responsible for photoreceptor degeneration, indicating that impaired pH homeostasis is the most likely cause underlying the RP17 phenotype.<ref>PMID:15563508</ref> | |||
== Function == | == Function == | ||
[https://www.uniprot.org/uniprot/CAH4_HUMAN CAH4_HUMAN] Reversible hydration of carbon dioxide. May stimulate the sodium/bicarbonate transporter activity of SLC4A4 that acts in pH homeostasis. It is essential for acid overload removal from the retina and retina epithelium, and acid release in the choriocapillaris in the choroid.<ref>PMID:15563508</ref> | |||
== Evolutionary Conservation == | == Evolutionary Conservation == | ||
[[Image:Consurf_key_small.gif|200px|right]] | [[Image:Consurf_key_small.gif|200px|right]] | ||
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__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: | [[Category: Homo sapiens]] | ||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Ferre | [[Category: Ferre RAA]] | ||
[[Category: Greasley | [[Category: Greasley SE]] | ||
[[Category: Pauly | [[Category: Pauly TA]] | ||
[[Category: Paz | [[Category: Paz R]] | ||
Latest revision as of 09:42, 6 September 2023
Crystal Structure of soluble domain of CA4 in complex with small molecule.Crystal Structure of soluble domain of CA4 in complex with small molecule.
Structural highlights
DiseaseCAH4_HUMAN Defects in CA4 are the cause of retinitis pigmentosa type 17 (RP17) [MIM:600852. RP leads to degeneration of retinal photoreceptor cells. Patients typically have night vision blindness and loss of midperipheral visual field. As their condition progresses, they lose their far peripheral visual field and eventually central vision as well. RP17 inheritance is autosomal dominant. Note=Defective acid overload removal from retina and retinal epithelium, due to mutant CA4, is responsible for photoreceptor degeneration, indicating that impaired pH homeostasis is the most likely cause underlying the RP17 phenotype.[1] FunctionCAH4_HUMAN Reversible hydration of carbon dioxide. May stimulate the sodium/bicarbonate transporter activity of SLC4A4 that acts in pH homeostasis. It is essential for acid overload removal from the retina and retina epithelium, and acid release in the choriocapillaris in the choroid.[2] Evolutionary Conservation Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf. Publication Abstract from PubMedA novel series of potent thioether benzenesulfonamide inhibitors of carbonic anhydrases II and IV was discovered using structure-based drug design. Synthesis, structure-activity relationship, and optimization of physicochemical properties are described. Low nanomolar potency was achieved, and selected compounds with improved thermodynamic solubility showed promising in vitro inhibition of carbonic anhydrase activity in rabbit iris ciliary body homogenate. Thioether benzenesulfonamide inhibitors of carbonic anhydrases II and IV: structure-based drug design, synthesis, and biological evaluation.,Vernier W, Chong W, Rewolinski D, Greasley S, Pauly T, Shaw M, Dinh D, Ferre RA, Nukui S, Ornelas M, Reyner E Bioorg Med Chem. 2010 May 1;18(9):3307-19. Epub 2010 Mar 11. PMID:20363633[3] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. See AlsoReferences
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