6rav: Difference between revisions

<table><tr><td colspan='2'>[[6rav]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. This structure supersedes the now removed PDB entry [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=6qsv 6qsv]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6RAV OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6RAV FirstGlance]. <br>

</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.7&#8491;</td></tr>

<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=JGQ:4-[(2~{S},4~{S})-4-ethoxy-1-[(5-methoxy-7-methyl-1~{H}-indol-4-yl)methyl]piperidin-2-yl]benzoic+acid'>JGQ</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></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=6rav FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6rav OCA], [https://pdbe.org/6rav PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6rav RCSB], [https://www.ebi.ac.uk/pdbsum/6rav PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6rav ProSAT]</span></td></tr>

[https://www.uniprot.org/uniprot/CFAB_HUMAN CFAB_HUMAN] Defects in CFB are a cause of susceptibility to hemolytic uremic syndrome atypical type 4 (AHUS4) [MIM:[https://omim.org/entry/612924 612924]. An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Note=Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype.<ref>PMID:17182750</ref> <ref>PMID:20513133</ref>  

[https://www.uniprot.org/uniprot/CFAB_HUMAN CFAB_HUMAN] Factor B which is part of the alternate pathway of the complement system is cleaved by factor D into 2 fragments: Ba and Bb. Bb, a serine protease, then combines with complement factor 3b to generate the C3 or C5 convertase. It has also been implicated in proliferation and differentiation of preactivated B-lymphocytes, rapid spreading of peripheral blood monocytes, stimulation of lymphocyte blastogenesis and lysis of erythrocytes. Ba inhibits the proliferation of preactivated B-lymphocytes.

[[Category: Homo sapiens]]

[[Category: Adams CM]]

[[Category: Anderson K]]

[[Category: Argikar U]]

[[Category: Crowley M]]

[[Category: Cumin F]]

[[Category: Eder J]]

[[Category: Ehara T]]

[[Category: Erbel P]]

[[Category: Flohr S]]

[[Category: Gerhartz B]]

[[Category: Harrison R]]

[[Category: Hughes N]]

[[Category: Jaffee B]]

[[Category: Karki R]]

[[Category: Mac Sweeney A]]

[[Category: Maibaum J]]

[[Category: Mainolfi N]]

[[Category: Mogi M]]

[[Category: Sedrani R]]

[[Category: Sellner H]]

[[Category: Sirockin F]]

[[Category: Smith TM]]

[[Category: Valeur E]]

[[Category: Wiesmann C]]