1dle: Difference between revisions

<StructureSection load='1dle' size='340' side='right'caption='[[1dle]], [[Resolution|resolution]] 2.10&Aring;' scene=''>

<table><tr><td colspan='2'>[[1dle]] 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=1DLE OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1DLE 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]] 2.1&#8491;</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=1dle FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1dle OCA], [https://pdbe.org/1dle PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1dle RCSB], [https://www.ebi.ac.uk/pdbsum/1dle PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1dle ProSAT]</span></td></tr>

</table>

[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.

     <scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/dl/1dle_consurf.spt"</scriptWhenChecked>

     <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview03.spt</scriptWhenUnchecked>

</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1dle ConSurf].

[[Category: Carson M]]

[[Category: Jing H]]

[[Category: Macon KJ]]

[[Category: Moore D]]

[[Category: Narayana SV]]

[[Category: Volanakis JE]]

[[Category: Xu Y]]