1dle: Difference between revisions

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~~[[Image:1dle.png|left|200px]]~~

===FACTOR B SERINE PROTEASE DOMAIN===

==~~=FACTOR B SERINE PROTEASE DOMAIN~~===

==Disease==

[[http://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:[http://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>

~~{{ABSTRACT_PUBMED_10637221}}~~

==Function==

[[http://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.

==About this Structure==

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==Reference==

[[Category: Homo sapiens]]

[[Category: Carson, M.]]

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@@ Line 1: / Line 1: @@
-[[Image:1dle.png|left|200px]]
 {{STRUCTURE_1dle|  PDB=1dle  |  SCENE=  }}
+===FACTOR B SERINE PROTEASE DOMAIN===
+{{ABSTRACT_PUBMED_10637221}}
-===FACTOR B SERINE PROTEASE DOMAIN===
+==Disease==
+[[http://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:[http://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>
-{{ABSTRACT_PUBMED_10637221}}
+==Function==
+[[http://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.
 ==About this Structure==
@@ Line 11: / Line 13: @@
 ==Reference==
-<ref group="xtra">PMID:010637221</ref><references group="xtra"/>
+<ref group="xtra">PMID:010637221</ref><references group="xtra"/><references/>
 [[Category: Homo sapiens]]
 [[Category: Carson, M.]]