1e88: Difference between revisions

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-[[Image:1e88.png|left|200px]]
 {{STRUCTURE_1e88|  PDB=1e88  |  SCENE=  }}
+===Solution structure of 6F11F22F2, a compact three-module fragment of the gelatin-binding domain of human fibronectin===
+{{ABSTRACT_PUBMED_11285216}}
-===Solution structure of 6F11F22F2, a compact three-module fragment of the gelatin-binding domain of human fibronectin===
+==Disease==
+[[http://www.uniprot.org/uniprot/FINC_HUMAN FINC_HUMAN]] Defects in FN1 are the cause of glomerulopathy with fibronectin deposits type 2 (GFND2) [MIM:[http://omim.org/entry/601894 601894]]; also known as familial glomerular nephritis with fibronectin deposits or fibronectin glomerulopathy. GFND is a genetically heterogeneous autosomal dominant disorder characterized clinically by proteinuria, microscopic hematuria, and hypertension that leads to end-stage renal failure in the second to fifth decade of life.<ref>PMID:18268355</ref>
-{{ABSTRACT_PUBMED_11285216}}
+==Function==
+[[http://www.uniprot.org/uniprot/FINC_HUMAN FINC_HUMAN]] Fibronectins bind cell surfaces and various compounds including collagen, fibrin, heparin, DNA, and actin. Fibronectins are involved in cell adhesion, cell motility, opsonization, wound healing, and maintenance of cell shape.<ref>PMID:8114919</ref><ref>PMID:11209058</ref><ref>PMID:15665290</ref><ref>PMID:19379667</ref>  Anastellin binds fibronectin and induces fibril formation. This fibronectin polymer, named superfibronectin, exhibits enhanced adhesive properties. Both anastellin and superfibronectin inhibit tumor growth, angiogenesis and metastasis. Anastellin activates p38 MAPK and inhibits lysophospholipid signaling.<ref>PMID:8114919</ref><ref>PMID:11209058</ref><ref>PMID:15665290</ref><ref>PMID:19379667</ref>
 ==About this Structure==
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 ==Reference==
-<ref group="xtra">PMID:011285216</ref><references group="xtra"/>
+<ref group="xtra">PMID:011285216</ref><references group="xtra"/><references/>
 [[Category: Homo sapiens]]
 [[Category: Boyd, J.]]