1klc: Difference between revisions
m Protected "1klc" [edit=sysop:move=sysop] |
No edit summary |
||
| Line 1: | Line 1: | ||
{{STRUCTURE_1klc| PDB=1klc | SCENE= }} | {{STRUCTURE_1klc| PDB=1klc | SCENE= }} | ||
===SOLUTION STRUCTURE OF TGF-B1, NMR, MINIMIZED AVERAGE STRUCTURE=== | |||
{{ABSTRACT_PUBMED_8679613}} | |||
=== | ==Disease== | ||
[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Defects in TGFB1 are the cause of Camurati-Engelmann disease (CE) [MIM:[http://omim.org/entry/131300 131300]]; also known as progressive diaphyseal dysplasia 1 (DPD1). CE is an autosomal dominant disorder characterized by hyperostosis and sclerosis of the diaphyses of long bones. The disease typically presents in early childhood with pain, muscular weakness and waddling gait, and in some cases other features such as exophthalmos, facial paralysis, hearing difficulties and loss of vision.<ref>PMID:10973241</ref><ref>PMID:11062463</ref><ref>PMID:12493741</ref><ref>PMID:12843182</ref><ref>PMID:15103729</ref> | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/TGFB1_HUMAN TGFB1_HUMAN]] Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts. | |||
==About this Structure== | ==About this Structure== | ||
| Line 11: | Line 13: | ||
==Reference== | ==Reference== | ||
<ref group="xtra">PMID:008679613</ref><references group="xtra"/> | <ref group="xtra">PMID:008679613</ref><references group="xtra"/><references/> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Archer, S J.]] | [[Category: Archer, S J.]] | ||