2dsq: Difference between revisions
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<StructureSection load='2dsq' size='340' side='right' caption='[[2dsq]], [[Resolution|resolution]] 2.80Å' scene=''> | <StructureSection load='2dsq' size='340' side='right' caption='[[2dsq]], [[Resolution|resolution]] 2.80Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[2dsq]] is a 6 chain structure with sequence from [http://en.wikipedia.org/wiki/ | <table><tr><td colspan='2'>[[2dsq]] is a 6 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2DSQ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2DSQ FirstGlance]. <br> | ||
</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1wqj|1wqj]], [[2dsp|2dsp]], [[2dsr|2dsr]]</td></tr> | </td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1wqj|1wqj]], [[2dsp|2dsp]], [[2dsr|2dsr]]</td></tr> | ||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2dsq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2dsq OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2dsq RCSB], [http://www.ebi.ac.uk/pdbsum/2dsq PDBsum]</span></td></tr> | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2dsq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2dsq OCA], [http://pdbe.org/2dsq PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2dsq RCSB], [http://www.ebi.ac.uk/pdbsum/2dsq PDBsum]</span></td></tr> | ||
</table> | </table> | ||
== Disease == | == Disease == | ||
[[http://www.uniprot.org/uniprot/ | [[http://www.uniprot.org/uniprot/IGF1_HUMAN IGF1_HUMAN]] Defects in IGF1 are the cause of insulin-like growth factor I deficiency (IGF1 deficiency) [MIM:[http://omim.org/entry/608747 608747]]. IGF1 deficiency is an autosomal recessive disorder characterized by growth retardation, sensorineural deafness and mental retardation. | ||
== Function == | == Function == | ||
[[http://www.uniprot.org/uniprot/IBP4_HUMAN IBP4_HUMAN]] IGF-binding proteins prolong the half-life of the IGFs and have been shown to either inhibit or stimulate the growth promoting effects of the IGFs on cell culture. They alter the interaction of IGFs with their cell surface receptors. [[http://www.uniprot.org/uniprot/IBP1_HUMAN IBP1_HUMAN]] IGF-binding proteins prolong the half-life of the IGFs and have been shown to either inhibit or stimulate the growth promoting effects of the IGFs on cell culture. They alter the interaction of IGFs with their cell surface receptors. Promotes cell migration.<ref>PMID:15972819</ref> [[http://www.uniprot.org/uniprot/ | [[http://www.uniprot.org/uniprot/IBP4_HUMAN IBP4_HUMAN]] IGF-binding proteins prolong the half-life of the IGFs and have been shown to either inhibit or stimulate the growth promoting effects of the IGFs on cell culture. They alter the interaction of IGFs with their cell surface receptors. [[http://www.uniprot.org/uniprot/IBP1_HUMAN IBP1_HUMAN]] IGF-binding proteins prolong the half-life of the IGFs and have been shown to either inhibit or stimulate the growth promoting effects of the IGFs on cell culture. They alter the interaction of IGFs with their cell surface receptors. Promotes cell migration.<ref>PMID:15972819</ref> [[http://www.uniprot.org/uniprot/IGF1_HUMAN IGF1_HUMAN]] The insulin-like growth factors, isolated from plasma, are structurally and functionally related to insulin but have a much higher growth-promoting activity. May be a physiological regulator of [1-14C]-2-deoxy-D-glucose (2DG) transport and glycogen synthesis in osteoblasts. Stimulates glucose transport in rat bone-derived osteoblastic (PyMS) cells and is effective at much lower concentrations than insulin, not only regarding glycogen and DNA synthesis but also with regard to enhancing glucose uptake.<ref>PMID:21076856</ref> | ||
== Evolutionary Conservation == | == Evolutionary Conservation == | ||
[[Image:Consurf_key_small.gif|200px|right]] | [[Image:Consurf_key_small.gif|200px|right]] | ||
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | ||
</div> | </div> | ||
<div class="pdbe-citations 2dsq" style="background-color:#fffaf0;"></div> | |||
==See Also== | ==See Also== | ||
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__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: | [[Category: Human]] | ||
[[Category: Holak, T A]] | [[Category: Holak, T A]] | ||
[[Category: Huber, R]] | [[Category: Huber, R]] |