6f08

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'''Unreleased structure'''
 
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The entry 6f08 is ON HOLD until Paper Publication
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==14-3-3 zeta in complex with the human Son of sevenless homolog 1 (SOS1)==
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<StructureSection load='6f08' size='340' side='right' caption='[[6f08]], [[Resolution|resolution]] 1.90&Aring;' scene=''>
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== Structural highlights ==
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<table><tr><td colspan='2'>[[6f08]] is a 8 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6F08 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6F08 FirstGlance]. <br>
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</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=1PE:PENTAETHYLENE+GLYCOL'>1PE</scene></td></tr>
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<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>
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<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=6f08 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6f08 OCA], [http://pdbe.org/6f08 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6f08 RCSB], [http://www.ebi.ac.uk/pdbsum/6f08 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6f08 ProSAT]</span></td></tr>
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</table>
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== Disease ==
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[[http://www.uniprot.org/uniprot/SOS1_HUMAN SOS1_HUMAN]] Defects in SOS1 are the cause of gingival fibromatosis 1 (GGF1) [MIM:[http://omim.org/entry/135300 135300]]; also known as GINGF1. Gingival fibromatosis is a rare overgrowth condition characterized by a benign, slowly progressive, nonhemorrhagic, fibrous enlargement of maxillary and mandibular keratinized gingiva. GGF1 is usually transmitted as an autosomal dominant trait, although sporadic cases are common.<ref>PMID:11868160</ref> Defects in SOS1 are the cause of Noonan syndrome type 4 (NS4) [MIM:[http://omim.org/entry/610733 610733]]. NS4 is an autosomal dominant disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis. It is a genetically heterogeneous and relatively common syndrome, with an estimated incidence of 1 in 1000-2500 live births. Rarely, NS4 is associated with juvenile myelomonocytic leukemia (JMML). SOS1 mutations engender a high prevalence of pulmonary valve disease; atrial septal defects are less common.<ref>PMID:17143285</ref> <ref>PMID:17143282</ref> <ref>PMID:19020799</ref> <ref>PMID:19438935</ref> <ref>PMID:20683980</ref> <ref>PMID:20673819</ref> <ref>PMID:19953625</ref> <ref>PMID:21387466</ref>
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== Function ==
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[[http://www.uniprot.org/uniprot/1433Z_HUMAN 1433Z_HUMAN]] Adapter protein implicated in the regulation of a large spectrum of both general and specialized signaling pathways. Binds to a large number of partners, usually by recognition of a phosphoserine or phosphothreonine motif. Binding generally results in the modulation of the activity of the binding partner.<ref>PMID:9360956</ref> <ref>PMID:14578935</ref> <ref>PMID:15071501</ref> <ref>PMID:15644438</ref> <ref>PMID:16376338</ref> [[http://www.uniprot.org/uniprot/SOS1_HUMAN SOS1_HUMAN]] Promotes the exchange of Ras-bound GDP by GTP.
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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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The deviant Ras activation machinery is found in approximately 30% of all human cancers. SOS1 is an important protagonist of this pathway that plays a key-role in aberrant cell proliferation and differentiation. Interaction of SOS1 with 14-3-3 proteins modulates SOS1 activity in Ras-MAPK signaling. In the present study, we analyze the 14-3-3/SOS1 protein-protein interaction (PPI) by different biochemical assays and report the high resolution crystal structure of a 13-mer motif of SOS1 bound to 14-3-3zeta. These structural and functional insights are important for the evaluation of this PPI interface for small-molecule stabilization as a new starting point for modulating the Ras-Raf-MAPK pathway.
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Authors:
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Structural characterization of 14-3-3zeta in complex with the human Son of sevenless homolog 1 (SOS1).,Ballone A, Centorrino F, Wolter M, Ottmann C J Struct Biol. 2018 Feb 1. pii: S1047-8477(18)30026-1. doi:, 10.1016/j.jsb.2018.01.011. PMID:29408703<ref>PMID:29408703</ref>
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Description:
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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[[Category: Unreleased Structures]]
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</div>
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<div class="pdbe-citations 6f08" style="background-color:#fffaf0;"></div>
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== References ==
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<references/>
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__TOC__
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</StructureSection>
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[[Category: Ballone, A]]
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[[Category: Centorrino, F]]
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[[Category: Guo, S]]
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[[Category: Leysen, S]]
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[[Category: Ottmann, C]]
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[[Category: 14-3-3]]
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[[Category: Dimer]]
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[[Category: Peptide binding protein]]
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[[Category: Phosphosite]]
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[[Category: Sos1]]

Revision as of 06:36, 15 February 2018

14-3-3 zeta in complex with the human Son of sevenless homolog 1 (SOS1)

6f08, resolution 1.90Å

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