2ii0

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{{Seed}}
 
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[[Image:2ii0.png|left|200px]]
 
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==Crystal Structure of catalytic domain of Son of sevenless (Rem-Cdc25) in the absence of Ras==
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The line below this paragraph, containing "STRUCTURE_2ii0", creates the "Structure Box" on the page.
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<StructureSection load='2ii0' size='340' side='right'caption='[[2ii0]], [[Resolution|resolution]] 2.02&Aring;' scene=''>
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You may change the PDB parameter (which sets the PDB file loaded into the applet)
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== Structural highlights ==
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or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
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<table><tr><td colspan='2'>[[2ii0]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2II0 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2II0 FirstGlance]. <br>
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or leave the SCENE parameter empty for the default display.
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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.02&#8491;</td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2ii0 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2ii0 OCA], [https://pdbe.org/2ii0 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2ii0 RCSB], [https://www.ebi.ac.uk/pdbsum/2ii0 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2ii0 ProSAT]</span></td></tr>
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{{STRUCTURE_2ii0| PDB=2ii0 | SCENE= }}
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</table>
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== Disease ==
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[https://www.uniprot.org/uniprot/SOS1_HUMAN SOS1_HUMAN] Defects in SOS1 are the cause of gingival fibromatosis 1 (GGF1) [MIM:[https://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:[https://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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[https://www.uniprot.org/uniprot/SOS1_HUMAN SOS1_HUMAN] Promotes the exchange of Ras-bound GDP by GTP.
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== Evolutionary Conservation ==
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[[Image:Consurf_key_small.gif|200px|right]]
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Check<jmol>
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<jmolCheckbox>
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<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/ii/2ii0_consurf.spt"</scriptWhenChecked>
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<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
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<text>to colour the structure by Evolutionary Conservation</text>
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</jmolCheckbox>
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</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=2ii0 ConSurf].
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<div style="clear:both"></div>
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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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The Ras-specific guanine nucleotide-exchange factors Son of sevenless (Sos) and Ras guanine nucleotide-releasing factor 1 (RasGRF1) transduce extracellular stimuli into Ras activation by catalyzing the exchange of Ras-bound GDP for GTP. A truncated form of RasGRF1 containing only the core catalytic Cdc25 domain is sufficient for stimulating Ras nucleotide exchange, whereas the isolated Cdc25 domain of Sos is inactive. At a site distal to the catalytic site, nucleotide-bound Ras binds to Sos, making contacts with the Cdc25 domain and with a Ras exchanger motif (Rem) domain. This allosteric Ras binding stimulates nucleotide exchange by Sos, but the mechanism by which this stimulation occurs has not been defined. We present a crystal structure of the Rem and Cdc25 domains of Sos determined at 2.0-A resolution in the absence of Ras. Differences between this structure and that of Sos bound to two Ras molecules show that allosteric activation of Sos by Ras occurs through a rotation of the Rem domain that is coupled to a rotation of a helical hairpin at the Sos catalytic site. This motion relieves steric occlusion of the catalytic site, allowing substrate Ras binding and nucleotide exchange. A structure of the isolated RasGRF1 Cdc25 domain determined at 2.2-A resolution, combined with computational analyses, suggests that the Cdc25 domain of RasGRF1 is able to maintain an active conformation in isolation because the helical hairpin has strengthened interactions with the Cdc25 domain core. These results indicate that RasGRF1 lacks the allosteric activation switch that is crucial for Sos activity.
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===Crystal Structure of catalytic domain of Son of sevenless (Rem-Cdc25) in the absence of Ras===
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A Ras-induced conformational switch in the Ras activator Son of sevenless.,Freedman TS, Sondermann H, Friedland GD, Kortemme T, Bar-Sagi D, Marqusee S, Kuriyan J Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):16692-7. Epub 2006 Oct 30. PMID:17075039<ref>PMID:17075039</ref>
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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</div>
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<div class="pdbe-citations 2ii0" style="background-color:#fffaf0;"></div>
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==See Also==
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The line below this paragraph, {{ABSTRACT_PUBMED_17075039}}, adds the Publication Abstract to the page
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*[[Son of sevenless|Son of sevenless]]
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(as it appears on PubMed at http://www.pubmed.gov), where 17075039 is the PubMed ID number.
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== References ==
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<references/>
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{{ABSTRACT_PUBMED_17075039}}
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__TOC__
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</StructureSection>
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==Disease==
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Known disease associated with this structure: Fibromatosis, gingival OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=182530 182530]], Noonan syndrome 4 OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=182530 182530]]
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==About this Structure==
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2II0 is a [[Single protein]] structure of sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2II0 OCA].
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==Reference==
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A Ras-induced conformational switch in the Ras activator Son of sevenless., Freedman TS, Sondermann H, Friedland GD, Kortemme T, Bar-Sagi D, Marqusee S, Kuriyan J, Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):16692-7. Epub 2006 Oct 30. PMID:[http://www.ncbi.nlm.nih.gov/pubmed/17075039 17075039]
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[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
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[[Category: Single protein]]
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[[Category: Large Structures]]
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[[Category: Bar-Sagi, D.]]
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[[Category: Bar-Sagi D]]
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[[Category: Freedman, T S.]]
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[[Category: Freedman TS]]
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[[Category: Friedland, G D.]]
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[[Category: Friedland GD]]
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[[Category: Kortemme, T.]]
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[[Category: Kortemme T]]
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[[Category: Kuriyan, J.]]
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[[Category: Kuriyan J]]
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[[Category: Marqusee, S.]]
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[[Category: Marqusee S]]
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[[Category: Sondermann, H.]]
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[[Category: Sondermann H]]
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[[Category: Signaling protein]]
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Mon Jul 28 09:43:15 2008''
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Current revision

Crystal Structure of catalytic domain of Son of sevenless (Rem-Cdc25) in the absence of Ras

PDB ID 2ii0

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