3con: Difference between revisions

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<StructureSection load='3con' size='340' side='right'caption='[[3con]], [[Resolution|resolution]] 1.65&Aring;' scene=''>
<StructureSection load='3con' size='340' side='right'caption='[[3con]], [[Resolution|resolution]] 1.65&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[3con]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3CON OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3CON FirstGlance]. <br>
<table><tr><td colspan='2'>[[3con]] 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=3CON OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3CON FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=UNX:UNKNOWN+ATOM+OR+ION'>UNX</scene></td></tr>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.649&#8491;</td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">NRAS, HRAS1 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=UNX:UNKNOWN+ATOM+OR+ION'>UNX</scene></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3con FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3con OCA], [https://pdbe.org/3con PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3con RCSB], [https://www.ebi.ac.uk/pdbsum/3con PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3con ProSAT]</span></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3con FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3con OCA], [https://pdbe.org/3con PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3con RCSB], [https://www.ebi.ac.uk/pdbsum/3con PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3con ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[https://www.uniprot.org/uniprot/RASN_HUMAN RASN_HUMAN]] Defects in NRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:[https://omim.org/entry/607785 607785]]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia.  Defects in NRAS are the cause of Noonan syndrome type 6 (NS6) [MIM:[https://omim.org/entry/613224 613224]]. A syndrome characterized by facial dysmorphic features such as hypertelorism, a downward eyeslant and low-set posteriorly rotated ears. Other features can include short stature, a short neck with webbing or redundancy of skin, cardiac anomalies, deafness, motor delay and variable intellectual deficits.<ref>PMID:19966803</ref>  Defects in NRAS are the cause of autoimmune lymphoproliferative syndrome type 4 (ALPS4) [MIM:[https://omim.org/entry/614470 614470]]. A disorder of apoptosis, characterized by chronic accumulation of non-malignant lymphocytes, defective lymphocyte apoptosis, and an increased risk for the development of hematologic malignancies.<ref>PMID:17517660</ref>
[https://www.uniprot.org/uniprot/RASN_HUMAN RASN_HUMAN] Defects in NRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:[https://omim.org/entry/607785 607785]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia.  Defects in NRAS are the cause of Noonan syndrome type 6 (NS6) [MIM:[https://omim.org/entry/613224 613224]. A syndrome characterized by facial dysmorphic features such as hypertelorism, a downward eyeslant and low-set posteriorly rotated ears. Other features can include short stature, a short neck with webbing or redundancy of skin, cardiac anomalies, deafness, motor delay and variable intellectual deficits.<ref>PMID:19966803</ref>  Defects in NRAS are the cause of autoimmune lymphoproliferative syndrome type 4 (ALPS4) [MIM:[https://omim.org/entry/614470 614470]. A disorder of apoptosis, characterized by chronic accumulation of non-malignant lymphocytes, defective lymphocyte apoptosis, and an increased risk for the development of hematologic malignancies.<ref>PMID:17517660</ref>  
== Function ==
== Function ==
[[https://www.uniprot.org/uniprot/RASN_HUMAN RASN_HUMAN]] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.  
[https://www.uniprot.org/uniprot/RASN_HUMAN RASN_HUMAN] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
== Evolutionary Conservation ==
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
[[Image:Consurf_key_small.gif|200px|right]]
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__TOC__
__TOC__
</StructureSection>
</StructureSection>
[[Category: Human]]
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Large Structures]]
[[Category: Arrowsmith, C H]]
[[Category: Arrowsmith CH]]
[[Category: Bochkarev, A]]
[[Category: Bochkarev A]]
[[Category: Bountra, C]]
[[Category: Bountra C]]
[[Category: Edwards, A M]]
[[Category: Edwards AM]]
[[Category: Loppnau, P]]
[[Category: Loppnau P]]
[[Category: Nedyalkova, L]]
[[Category: Nedyalkova L]]
[[Category: Park, H]]
[[Category: Park H]]
[[Category: Structural genomic]]
[[Category: Shen L]]
[[Category: Shen, L]]
[[Category: Tempel W]]
[[Category: Tempel, W]]
[[Category: Tong Y]]
[[Category: Tong, Y]]
[[Category: Weigelt J]]
[[Category: Weigelt, J]]
[[Category: Disease mutation]]
[[Category: Gdp]]
[[Category: Golgi apparatus]]
[[Category: Gtp-binding]]
[[Category: Gtpase]]
[[Category: Hydrolase]]
[[Category: Lipoprotein]]
[[Category: Membrane]]
[[Category: Methylation]]
[[Category: Nucleotide-binding]]
[[Category: Oncogene]]
[[Category: Palmitate]]
[[Category: Prenylation]]
[[Category: Proto-oncogene]]
[[Category: Sgc]]

Latest revision as of 15:31, 30 August 2023

Crystal structure of the human NRAS GTPase bound with GDPCrystal structure of the human NRAS GTPase bound with GDP

Structural highlights

3con is a 1 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance.
Method:X-ray diffraction, Resolution 1.649Å
Ligands:, ,
Resources:FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT

Disease

RASN_HUMAN Defects in NRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:607785. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. Defects in NRAS are the cause of Noonan syndrome type 6 (NS6) [MIM:613224. A syndrome characterized by facial dysmorphic features such as hypertelorism, a downward eyeslant and low-set posteriorly rotated ears. Other features can include short stature, a short neck with webbing or redundancy of skin, cardiac anomalies, deafness, motor delay and variable intellectual deficits.[1] Defects in NRAS are the cause of autoimmune lymphoproliferative syndrome type 4 (ALPS4) [MIM:614470. A disorder of apoptosis, characterized by chronic accumulation of non-malignant lymphocytes, defective lymphocyte apoptosis, and an increased risk for the development of hematologic malignancies.[2]

Function

RASN_HUMAN Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.

Evolutionary Conservation

Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf.

References

  1. ↑ Cirstea IC, Kutsche K, Dvorsky R, Gremer L, Carta C, Horn D, Roberts AE, Lepri F, Merbitz-Zahradnik T, Konig R, Kratz CP, Pantaleoni F, Dentici ML, Joshi VA, Kucherlapati RS, Mazzanti L, Mundlos S, Patton MA, Silengo MC, Rossi C, Zampino G, Digilio C, Stuppia L, Seemanova E, Pennacchio LA, Gelb BD, Dallapiccola B, Wittinghofer A, Ahmadian MR, Tartaglia M, Zenker M. A restricted spectrum of NRAS mutations causes Noonan syndrome. Nat Genet. 2010 Jan;42(1):27-9. Epub 2009 Dec 6. PMID:19966803 doi:10.1038/ng.497
  2. ↑ Oliveira JB, Bidere N, Niemela JE, Zheng L, Sakai K, Nix CP, Danner RL, Barb J, Munson PJ, Puck JM, Dale J, Straus SE, Fleisher TA, Lenardo MJ. NRAS mutation causes a human autoimmune lymphoproliferative syndrome. Proc Natl Acad Sci U S A. 2007 May 22;104(21):8953-8. Epub 2007 May 16. PMID:17517660 doi:10.1073/pnas.0702975104

3con, resolution 1.65Å

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