24sr: Difference between revisions

Latest revision as of 08:20, 16 September 2026

Human NRAS WT (GDP-bound) in complex with macrocyclic peptide inhibitor AP6296

Structural highlights

24sr is a 6 chain structure with sequence from Homo sapiens and Synthetic construct. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance.
Method:	X-ray diffraction, Resolution 1.232Å
Ligands:	6LR, 7VN, A1MFM, A1MFN, AC5, EDO, GDP, MG, MLE, PO4, SAR, SOQ
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.

References

↑ 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
↑ 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

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OCA

[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

[1]

[2]

@@ Line 1: / Line 1: @@
-'''Unreleased structure'''
-The entry 24sr is ON HOLD  until Paper Publication
+==Human NRAS WT (GDP-bound) in complex with macrocyclic peptide inhibitor AP6296==
+<StructureSection load='24sr' size='340' side='right'caption='[[24sr]], [[Resolution|resolution]] 1.23&Aring;' scene=''>
-Authors:
+== Structural highlights ==
+<table><tr><td colspan='2'>[[24sr]] is a 6 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Synthetic_construct Synthetic construct]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=24SR OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=24SR FirstGlance]. <br>
-Description:
+</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.232&#8491;</td></tr>
-[[Category: Unreleased Structures]]
+<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=6LR:MORPHOLINE'>6LR</scene>, <scene name='pdbligand=7VN:(2~{S})-2-cyclopentyl-2-(methylamino)ethanoic+acid'>7VN</scene>, <scene name='pdbligand=A1MFM:(2~{S})-2-azanyl-4-[3-chloranyl-4-(trifluoromethyl)phenyl]butanoic+acid'>A1MFM</scene>, <scene name='pdbligand=A1MFN:(2~{S})-3-(4-methylphenyl)-2-(propylamino)propanoic+acid'>A1MFN</scene>, <scene name='pdbligand=AC5:1-AMINOCYCLOPENTANECARBOXYLIC+ACID'>AC5</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=MLE:N-METHYLLEUCINE'>MLE</scene>, <scene name='pdbligand=PO4:PHOSPHATE+ION'>PO4</scene>, <scene name='pdbligand=SAR:SARCOSINE'>SAR</scene>, <scene name='pdbligand=SOQ:(2~{S})-2-(methylamino)butanedioic+acid'>SOQ</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=24sr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=24sr OCA], [https://pdbe.org/24sr PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=24sr RCSB], [https://www.ebi.ac.uk/pdbsum/24sr PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=24sr ProSAT]</span></td></tr>
+</table>
+== 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>
+== Function ==
+[https://www.uniprot.org/uniprot/RASN_HUMAN RASN_HUMAN] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
+== References ==
+<references/>
+__TOC__
+</StructureSection>
+[[Category: Homo sapiens]]
+[[Category: Large Structures]]
+[[Category: Synthetic construct]]
+[[Category: Fukami TA]]
+[[Category: Irie M]]
+[[Category: Kage M]]
+[[Category: Tanada M]]
+[[Category: Torizawa T]]
+[[Category: Yamano T]]

24sr: Difference between revisions

Latest revision as of 08:20, 16 September 2026

Human NRAS WT (GDP-bound) in complex with macrocyclic peptide inhibitor AP6296

Structural highlights

Disease

Function

References

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