6ziz - Revision history

OCA at 11:53, 1 February 2024

OCA — Thu, 01 Feb 2024 11:53:10 GMT

←Older revision		Revision as of 11:53, 1 February 2024
Line 3:		Line 3:
	<StructureSection load='6ziz' size='340' side='right'caption='[[6ziz]], [[Resolution\|resolution]] 1.79Å' scene=''>		<StructureSection load='6ziz' size='340' side='right'caption='[[6ziz]], [[Resolution\|resolution]] 1.79Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6ziz]] is a 2 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=6ZIZ OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=6ZIZ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6ziz]] is a 2 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=6ZIZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6ZIZ FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EZZ:(3~{S})-3-[2-[(dimethylamino)methyl]-1~{H}-indol-3-yl]-5-oxidanyl-2,3-dihydroisoindol-1-one'>EZZ</scene>, <scene name='pdbligand=GTP:GUANOSINE-5-TRIPHOSPHATE'>GTP</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</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]] 1.785Å</td></tr>
-	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">NRAS, HRAS1 ([http://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=EZZ:(3~{S})-3-[2-[(dimethylamino)methyl]-1~{H}-indol-3-yl]-5-oxidanyl-2,3-dihydroisoindol-1-one'>EZZ</scene>, <scene name='pdbligand=GTP:GUANOSINE-5-TRIPHOSPHATE'>GTP</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=6ziz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ziz OCA], [~~http~~://pdbe.org/6ziz PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6ziz RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6ziz PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6ziz 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=6ziz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ziz OCA], [https://pdbe.org/6ziz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6ziz RCSB], [https://www.ebi.ac.uk/pdbsum/6ziz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6ziz ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/RASN_HUMAN RASN_HUMAN]] Defects in NRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:[~~http~~://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:[~~http~~://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:[~~http~~://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 ==
-	[~~[http~~://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.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 25:		Line 25:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Boettcher, J]]	+	[[Category: Boettcher J]]
-	[[Category: Fischer, G]]	+	[[Category: Fischer G]]
-	[[Category: Kessler, D]]	+	[[Category: Kessler D]]
-	~~[[Category: Gtpase]]~~	+
-	~~[[Category: Hydrolase~~]]	+

OCA at 07:14, 25 November 2020

OCA — Wed, 25 Nov 2020 07:14:47 GMT

←Older revision		Revision as of 07:14, 25 November 2020
Line 1:		Line 1:

	==CRYSTAL STRUCTURE OF NRAS Q61R IN COMPLEX WITH GTP AND COMPOUND 18==		==CRYSTAL STRUCTURE OF NRAS Q61R IN COMPLEX WITH GTP AND COMPOUND 18==
-	<StructureSection load='6ziz' size='340' side='right'caption='[[6ziz]]' scene=''>	+	<StructureSection load='6ziz' size='340' side='right'caption='[[6ziz]], [[Resolution\|resolution]] 1.79Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6ZIZ OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=6ZIZ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6ziz]] is a 2 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=6ZIZ OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=6ZIZ FirstGlance]. <br>
-	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=6ziz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ziz OCA], [http://pdbe.org/6ziz PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6ziz RCSB], [http://www.ebi.ac.uk/pdbsum/6ziz PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6ziz ProSAT]</span></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EZZ:(3~{S})-3-[2-[(dimethylamino)methyl]-1~{H}-indol-3-yl]-5-oxidanyl-2,3-dihydroisoindol-1-one'>EZZ</scene>, <scene name='pdbligand=GTP:GUANOSINE-5-TRIPHOSPHATE'>GTP</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">NRAS, HRAS1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
		+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=6ziz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ziz OCA], [http://pdbe.org/6ziz PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6ziz RCSB], [http://www.ebi.ac.uk/pdbsum/6ziz PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6ziz ProSAT]</span></td></tr>
	</table>		</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/RASN_HUMAN RASN_HUMAN]] Defects in NRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:[http://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:[http://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:[http://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 ==
		+	[[http://www.uniprot.org/uniprot/RASN_HUMAN RASN_HUMAN]] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Activating mutations in the three human RAS genes, KRAS, NRAS and HRAS, are among the most common oncogenic drivers in human cancers. Covalent KRAS(G12C) inhibitors, which bind to the switch II pocket in the 'off state' of KRAS, represent the first direct KRAS drugs that entered human clinical trials. However, the remaining 85% of non-KRAS(G12C)-driven cancers remain undrugged as do NRAS and HRAS and no drugs targeting the 'on state' have been discovered so far. The switch I/II pocket is a second pocket for which the nanomolar inhibitor BI-2852 has been discovered. Here, we elucidate inhibitor binding modes in KRAS, NRAS and HRAS on and off and discuss future strategies to drug all RAS isoforms with this one pocket.
		+
		+	Drugging all RAS isoforms with one pocket.,Kessler D, Bergner A, Bottcher J, Fischer G, Dobel S, Hinkel M, Mullauer B, Weiss-Puxbaum A, McConnell DB Future Med Chem. 2020 Aug 11. doi: 10.4155/fmc-2020-0221. PMID:32779487<ref>PMID:32779487</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 6ziz" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Boettcher J]]	+	[[Category: Boettcher, J]]
-	[[Category: Fischer G]]	+	[[Category: Fischer, G]]
-	[[Category: Kessler D]]	+	[[Category: Kessler, D]]
		+	[[Category: Gtpase]]
		+	[[Category: Hydrolase]]

OCA at 06:24, 19 August 2020

OCA — Wed, 19 Aug 2020 06:24:15 GMT

←Older revision		Revision as of 06:24, 19 August 2020
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 6ziz is ~~ON HOLD until Paper Publication~~	+	==CRYSTAL STRUCTURE OF NRAS Q61R IN COMPLEX WITH GTP AND COMPOUND 18==
-		+	<StructureSection load='6ziz' size='340' side='right'caption='[[6ziz]]' scene=''>
-	~~Authors~~:	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6ZIZ OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=6ZIZ FirstGlance]. <br>
-	~~Description~~:	+	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=6ziz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ziz OCA], [http://pdbe.org/6ziz PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6ziz RCSB], [http://www.ebi.ac.uk/pdbsum/6ziz PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6ziz ProSAT]</span></td></tr>
-	[[Category: ~~Unreleased Structures~~]]	+	</table>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Boettcher J]]
		+	[[Category: Fischer G]]
		+	[[Category: Kessler D]]

OCA at 09:29, 29 July 2020

OCA — Wed, 29 Jul 2020 09:29:26 GMT

←Older revision		Revision as of 09:29, 29 July 2020
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 6ziz is ON HOLD	+	The entry 6ziz is ON HOLD until Paper Publication

	Authors:		Authors:

OCA: Protected "6ziz" [edit=sysop:move=sysop]

OCA — Wed, 08 Jul 2020 11:12:28 GMT

Protected "6ziz" [edit=sysop:move=sysop]

←Older revision

Revision as of 11:12, 8 July 2020

OCA: New page: '''Unreleased structure''' The entry 6ziz is ON HOLD Authors: Description: Category: Unreleased Structures

OCA — Wed, 08 Jul 2020 11:12:26 GMT

New page: '''Unreleased structure''' The entry 6ziz is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 6ziz is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]