3nw6 - Revision history

OCA at 10:31, 21 February 2024

2024-02-21T10:31:13Z

←Older revision		Revision as of 10:31, 21 February 2024
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	==Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)==		==Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)==
-	<StructureSection load='3nw6' size='340' side='right' caption='[[3nw6]], [[Resolution\|resolution]] 2.20Å' scene=''>	+	<StructureSection load='3nw6' size='340' side='right'caption='[[3nw6]], [[Resolution\|resolution]] 2.20Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3nw6]] is a 1 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=3NW6 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3NW6 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3nw6]] 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=3NW6 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3NW6 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=LGW:N-(5-CYCLOPROPYL-1H-PYRAZOL-3-YL)-2-{(2S)-1-[(6-FLUOROPYRIDIN-3-YL)CARBONYL]PYRROLIDIN-2-YL}PYRROLO[2,1-F][1,2,4]TRIAZIN-4-AMINE'>LGW</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]] 2.2Å</td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3nw5\|3nw5]], [[3nw7\|3nw7]]</td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=LGW:N-(5-CYCLOPROPYL-1H-PYRAZOL-3-YL)-2-{(2S)-1-[(6-FLUOROPYRIDIN-3-YL)CARBONYL]PYRROLIDIN-2-YL}PYRROLO[2,1-F][1,2,4]TRIAZIN-4-AMINE'>LGW</scene></td></tr>
-	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">IGF1R ([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'>[https://proteopedia.org/fgij/fg.htm?mol=3nw6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nw6 OCA], [https://pdbe.org/3nw6 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3nw6 RCSB], [https://www.ebi.ac.uk/pdbsum/3nw6 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3nw6 ProSAT]</span></td></tr>
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Receptor_protein-tyrosine_kinase Receptor protein-tyrosine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.10.1 2.7.10.1] </span></td></tr>	+
-	<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=3nw6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nw6 OCA], [~~http~~://pdbe.org/3nw6 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3nw6 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3nw6 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3nw6 ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/IGF1R_HUMAN IGF1R_HUMAN]] Defects in IGF1R are a cause of insulin-like growth factor 1 resistance (IGF1RES) [MIM:[~~http~~://omim.org/entry/270450 270450]]. It is a disorder characterized by intrauterine growth retardation and poor postnatal growth accompanied with increased plasma IGF1.<ref>PMID:14657428</ref> <ref>PMID:15928254</ref>	+	[https://www.uniprot.org/uniprot/IGF1R_HUMAN IGF1R_HUMAN] Defects in IGF1R are a cause of insulin-like growth factor 1 resistance (IGF1RES) [MIM:[https://omim.org/entry/270450 270450]. It is a disorder characterized by intrauterine growth retardation and poor postnatal growth accompanied with increased plasma IGF1.<ref>PMID:14657428</ref> <ref>PMID:15928254</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/IGF1R_HUMAN IGF1R_HUMAN]] Receptor tyrosine kinase which mediates actions of insulin-like growth factor 1 (IGF1). Binds IGF1 with high affinity and IGF2 and insulin (INS) with a lower affinity. The activated IGF1R is involved in cell growth and survival control. IGF1R is crucial for tumor transformation and survival of malignant cell. Ligand binding activates the receptor kinase, leading to receptor autophosphorylation, and tyrosines phosphorylation of multiple substrates, that function as signaling adapter proteins including, the insulin-receptor substrates (IRS1/2), Shc and 14-3-3 proteins. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway and the Ras-MAPK pathway. The result of activating the MAPK pathway is increased cellular proliferation, whereas activating the PI3K pathway inhibits apoptosis and stimulates protein synthesis. Phosphorylated IRS1 can activate the 85 kDa regulatory subunit of PI3K (PIK3R1), leading to activation of several downstream substrates, including protein AKT/PKB. AKT phosphorylation, in turn, enhances protein synthesis through mTOR activation and triggers the antiapoptotic effects of IGFIR through phosphorylation and inactivation of BAD. In parallel to PI3K-driven signaling, recruitment of Grb2/SOS by phosphorylated IRS1 or Shc leads to recruitment of Ras and activation of the ras-MAPK pathway. In addition to these two main signaling pathways IGF1R signals also through the Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT). Phosphorylation of JAK proteins can lead to phosphorylation/activation of signal transducers and activators of transcription (STAT) proteins. In particular activation of STAT3, may be essential for the transforming activity of IGF1R. The JAK/STAT pathway activates gene transcription and may be responsible for the transforming activity. JNK kinases can also be activated by the IGF1R. IGF1 exerts inhibiting activities on JNK activation via phosphorylation and inhibition of MAP3K5/ASK1, which is able to directly associate with the IGF1R.<ref>PMID:8257688</ref> <ref>PMID:1846292</ref> <ref>PMID:8452530</ref> <ref>PMID:7679099</ref> <ref>PMID:10579905</ref> <ref>PMID:10747872</ref> <ref>PMID:12138094</ref> <ref>PMID:12556535</ref> <ref>PMID:16831875</ref> When present in a hybrid receptor with INSR, binds IGF1. PubMed:12138094 shows that hybrid receptors composed of IGF1R and INSR isoform Long are activated with a high affinity by IGF1, with low affinity by IGF2 and not significantly activated by insulin, and that hybrid receptors composed of IGF1R and INSR isoform Short are activated by IGF1, IGF2 and insulin. In contrast, PubMed:16831875 shows that hybrid receptors composed of IGF1R and INSR isoform Long and hybrid receptors composed of IGF1R and INSR isoform Short have similar binding characteristics, both bind IGF1 and have a low affinity for insulin.<ref>PMID:8257688</ref> <ref>PMID:1846292</ref> <ref>PMID:8452530</ref> <ref>PMID:7679099</ref> <ref>PMID:10579905</ref> <ref>PMID:10747872</ref> <ref>PMID:12138094</ref> <ref>PMID:12556535</ref> <ref>PMID:16831875</ref>	+	[https://www.uniprot.org/uniprot/IGF1R_HUMAN IGF1R_HUMAN] Receptor tyrosine kinase which mediates actions of insulin-like growth factor 1 (IGF1). Binds IGF1 with high affinity and IGF2 and insulin (INS) with a lower affinity. The activated IGF1R is involved in cell growth and survival control. IGF1R is crucial for tumor transformation and survival of malignant cell. Ligand binding activates the receptor kinase, leading to receptor autophosphorylation, and tyrosines phosphorylation of multiple substrates, that function as signaling adapter proteins including, the insulin-receptor substrates (IRS1/2), Shc and 14-3-3 proteins. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway and the Ras-MAPK pathway. The result of activating the MAPK pathway is increased cellular proliferation, whereas activating the PI3K pathway inhibits apoptosis and stimulates protein synthesis. Phosphorylated IRS1 can activate the 85 kDa regulatory subunit of PI3K (PIK3R1), leading to activation of several downstream substrates, including protein AKT/PKB. AKT phosphorylation, in turn, enhances protein synthesis through mTOR activation and triggers the antiapoptotic effects of IGFIR through phosphorylation and inactivation of BAD. In parallel to PI3K-driven signaling, recruitment of Grb2/SOS by phosphorylated IRS1 or Shc leads to recruitment of Ras and activation of the ras-MAPK pathway. In addition to these two main signaling pathways IGF1R signals also through the Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT). Phosphorylation of JAK proteins can lead to phosphorylation/activation of signal transducers and activators of transcription (STAT) proteins. In particular activation of STAT3, may be essential for the transforming activity of IGF1R. The JAK/STAT pathway activates gene transcription and may be responsible for the transforming activity. JNK kinases can also be activated by the IGF1R. IGF1 exerts inhibiting activities on JNK activation via phosphorylation and inhibition of MAP3K5/ASK1, which is able to directly associate with the IGF1R.<ref>PMID:8257688</ref> <ref>PMID:1846292</ref> <ref>PMID:8452530</ref> <ref>PMID:7679099</ref> <ref>PMID:10579905</ref> <ref>PMID:10747872</ref> <ref>PMID:12138094</ref> <ref>PMID:12556535</ref> <ref>PMID:16831875</ref> When present in a hybrid receptor with INSR, binds IGF1. PubMed:12138094 shows that hybrid receptors composed of IGF1R and INSR isoform Long are activated with a high affinity by IGF1, with low affinity by IGF2 and not significantly activated by insulin, and that hybrid receptors composed of IGF1R and INSR isoform Short are activated by IGF1, IGF2 and insulin. In contrast, PubMed:16831875 shows that hybrid receptors composed of IGF1R and INSR isoform Long and hybrid receptors composed of IGF1R and INSR isoform Short have similar binding characteristics, both bind IGF1 and have a low affinity for insulin.<ref>PMID:8257688</ref> <ref>PMID:1846292</ref> <ref>PMID:8452530</ref> <ref>PMID:7679099</ref> <ref>PMID:10579905</ref> <ref>PMID:10747872</ref> <ref>PMID:12138094</ref> <ref>PMID:12556535</ref> <ref>PMID:16831875</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
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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=3nw6 ConSurf].		</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=3nw6 ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
-	<div style="background-color:#fffaf0;">
-	== Publication Abstract from PubMed ==
-	Pyrrolidine, pyrrolidinone, carbocyclic, and acyclic groups were used as isosteric proline replacements in a series of insulin-like growth factor I receptor kinase/insulin receptor kinase inhibitors. Examples that were similar in potency to proline-containing reference compounds were shown to project a key fluoropyridine amide into a common space, while less potent compounds were not able to do so for reasons of stereochemistry or structural rigidity.
-
-	Proline isosteres in a series of 2,4-disubstituted pyrrolo[1,2-f][1,2,4]triazine inhibitors of IGF-1R kinase and IR kinase.,Sampognaro AJ, Wittman MD, Carboni JM, Chang C, Greer AF, Hurlburt WW, Sack JS, Vyas DM Bioorg Med Chem Lett. 2010 Sep 1;20(17):5027-30. Epub 2010 Jul 15. PMID:20675137<ref>PMID:20675137</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 3nw6" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 40:		Line 29:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
-	[[Category: ~~Receptor protein-tyrosine kinase~~]]	+	[[Category: Large Structures]]
-	[[Category: Sack~~, J S]]~~	+	[[Category: Sack JS]]
-	~~[[Category: Hormone/growth factor]]~~	+
-	~~[[Category: Igf-1r]]~~	+
-	~~[[Category: Kinase domain]]~~	+
-	~~[[Category: Transferase~~]]	+

OCA at 10:02, 30 January 2019

2019-01-30T10:02:44Z

←Older revision		Revision as of 10:02, 30 January 2019
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	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/nw/3nw6_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/nw/3nw6_consurf.spt"</scriptWhenChecked>
	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>		<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
Line 35:		Line 35:

	==See Also==		==See Also==
-	*[[Hormone\|Hormone]]
	*[[Insulin-like growth factor receptor\|Insulin-like growth factor receptor]]		*[[Insulin-like growth factor receptor\|Insulin-like growth factor receptor]]
	== References ==		== References ==

OCA at 13:52, 4 August 2016

2016-08-04T13:52:31Z

←Older revision		Revision as of 13:52, 4 August 2016
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		+
	==Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)==		==Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)==
	<StructureSection load='3nw6' size='340' side='right' caption='[[3nw6]], [[Resolution\|resolution]] 2.20Å' scene=''>		<StructureSection load='3nw6' size='340' side='right' caption='[[3nw6]], [[Resolution\|resolution]] 2.20Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3nw6]] is a 1 chain structure with 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=3NW6 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3NW6 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3nw6]] is a 1 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=3NW6 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3NW6 FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=LGW:N-(5-CYCLOPROPYL-1H-PYRAZOL-3-YL)-2-{(2S)-1-[(6-FLUOROPYRIDIN-3-YL)CARBONYL]PYRROLIDIN-2-YL}PYRROLO[2,1-F][1,2,4]TRIAZIN-4-AMINE'>LGW</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=LGW:N-(5-CYCLOPROPYL-1H-PYRAZOL-3-YL)-2-{(2S)-1-[(6-FLUOROPYRIDIN-3-YL)CARBONYL]PYRROLIDIN-2-YL}PYRROLO[2,1-F][1,2,4]TRIAZIN-4-AMINE'>LGW</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3nw5\|3nw5]], [[3nw7\|3nw7]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3nw5\|3nw5]], [[3nw7\|3nw7]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">IGF1R ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">IGF1R ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Receptor_protein-tyrosine_kinase Receptor protein-tyrosine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.10.1 2.7.10.1] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Receptor_protein-tyrosine_kinase Receptor protein-tyrosine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.10.1 2.7.10.1] </span></td></tr>
-	<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=3nw6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nw6 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3nw6 RCSB], [http://www.ebi.ac.uk/pdbsum/3nw6 PDBsum]</span></td></tr>	+	<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=3nw6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nw6 OCA], [http://pdbe.org/3nw6 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3nw6 RCSB], [http://www.ebi.ac.uk/pdbsum/3nw6 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3nw6 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
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	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
	</jmolCheckbox>		</jmolCheckbox>
-	</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/~~chain_selection~~.php?pdb_ID=~~2ata~~ ConSurf].	+	</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=3nw6 ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 31:		Line 32:
	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
		+	<div class="pdbe-citations 3nw6" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 39:		Line 41:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Receptor protein-tyrosine kinase]]		[[Category: Receptor protein-tyrosine kinase]]
	[[Category: Sack, J S]]		[[Category: Sack, J S]]

OCA at 06:56, 19 December 2014

2014-12-19T06:56:54Z

←Older revision		Revision as of 06:56, 19 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3nw6\| PDB=3nw6 \| SCENE= }}~~	+	==Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)==
-	===Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)===	+	<StructureSection load='3nw6' size='340' side='right' caption='[[3nw6]], [[Resolution\|resolution]] 2.20Å' scene=''>
-	{~~{ABSTRACT_PUBMED_20675137}~~}	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3nw6]] is a 1 chain structure with 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=3NW6 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3NW6 FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=LGW:N-(5-CYCLOPROPYL-1H-PYRAZOL-3-YL)-2-{(2S)-1-[(6-FLUOROPYRIDIN-3-YL)CARBONYL]PYRROLIDIN-2-YL}PYRROLO[2,1-F][1,2,4]TRIAZIN-4-AMINE'>LGW</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3nw5\|3nw5]], [[3nw7\|3nw7]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">IGF1R ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
		+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Receptor_protein-tyrosine_kinase Receptor protein-tyrosine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.10.1 2.7.10.1] </span></td></tr>
		+	<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=3nw6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3nw6 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3nw6 RCSB], [http://www.ebi.ac.uk/pdbsum/3nw6 PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/IGF1R_HUMAN IGF1R_HUMAN]] Defects in IGF1R are a cause of insulin-like growth factor 1 resistance (IGF1RES) [MIM:[http://omim.org/entry/270450 270450]]. It is a disorder characterized by intrauterine growth retardation and poor postnatal growth accompanied with increased plasma IGF1.<ref>PMID:14657428</ref> <ref>PMID:15928254</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/IGF1R_HUMAN IGF1R_HUMAN]] Receptor tyrosine kinase which mediates actions of insulin-like growth factor 1 (IGF1). Binds IGF1 with high affinity and IGF2 and insulin (INS) with a lower affinity. The activated IGF1R is involved in cell growth and survival control. IGF1R is crucial for tumor transformation and survival of malignant cell. Ligand binding activates the receptor kinase, leading to receptor autophosphorylation, and tyrosines phosphorylation of multiple substrates, that function as signaling adapter proteins including, the insulin-receptor substrates (IRS1/2), Shc and 14-3-3 proteins. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway and the Ras-MAPK pathway. The result of activating the MAPK pathway is increased cellular proliferation, whereas activating the PI3K pathway inhibits apoptosis and stimulates protein synthesis. Phosphorylated IRS1 can activate the 85 kDa regulatory subunit of PI3K (PIK3R1), leading to activation of several downstream substrates, including protein AKT/PKB. AKT phosphorylation, in turn, enhances protein synthesis through mTOR activation and triggers the antiapoptotic effects of IGFIR through phosphorylation and inactivation of BAD. In parallel to PI3K-driven signaling, recruitment of Grb2/SOS by phosphorylated IRS1 or Shc leads to recruitment of Ras and activation of the ras-MAPK pathway. In addition to these two main signaling pathways IGF1R signals also through the Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT). Phosphorylation of JAK proteins can lead to phosphorylation/activation of signal transducers and activators of transcription (STAT) proteins. In particular activation of STAT3, may be essential for the transforming activity of IGF1R. The JAK/STAT pathway activates gene transcription and may be responsible for the transforming activity. JNK kinases can also be activated by the IGF1R. IGF1 exerts inhibiting activities on JNK activation via phosphorylation and inhibition of MAP3K5/ASK1, which is able to directly associate with the IGF1R.<ref>PMID:8257688</ref> <ref>PMID:1846292</ref> <ref>PMID:8452530</ref> <ref>PMID:7679099</ref> <ref>PMID:10579905</ref> <ref>PMID:10747872</ref> <ref>PMID:12138094</ref> <ref>PMID:12556535</ref> <ref>PMID:16831875</ref> When present in a hybrid receptor with INSR, binds IGF1. PubMed:12138094 shows that hybrid receptors composed of IGF1R and INSR isoform Long are activated with a high affinity by IGF1, with low affinity by IGF2 and not significantly activated by insulin, and that hybrid receptors composed of IGF1R and INSR isoform Short are activated by IGF1, IGF2 and insulin. In contrast, PubMed:16831875 shows that hybrid receptors composed of IGF1R and INSR isoform Long and hybrid receptors composed of IGF1R and INSR isoform Short have similar binding characteristics, both bind IGF1 and have a low affinity for insulin.<ref>PMID:8257688</ref> <ref>PMID:1846292</ref> <ref>PMID:8452530</ref> <ref>PMID:7679099</ref> <ref>PMID:10579905</ref> <ref>PMID:10747872</ref> <ref>PMID:12138094</ref> <ref>PMID:12556535</ref> <ref>PMID:16831875</ref>
		+	== Evolutionary Conservation ==
		+	[[Image:Consurf_key_small.gif\|200px\|right]]
		+	Check<jmol>
		+	<jmolCheckbox>
		+	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/nw/3nw6_consurf.spt"</scriptWhenChecked>
		+	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
		+	<text>to colour the structure by Evolutionary Conservation</text>
		+	</jmolCheckbox>
		+	</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/chain_selection.php?pdb_ID=2ata ConSurf].
		+	<div style="clear:both"></div>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Pyrrolidine, pyrrolidinone, carbocyclic, and acyclic groups were used as isosteric proline replacements in a series of insulin-like growth factor I receptor kinase/insulin receptor kinase inhibitors. Examples that were similar in potency to proline-containing reference compounds were shown to project a key fluoropyridine amide into a common space, while less potent compounds were not able to do so for reasons of stereochemistry or structural rigidity.

-	~~==Disease==~~	+	Proline isosteres in a series of 2,4-disubstituted pyrrolo[1,2-f][1,2,4]triazine inhibitors of IGF-1R kinase and IR kinase.,Sampognaro AJ, Wittman MD, Carboni JM, Chang C, Greer AF, Hurlburt WW, Sack JS, Vyas DM Bioorg Med Chem Lett. 2010 Sep 1;20(17):5027-30. Epub 2010 Jul 15. PMID:20675137<ref>PMID:20675137</ref>
-	[[~~http://www.uniprot.org/uniprot/IGF1R_HUMAN IGF1R_HUMAN~~]~~] Defects in IGF1R are a cause~~ of ~~insulin~~-~~like growth factor~~ 1 ~~resistance~~ (~~IGF1RES~~) ~~[MIM~~:~~[http://omim~~.~~org/entry/270450 270450]]~~. ~~It is a disorder characterized by intrauterine growth retardation and poor postnatal growth accompanied with increased plasma IGF1.<ref>~~PMID:~~14657428</ref>~~<ref>PMID:~~15928254~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www.uniprot.org/uniprot/IGF1R_HUMAN IGF1R_HUMAN]] Receptor tyrosine kinase which mediates actions of insulin-like growth factor 1 (IGF1). Binds IGF1 with high affinity and IGF2 and insulin (INS) with~~ a ~~lower affinity. The activated IGF1R is involved in cell growth and survival control. IGF1R is crucial for tumor transformation and survival~~ of ~~malignant cell. Ligand binding activates~~ the receptor kinase, leading to receptor autophosphorylation, and tyrosines phosphorylation of multiple substrates, that function as signaling adapter proteins including, the insulin-receptor substrates (IRS1/2), Shc and 14-3-3 proteins. ~~Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway and the Ras-MAPK pathway~~. ~~The result~~ of activating the MAPK pathway is increased cellular proliferation, whereas activating the PI3K pathway inhibits apoptosis and stimulates protein synthesis. Phosphorylated IRS1 can activate the 85 kDa regulatory subunit of PI3K (PIK3R1), leading to activation of several downstream substrates, including protein AKT/PKB. AKT phosphorylation, in turn, enhances protein synthesis through mTOR activation and triggers the antiapoptotic effects of IGFIR through phosphorylation and inactivation of BAD. In parallel to PI3K-driven signaling, recruitment of Grb2/SOS by phosphorylated IRS1 or Shc leads to recruitment of Ras and activation of the ras-MAPK pathway. In addition to these two main signaling pathways IGF1R signals also through the Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT). Phosphorylation of JAK proteins can lead to phosphorylation/activation of signal transducers and activators of transcription (STAT) proteins. In particular activation of STAT3, may be essential for the transforming activity of IGF1R. The JAK/STAT pathway activates gene transcription and may be responsible for the transforming activity. JNK kinases can also be activated by the IGF1R. IGF1 exerts inhibiting activities on JNK activation via phosphorylation and inhibition of MAP3K5/ASK1, which is able to directly associate with the IGF1R.<~~ref~~>~~PMID:8257688~~</~~ref~~><ref>PMID:1846292</ref><ref>PMID:8452530</ref><ref>PMID:7679099</ref><ref>PMID:10579905</ref><ref>PMID:10747872</ref><ref>PMID:12138094</ref><ref>PMID:12556535</ref><ref>PMID:16831875</ref> When present in a hybrid receptor with INSR, binds IGF1. PubMed:12138094 shows that hybrid receptors composed of IGF1R and INSR isoform Long are activated with a high affinity by IGF1, with low affinity by IGF2 and not significantly activated by insulin, and that hybrid receptors composed of IGF1R and INSR isoform Short are activated by IGF1, IGF2 and insulin. In contrast, PubMed:16831875 shows that hybrid receptors composed of IGF1R and INSR isoform Long and hybrid receptors composed of IGF1R and INSR isoform Short have similar binding characteristics, both bind IGF1 and have a low affinity for insulin.<ref>PMID:8257688</ref><ref>PMID:1846292</ref><ref>PMID:8452530</ref><ref>PMID:7679099</ref><ref>PMID:10579905</ref><ref>PMID:10747872</ref><ref>PMID:12138094</ref><ref>PMID:12556535</ref><ref>PMID:16831875</ref>	+	</div>
-		+
-	~~==About this Structure==~~	+
-	[[3nw6]] is a 1 chain structure with 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=3NW6 OCA].	+

	==See Also==		==See Also==
	*[[Hormone\|Hormone]]		*[[Hormone\|Hormone]]
	*[[Insulin-like growth factor receptor\|Insulin-like growth factor receptor]]		*[[Insulin-like growth factor receptor\|Insulin-like growth factor receptor]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:020675137</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Receptor protein-tyrosine kinase]]		[[Category: Receptor protein-tyrosine kinase]]
-	[[Category: Sack, J S.]]	+	[[Category: Sack, J S]]
	[[Category: Hormone/growth factor]]		[[Category: Hormone/growth factor]]
	[[Category: Igf-1r]]		[[Category: Igf-1r]]
	[[Category: Kinase domain]]		[[Category: Kinase domain]]
	[[Category: Transferase]]		[[Category: Transferase]]

OCA at 19:48, 24 March 2013

2013-03-24T19:48:25Z

←Older revision		Revision as of 19:48, 24 March 2013
Line 1:		Line 1:
-	[[Image:3nw6.png\|left\|200px]]
-
	{{STRUCTURE_3nw6\| PDB=3nw6 \| SCENE= }}		{{STRUCTURE_3nw6\| PDB=3nw6 \| SCENE= }}
-
	===Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)===		===Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)===
		+	{{ABSTRACT_PUBMED_20675137}}

-	~~{{ABSTRACT_PUBMED_20675137}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/IGF1R_HUMAN IGF1R_HUMAN]] Defects in IGF1R are a cause of insulin-like growth factor 1 resistance (IGF1RES) [MIM:[http://omim.org/entry/270450 270450]]. It is a disorder characterized by intrauterine growth retardation and poor postnatal growth accompanied with increased plasma IGF1.<ref>PMID:14657428</ref><ref>PMID:15928254</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/IGF1R_HUMAN IGF1R_HUMAN]] Receptor tyrosine kinase which mediates actions of insulin-like growth factor 1 (IGF1). Binds IGF1 with high affinity and IGF2 and insulin (INS) with a lower affinity. The activated IGF1R is involved in cell growth and survival control. IGF1R is crucial for tumor transformation and survival of malignant cell. Ligand binding activates the receptor kinase, leading to receptor autophosphorylation, and tyrosines phosphorylation of multiple substrates, that function as signaling adapter proteins including, the insulin-receptor substrates (IRS1/2), Shc and 14-3-3 proteins. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway and the Ras-MAPK pathway. The result of activating the MAPK pathway is increased cellular proliferation, whereas activating the PI3K pathway inhibits apoptosis and stimulates protein synthesis. Phosphorylated IRS1 can activate the 85 kDa regulatory subunit of PI3K (PIK3R1), leading to activation of several downstream substrates, including protein AKT/PKB. AKT phosphorylation, in turn, enhances protein synthesis through mTOR activation and triggers the antiapoptotic effects of IGFIR through phosphorylation and inactivation of BAD. In parallel to PI3K-driven signaling, recruitment of Grb2/SOS by phosphorylated IRS1 or Shc leads to recruitment of Ras and activation of the ras-MAPK pathway. In addition to these two main signaling pathways IGF1R signals also through the Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT). Phosphorylation of JAK proteins can lead to phosphorylation/activation of signal transducers and activators of transcription (STAT) proteins. In particular activation of STAT3, may be essential for the transforming activity of IGF1R. The JAK/STAT pathway activates gene transcription and may be responsible for the transforming activity. JNK kinases can also be activated by the IGF1R. IGF1 exerts inhibiting activities on JNK activation via phosphorylation and inhibition of MAP3K5/ASK1, which is able to directly associate with the IGF1R.<ref>PMID:8257688</ref><ref>PMID:1846292</ref><ref>PMID:8452530</ref><ref>PMID:7679099</ref><ref>PMID:10579905</ref><ref>PMID:10747872</ref><ref>PMID:12138094</ref><ref>PMID:12556535</ref><ref>PMID:16831875</ref> When present in a hybrid receptor with INSR, binds IGF1. PubMed:12138094 shows that hybrid receptors composed of IGF1R and INSR isoform Long are activated with a high affinity by IGF1, with low affinity by IGF2 and not significantly activated by insulin, and that hybrid receptors composed of IGF1R and INSR isoform Short are activated by IGF1, IGF2 and insulin. In contrast, PubMed:16831875 shows that hybrid receptors composed of IGF1R and INSR isoform Long and hybrid receptors composed of IGF1R and INSR isoform Short have similar binding characteristics, both bind IGF1 and have a low affinity for insulin.<ref>PMID:8257688</ref><ref>PMID:1846292</ref><ref>PMID:8452530</ref><ref>PMID:7679099</ref><ref>PMID:10579905</ref><ref>PMID:10747872</ref><ref>PMID:12138094</ref><ref>PMID:12556535</ref><ref>PMID:16831875</ref>

	==About this Structure==		==About this Structure==
Line 15:		Line 17:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:020675137</ref><references group="xtra"/>	+	<ref group="xtra">PMID:020675137</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Receptor protein-tyrosine kinase]]		[[Category: Receptor protein-tyrosine kinase]]

OCA at 15:19, 20 October 2012

2012-10-20T15:19:33Z

←Older revision		Revision as of 15:19, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3nw6]] is a 1 chain structure ~~of [[Hormone]]~~ with 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=3NW6 OCA].	+	[[3nw6]] is a 1 chain structure with 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=3NW6 OCA].

	==See Also==		==See Also==
	*[[Hormone\|Hormone]]		*[[Hormone\|Hormone]]
		+	*[[Insulin-like growth factor receptor\|Insulin-like growth factor receptor]]

	==Reference==		==Reference==

OCA: Protected "3nw6" [edit=sysop:move=sysop]

2012-07-26T18:01:24Z

Protected "3nw6" [edit=sysop:move=sysop]

←Older revision

Revision as of 18:01, 26 July 2012

OCA at 18:01, 26 July 2012

2012-07-26T18:01:22Z

←Older revision		Revision as of 18:01, 26 July 2012
Line 1:		Line 1:
-	{{Seed}}
	[[Image:3nw6.png\|left\|200px]]		[[Image:3nw6.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_3nw6", creates the "Structure Box" on the page.
-	You may change the PDB parameter (which sets the PDB file loaded into the applet)
-	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
-	or leave the SCENE parameter empty for the default display.
-	-->
	{{STRUCTURE_3nw6\| PDB=3nw6 \| SCENE= }}		{{STRUCTURE_3nw6\| PDB=3nw6 \| SCENE= }}

	===Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)===		===Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_20675137}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 20675137 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_20675137}}		{{ABSTRACT_PUBMED_20675137}}

	==About this Structure==		==About this Structure==
-	~~3NW6~~ is a 1 chain structure with 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=3NW6 OCA].	+	[[3nw6]] is a 1 chain structure of [[Hormone]] with 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=3NW6 OCA].
		+
		+	==See Also==
		+	*[[Hormone\|Hormone]]

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~20675137~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:020675137</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Receptor protein-tyrosine kinase]]		[[Category: Receptor protein-tyrosine kinase]]
Line 31:		Line 22:
	[[Category: Kinase domain]]		[[Category: Kinase domain]]
	[[Category: Transferase]]		[[Category: Transferase]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Fri Sep 10 13:36:09 2010''

OCA at 09:27, 10 September 2010

2010-09-10T09:27:39Z

←Older revision		Revision as of 09:27, 10 September 2010
Line 1:		Line 1:
	{{Seed}}		{{Seed}}
-	[[Image:3nw6.~~jpg~~\|left\|200px]]	+	[[Image:3nw6.png\|left\|200px]]

	<!--		<!--
Line 12:		Line 12:
	===Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)===		===Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)===

		+
		+	<!--
		+	The line below this paragraph, {{ABSTRACT_PUBMED_20675137}}, adds the Publication Abstract to the page
		+	(as it appears on PubMed at http://www.pubmed.gov), where 20675137 is the PubMed ID number.
		+	-->
		+	{{ABSTRACT_PUBMED_20675137}}

	==About this Structure==		==About this Structure==
	3NW6 is a 1 chain structure with 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=3NW6 OCA].		3NW6 is a 1 chain structure with 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=3NW6 OCA].
		+
		+	==Reference==
		+	<ref group="xtra">PMID:20675137</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Receptor protein-tyrosine kinase]]		[[Category: Receptor protein-tyrosine kinase]]
Line 23:		Line 32:
	[[Category: Transferase]]		[[Category: Transferase]]

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on ~~Wed Jul 28 12~~:44:23 2010''	+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Fri Sep 10 13:36:09 2010''

OCA at 08:37, 28 July 2010

2010-07-28T08:37:41Z

←Older revision		Revision as of 08:37, 28 July 2010
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	{{Seed}}
		+	[[Image:3nw6.jpg\|left\|200px]]

-	The ~~entry 3nw6~~ is ~~ON HOLD~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_3nw6", creates the "Structure Box" on the page.
		+	You may change the PDB parameter (which sets the PDB file loaded into the applet)
		+	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
		+	or leave the SCENE parameter empty for the default display.
		+	-->
		+	{{STRUCTURE_3nw6\| PDB=3nw6 \| SCENE= }}

-	~~Authors: Sack, J.S.~~	+	===Crystal structure of insulin-like growth factor 1 receptor (IGF-1R-WT) complex with a carbon-linked proline isostere inhibitor (11A)===

-	Description: CRYSTAL STRUCTURE OF INSULIN-LIKE GROWTH FACTOR 1 RECEPTOR (IGF-1R-WT) COMPLEX WITH A CARBON-LINKED PROLINE ISOSTERE INHIBITOR (11A)

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Jul ~~21 10~~:06:21 2010''	+	==About this Structure==
		+	3NW6 is a 1 chain structure with 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=3NW6 OCA].
		+	[[Category: Homo sapiens]]
		+	[[Category: Receptor protein-tyrosine kinase]]
		+	[[Category: Sack, J S.]]
		+	[[Category: Hormone/growth factor]]
		+	[[Category: Igf-1r]]
		+	[[Category: Kinase domain]]
		+	[[Category: Transferase]]
		+
		+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Jul 28 12:44:23 2010''