3kq6 - Revision history

OCA at 08:21, 6 September 2023

OCA — Wed, 06 Sep 2023 08:21:21 GMT

←Older revision		Revision as of 08:21, 6 September 2023
Line 3:		Line 3:
	<StructureSection load='3kq6' size='340' side='right'caption='[[3kq6]], [[Resolution\|resolution]] 1.90Å' scene=''>		<StructureSection load='3kq6' size='340' side='right'caption='[[3kq6]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3kq6]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KQ6 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3KQ6 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3kq6]] is a 4 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=3KQ6 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3KQ6 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</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]] 1.9Å</td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1rwe\|1rwe]]</div~~></td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</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=3kq6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kq6 OCA], [https://pdbe.org/3kq6 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3kq6 RCSB], [https://www.ebi.ac.uk/pdbsum/3kq6 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3kq6 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=3kq6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kq6 OCA], [https://pdbe.org/3kq6 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3kq6 RCSB], [https://www.ebi.ac.uk/pdbsum/3kq6 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3kq6 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[https://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[https://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[https://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[https://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>	+	[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[https://omim.org/entry/176730 176730].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[https://omim.org/entry/125852 125852]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[https://omim.org/entry/606176 606176]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[https://omim.org/entry/613370 613370]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.	+	[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 38:		Line 38:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Hu~~, S Q~~]]	+	[[Category: Hu SQ]]
-	[[Category: Ismail-Beigi, F]]	+	[[Category: Ismail-Beigi F]]
-	[[Category: Phillips~~, N B~~]]	+	[[Category: Phillips NB]]
-	[[Category: Wan~~, Z L~~]]	+	[[Category: Wan ZL]]
-	[[Category: Weiss~~, M A~~]]	+	[[Category: Weiss MA]]
-	[[Category: Whittake, J]]	+	[[Category: Whittake J]]
-	[[Category: Whittaker, L]]	+	[[Category: Whittaker L]]
-	~~[[Category: Carbohydrate metabolism]]~~	+
-	~~[[Category: Cleavage on pair of basic residue]]~~	+
-	~~[[Category: Diabetes mellitus]]~~	+
-	~~[[Category: Disease mutation]]~~	+
-	~~[[Category: Disulfide bond]]~~	+
-	~~[[Category: Glucose metabolism]]~~	+
-	~~[[Category: Hormone]]~~	+
-	~~[[Category: Long-acting insulin analog]]~~	+
-	~~[[Category: Pharmaceutical]]~~	+
-	~~[[Category: Receptor binding]]~~	+
-	~~[[Category: Secreted]]~~	+
-	~~[[Category: Zinc-binding site~~]]	+

OCA at 12:28, 13 October 2021

OCA — Wed, 13 Oct 2021 12:28:14 GMT

OCA at 07:03, 7 October 2020

OCA — Wed, 07 Oct 2020 07:03:01 GMT

←Older revision		Revision as of 07:03, 7 October 2020
Line 1:		Line 1:

	==Enhancing the Therapeutic Properties of a Protein by a Designed Zinc-Binding Site, Structural principles of a novel long-acting insulin analog==		==Enhancing the Therapeutic Properties of a Protein by a Designed Zinc-Binding Site, Structural principles of a novel long-acting insulin analog==
-	<StructureSection load='3kq6' size='340' side='right' caption='[[3kq6]], [[Resolution\|resolution]] 1.90Å' scene=''>	+	<StructureSection load='3kq6' size='340' side='right'caption='[[3kq6]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3kq6]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KQ6 OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3KQ6 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3kq6]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KQ6 OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=3KQ6 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rwe\|1rwe]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rwe\|1rwe]]</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=3kq6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kq6 OCA], [http://pdbe.org/3kq6 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3kq6 RCSB], [http://www.ebi.ac.uk/pdbsum/3kq6 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3kq6 ProSAT]</span></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=3kq6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kq6 OCA], [http://pdbe.org/3kq6 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3kq6 RCSB], [http://www.ebi.ac.uk/pdbsum/3kq6 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3kq6 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 33:		Line 33:

	==See Also==		==See Also==
-	*[[~~Molecular Playground/~~Insulin\|~~Molecular Playground/~~Insulin]]	+	*[[Insulin 3D Structures\|Insulin 3D Structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Large Structures]]
	[[Category: Hu, S Q]]		[[Category: Hu, S Q]]
	[[Category: Ismail-Beigi, F]]		[[Category: Ismail-Beigi, F]]

OCA at 06:40, 2 January 2019

OCA — Wed, 02 Jan 2019 06:40:34 GMT

←Older revision		Revision as of 06:40, 2 January 2019
Line 1:		Line 1:
		+
	==Enhancing the Therapeutic Properties of a Protein by a Designed Zinc-Binding Site, Structural principles of a novel long-acting insulin analog==		==Enhancing the Therapeutic Properties of a Protein by a Designed Zinc-Binding Site, Structural principles of a novel long-acting insulin analog==
	<StructureSection load='3kq6' size='340' side='right' caption='[[3kq6]], [[Resolution\|resolution]] 1.90Å' scene=''>		<StructureSection load='3kq6' size='340' side='right' caption='[[3kq6]], [[Resolution\|resolution]] 1.90Å' scene=''>
Line 5:		Line 6:
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rwe\|1rwe]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rwe\|1rwe]]</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=3kq6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kq6 OCA], [http://pdbe.org/3kq6 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3kq6 RCSB], [http://www.ebi.ac.uk/pdbsum/3kq6 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=3kq6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kq6 OCA], [http://pdbe.org/3kq6 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3kq6 RCSB], [http://www.ebi.ac.uk/pdbsum/3kq6 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3kq6 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 15:		Line 16:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/kq/3kq6_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/kq/3kq6_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 52:		Line 53:
	[[Category: Hormone]]		[[Category: Hormone]]
	[[Category: Long-acting insulin analog]]		[[Category: Long-acting insulin analog]]
		+	[[Category: Pharmaceutical]]
	[[Category: Receptor binding]]		[[Category: Receptor binding]]
	[[Category: Secreted]]		[[Category: Secreted]]
	[[Category: Zinc-binding site]]		[[Category: Zinc-binding site]]

OCA at 21:25, 8 February 2016

OCA — Mon, 08 Feb 2016 21:25:01 GMT

←Older revision		Revision as of 21:25, 8 February 2016
Line 5:		Line 5:
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rwe\|1rwe]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rwe\|1rwe]]</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=3kq6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kq6 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3kq6 RCSB], [http://www.ebi.ac.uk/pdbsum/3kq6 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=3kq6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kq6 OCA], [http://pdbe.org/3kq6 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3kq6 RCSB], [http://www.ebi.ac.uk/pdbsum/3kq6 PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 19:		Line 19:
	<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=3kq6 ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 29:		Line 29:
	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 3kq6" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==

OCA at 17:29, 18 December 2014

OCA — Thu, 18 Dec 2014 17:29:26 GMT

←Older revision		Revision as of 17:29, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3kq6\| PDB=3kq6 \| SCENE= }}~~	+	==Enhancing the Therapeutic Properties of a Protein by a Designed Zinc-Binding Site, Structural principles of a novel long-acting insulin analog==
-	===Enhancing the Therapeutic Properties of a Protein by a Designed Zinc-Binding Site, Structural principles of a novel long-acting insulin analog===	+	<StructureSection load='3kq6' size='340' side='right' caption='[[3kq6]], [[Resolution\|resolution]] 1.90Å' scene=''>
-	~~{{ABSTRACT_PUBMED_20181952}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3kq6]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KQ6 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3KQ6 FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rwe\|1rwe]]</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=3kq6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kq6 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3kq6 RCSB], [http://www.ebi.ac.uk/pdbsum/3kq6 PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[http://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[http://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[http://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[http://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.
		+	== 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/kq/3kq6_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 ==
		+	Bottom-up control of supramolecular protein assembly can provide a therapeutic nanobiotechnology. We demonstrate that the pharmacological properties of insulin can be enhanced by design of "zinc staples" between hexamers. Paired (i, i+4) His substitutions were introduced at an alpha-helical surface. The crystal structure contains both classical axial zinc ions and novel zinc ions at hexamer-hexamer interfaces. Although soluble at pH 4, the combined electrostatic effects of the substitutions and bridging zinc ions cause isoelectric precipitation at neutral pH. Following subcutaneous injection in a diabetic rat, the analog effected glycemic control with a time course similar to that of long acting formulation Lantus. Relative to Lantus, however, the analog discriminates at least 30-fold more stringently between the insulin receptor and mitogenic insulin-like growth factor receptor. Because aberrant mitogenic signaling may be associated with elevated cancer risk, such enhanced specificity may improve safety. Zinc stapling provides a general strategy to modify the pharmacokinetic and biological properties of a subcutaneous protein depot.

-	~~==Disease==~~	+	Supramolecular protein engineering: design of zinc-stapled insulin hexamers as a long acting depot.,Phillips NB, Wan ZL, Whittaker L, Hu SQ, Huang K, Hua QX, Whittaker J, Ismail-Beigi F, Weiss MA J Biol Chem. 2010 Apr 16;285(16):11755-9. Epub 2010 Feb 24. PMID:20181952<ref>PMID:20181952</ref>
-	~~[[http~~:~~//www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause~~ of familial hyperproinsulinemia (FHPRI) [MIM:[http://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref><ref>PMID:2196279</ref><ref>PMID:4019786</ref><ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin~~-dependent type 2 (IDDM2) [MIM:[http://omim.org/entry/125852 125852]]. IDDM2 is~~ a ~~multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy~~. ~~Clinical fetaures are polydipsia~~, ~~polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes~~, ~~kidneys~~, ~~nerves~~, ~~and blood vessels~~.~~<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal~~ (~~PNDM~~) ~~[MIM~~:~~[http://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood~~-~~onset autoimmune diabetes mellitus type 1~~. ~~It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life~~. ~~Permanent neonatal diabetes requires lifelong therapy.<ref>~~PMID:17855560</ref><ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[http://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref><ref>PMID:18162506</ref><ref>PMID:~~20226046~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis~~, the ~~pentose phosphate cycle, and glycogen synthesis in liver~~.	+	</div>
-		+
-	~~==About this Structure==~~	+
-	~~[[3kq6]] is a 4 chain structure~~. ~~Full crystallographic information is available from [http://oca~~.~~weizmann.ac.il~~/~~oca-bin/ocashort?id=3KQ6 OCA].~~	+

	==See Also==		==See Also==
	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]		*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:020181952</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
-	[[Category: Hu, S Q.]]	+	</StructureSection>
-	[[Category: Ismail-Beigi, F.]]	+	[[Category: Hu, S Q]]
-	[[Category: Phillips, N B.]]	+	[[Category: Ismail-Beigi, F]]
-	[[Category: Wan, Z L.]]	+	[[Category: Phillips, N B]]
-	[[Category: Weiss, M A.]]	+	[[Category: Wan, Z L]]
-	[[Category: Whittake, J.]]	+	[[Category: Weiss, M A]]
-	[[Category: Whittaker, L.]]	+	[[Category: Whittake, J]]
		+	[[Category: Whittaker, L]]
	[[Category: Carbohydrate metabolism]]		[[Category: Carbohydrate metabolism]]
	[[Category: Cleavage on pair of basic residue]]		[[Category: Cleavage on pair of basic residue]]

OCA at 21:45, 24 March 2013

OCA — Sun, 24 Mar 2013 21:45:26 GMT

←Older revision		Revision as of 21:45, 24 March 2013
Line 1:		Line 1:
-	[[Image:3kq6.png\|left\|200px]]
-
	{{STRUCTURE_3kq6\| PDB=3kq6 \| SCENE= }}		{{STRUCTURE_3kq6\| PDB=3kq6 \| SCENE= }}
-
	===Enhancing the Therapeutic Properties of a Protein by a Designed Zinc-Binding Site, Structural principles of a novel long-acting insulin analog===		===Enhancing the Therapeutic Properties of a Protein by a Designed Zinc-Binding Site, Structural principles of a novel long-acting insulin analog===
		+	{{ABSTRACT_PUBMED_20181952}}

-	~~{{ABSTRACT_PUBMED_20181952}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[http://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref><ref>PMID:2196279</ref><ref>PMID:4019786</ref><ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[http://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[http://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref><ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[http://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref><ref>PMID:18162506</ref><ref>PMID:20226046</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.

	==About this Structure==		==About this Structure==
Line 14:		Line 16:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:020181952</ref><references group="xtra"/>	+	<ref group="xtra">PMID:020181952</ref><references group="xtra"/><references/>
	[[Category: Hu, S Q.]]		[[Category: Hu, S Q.]]
	[[Category: Ismail-Beigi, F.]]		[[Category: Ismail-Beigi, F.]]

OCA at 11:31, 20 October 2012

OCA — Sat, 20 Oct 2012 11:31:38 GMT

←Older revision		Revision as of 11:31, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3kq6]] is a 4 chain structure ~~of [[Molecular Playground/Insulin]]~~. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KQ6 OCA].	+	[[3kq6]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KQ6 OCA].

	==See Also==		==See Also==

OCA: Protected "3kq6" [edit=sysop:move=sysop]

OCA — Thu, 26 Jul 2012 05:40:39 GMT

Protected "3kq6" [edit=sysop:move=sysop]

←Older revision

Revision as of 05:40, 26 July 2012

OCA at 05:40, 26 July 2012

OCA — Thu, 26 Jul 2012 05:40:36 GMT

←Older revision		Revision as of 05:40, 26 July 2012
Line 1:		Line 1:
-	{{Seed}}
	[[Image:3kq6.png\|left\|200px]]		[[Image:3kq6.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_3kq6", 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_3kq6\| PDB=3kq6 \| SCENE= }}		{{STRUCTURE_3kq6\| PDB=3kq6 \| SCENE= }}

	===Enhancing the Therapeutic Properties of a Protein by a Designed Zinc-Binding Site, Structural principles of a novel long-acting insulin analog===		===Enhancing the Therapeutic Properties of a Protein by a Designed Zinc-Binding Site, Structural principles of a novel long-acting insulin analog===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_20181952}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 20181952 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_20181952}}		{{ABSTRACT_PUBMED_20181952}}

	==About this Structure==		==About this Structure==
-	~~3KQ6~~ is a 4 ~~chains~~ structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KQ6 OCA].	+	[[3kq6]] is a 4 chain structure of [[Molecular Playground/Insulin]]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KQ6 OCA].
		+
		+	==See Also==
		+	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~20181952~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:020181952</ref><references group="xtra"/>
	[[Category: Hu, S Q.]]		[[Category: Hu, S Q.]]
	[[Category: Ismail-Beigi, F.]]		[[Category: Ismail-Beigi, F.]]
Line 39:		Line 30:
	[[Category: Hormone]]		[[Category: Hormone]]
	[[Category: Long-acting insulin analog]]		[[Category: Long-acting insulin analog]]
-	[[Category: Pharmaceutical]]
	[[Category: Receptor binding]]		[[Category: Receptor binding]]
	[[Category: Secreted]]		[[Category: Secreted]]
	[[Category: Zinc-binding site]]		[[Category: Zinc-binding site]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Apr 28 10:54:43 2010''

←Older revision		Revision as of 12:28, 13 October 2021
Line 3:		Line 3:
	<StructureSection load='3kq6' size='340' side='right'caption='[[3kq6]], [[Resolution\|resolution]] 1.90Å' scene=''>		<StructureSection load='3kq6' size='340' side='right'caption='[[3kq6]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3kq6]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KQ6 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=3KQ6 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3kq6]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KQ6 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3KQ6 FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rwe\|1rwe]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1rwe\|1rwe]]</div></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=3kq6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kq6 OCA], [~~http~~://pdbe.org/3kq6 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3kq6 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3kq6 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3kq6 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=3kq6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kq6 OCA], [https://pdbe.org/3kq6 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3kq6 RCSB], [https://www.ebi.ac.uk/pdbsum/3kq6 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3kq6 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[~~http~~://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[~~http~~://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[~~http~~://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[~~http~~://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>	+	[[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[https://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[https://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[https://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[https://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.	+	[[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]