1uz9 - Revision history

OCA at 07:50, 12 July 2023

2023-07-12T07:50:39Z

←Older revision		Revision as of 07:50, 12 July 2023
Line 3:		Line 3:
	<StructureSection load='1uz9' size='340' side='right'caption='[[1uz9]], [[Resolution\|resolution]] 1.60Å' scene=''>		<StructureSection load='1uz9' size='340' side='right'caption='[[1uz9]], [[Resolution\|resolution]] 1.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1uz9]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1UZ9 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1UZ9 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1uz9]] 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=1UZ9 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1UZ9 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=CRS:M-CRESOL'>CRS</scene>, <scene name='pdbligand=UZ9:(2S)-2-AMINO-6-({(4R)-4-[(10R,13S)-10,13-DIMETHYL-3-OXOHEXADECAHYDRO-1H-CYCLOPENTA[A]PHENANTHREN-17-YL]PENTANOYL}AMINO)HEXANOIC+ACID'>UZ9</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]] 1.6Å</td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1efe\|1efe]], [[1ev3\|1ev3]], [[1ev6\|1ev6]], [[1evr\|1evr]], [[1fu2\|1fu2]], [[1fub\|1fub]], [[1g7a\|1g7a]], [[1g7b\|1g7b]], [[1guj\|1guj]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1kmf\|1kmf]], [[1lkq\|1lkq]], [[1lnp\|1lnp]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1mso\|1mso]], [[1os3\|1os3]], [[1os4\|1os4]], [[1q4v\|1q4v]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</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=CRS:M-CRESOL'>CRS</scene>, <scene name='pdbligand=UZ9:(2S)-2-AMINO-6-({(4R)-4-[(10R,13S)-10,13-DIMETHYL-3-OXOHEXADECAHYDRO-1H-CYCLOPENTA[A]PHENANTHREN-17-YL]PENTANOYL}AMINO)HEXANOIC+ACID'>UZ9</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=1uz9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1uz9 OCA], [https://pdbe.org/1uz9 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1uz9 RCSB], [https://www.ebi.ac.uk/pdbsum/1uz9 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1uz9 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=1uz9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1uz9 OCA], [https://pdbe.org/1uz9 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1uz9 RCSB], [https://www.ebi.ac.uk/pdbsum/1uz9 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1uz9 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.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Dodson~~, E J~~]]	+	[[Category: Dodson EJ]]
-	[[Category: Dodson~~, G G~~]]	+	[[Category: Dodson GG]]
-	[[Category: Havelund, S]]	+	[[Category: Havelund S]]
-	[[Category: Jonassen, I]]	+	[[Category: Jonassen I]]
-	[[Category: Roberts~~, S M~~]]	+	[[Category: Roberts SM]]
-	[[Category: Verma~~, C S~~]]	+	[[Category: Verma CS]]
-	[[Category: Whittingham~~, J L~~]]	+	[[Category: Whittingham JL]]
-	[[Category: Wilkinson~~, A J]]~~	+	[[Category: Wilkinson AJ]]
-	~~[[Category: Diabetes mellitus]]~~	+
-	~~[[Category: Hormone disease mutation]]~~	+
-	~~[[Category: Insulin]]~~	+
-	~~[[Category: Insulin family~~]]	+

OCA at 06:21, 6 October 2021

2021-10-06T06:21:18Z

OCA at 13:24, 1 January 2020

2020-01-01T13:24:34Z

←Older revision		Revision as of 13:24, 1 January 2020
Line 1:		Line 1:

	==Crystallographic and solution studies of N-lithocholyl insulin: a new generation of prolonged-acting insulins.==		==Crystallographic and solution studies of N-lithocholyl insulin: a new generation of prolonged-acting insulins.==
-	<StructureSection load='1uz9' size='340' side='right' caption='[[1uz9]], [[Resolution\|resolution]] 1.60Å' scene=''>	+	<StructureSection load='1uz9' size='340' side='right'caption='[[1uz9]], [[Resolution\|resolution]] 1.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1uz9]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1UZ9 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1UZ9 FirstGlance]. <br>		<table><tr><td colspan='2'>[[1uz9]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1UZ9 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1UZ9 FirstGlance]. <br>
Line 23:		Line 23:

	==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: Dodson, E J]]		[[Category: Dodson, E J]]
	[[Category: Dodson, G G]]		[[Category: Dodson, G G]]

OCA at 08:13, 28 March 2018

2018-03-28T08:13:09Z

←Older revision		Revision as of 08:13, 28 March 2018
Line 1:		Line 1:
-	==~~CRYSTALLOGRAPHIC AND SOLUTION STUDIES OF~~ N-~~LITHOCHOLYL INSULIN~~: ~~A NEW GENERATION OF PROLONGED~~-~~ACTING INSULINS~~.==	+
		+	==Crystallographic and solution studies of N-lithocholyl insulin: a new generation of prolonged-acting insulins.==
	<StructureSection load='1uz9' size='340' side='right' caption='[[1uz9]], [[Resolution\|resolution]] 1.60Å' scene=''>		<StructureSection load='1uz9' size='340' side='right' caption='[[1uz9]], [[Resolution\|resolution]] 1.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
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=CRS:M-CRESOL'>CRS</scene>, <scene name='pdbligand=UZ9:(2S)-2-AMINO-6-({(4R)-4-[(10R,13S)-10,13-DIMETHYL-3-OXOHEXADECAHYDRO-1H-CYCLOPENTA[A]PHENANTHREN-17-YL]PENTANOYL}AMINO)HEXANOIC+ACID'>UZ9</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=CRS:M-CRESOL'>CRS</scene>, <scene name='pdbligand=UZ9:(2S)-2-AMINO-6-({(4R)-4-[(10R,13S)-10,13-DIMETHYL-3-OXOHEXADECAHYDRO-1H-CYCLOPENTA[A]PHENANTHREN-17-YL]PENTANOYL}AMINO)HEXANOIC+ACID'>UZ9</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">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1efe\|1efe]], [[1ev3\|1ev3]], [[1ev6\|1ev6]], [[1evr\|1evr]], [[1fu2\|1fu2]], [[1fub\|1fub]], [[1g7a\|1g7a]], [[1g7b\|1g7b]], [[1guj\|1guj]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1kmf\|1kmf]], [[1lkq\|1lkq]], [[1lnp\|1lnp]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1mso\|1mso]], [[1os3\|1os3]], [[1os4\|1os4]], [[1q4v\|1q4v]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1efe\|1efe]], [[1ev3\|1ev3]], [[1ev6\|1ev6]], [[1evr\|1evr]], [[1fu2\|1fu2]], [[1fub\|1fub]], [[1g7a\|1g7a]], [[1g7b\|1g7b]], [[1guj\|1guj]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1kmf\|1kmf]], [[1lkq\|1lkq]], [[1lnp\|1lnp]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1mso\|1mso]], [[1os3\|1os3]], [[1os4\|1os4]], [[1q4v\|1q4v]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</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=1uz9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1uz9 OCA], [http://pdbe.org/1uz9 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1uz9 RCSB], [http://www.ebi.ac.uk/pdbsum/1uz9 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=1uz9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1uz9 OCA], [http://pdbe.org/1uz9 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1uz9 RCSB], [http://www.ebi.ac.uk/pdbsum/1uz9 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1uz9 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==

OCA at 14:08, 11 September 2015

2015-09-11T14:08:31Z

←Older revision		Revision as of 14:08, 11 September 2015
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=CRS:M-CRESOL'>CRS</scene>, <scene name='pdbligand=UZ9:(2S)-2-AMINO-6-({(4R)-4-[(10R,13S)-10,13-DIMETHYL-3-OXOHEXADECAHYDRO-1H-CYCLOPENTA[A]PHENANTHREN-17-YL]PENTANOYL}AMINO)HEXANOIC+ACID'>UZ9</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=CRS:M-CRESOL'>CRS</scene>, <scene name='pdbligand=UZ9:(2S)-2-AMINO-6-({(4R)-4-[(10R,13S)-10,13-DIMETHYL-3-OXOHEXADECAHYDRO-1H-CYCLOPENTA[A]PHENANTHREN-17-YL]PENTANOYL}AMINO)HEXANOIC+ACID'>UZ9</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">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1efe\|1efe]], [[1ev3\|1ev3]], [[1ev6\|1ev6]], [[1evr\|1evr]], [[1fu2\|1fu2]], [[1fub\|1fub]], [[1g7a\|1g7a]], [[1g7b\|1g7b]], [[1guj\|1guj]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1kmf\|1kmf]], [[1lkq\|1lkq]], [[1lnp\|1lnp]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1mso\|1mso]], [[1os3\|1os3]], [[1os4\|1os4]], [[1q4v\|1q4v]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1efe\|1efe]], [[1ev3\|1ev3]], [[1ev6\|1ev6]], [[1evr\|1evr]], [[1fu2\|1fu2]], [[1fub\|1fub]], [[1g7a\|1g7a]], [[1g7b\|1g7b]], [[1guj\|1guj]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1kmf\|1kmf]], [[1lkq\|1lkq]], [[1lnp\|1lnp]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1mso\|1mso]], [[1os3\|1os3]], [[1os4\|1os4]], [[1q4v\|1q4v]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</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=1uz9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1uz9 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1uz9 RCSB], [http://www.ebi.ac.uk/pdbsum/1uz9 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=1uz9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1uz9 OCA], [http://pdbe.org/1uz9 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1uz9 RCSB], [http://www.ebi.ac.uk/pdbsum/1uz9 PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 19:		Line 19:
	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 1uz9" style="background-color:#fffaf0;"></div>

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

OCA at 12:50, 18 December 2014

2014-12-18T12:50:04Z

←Older revision		Revision as of 12:50, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_1uz9\| PDB=1uz9 \| SCENE= }}~~	+	==CRYSTALLOGRAPHIC AND SOLUTION STUDIES OF N-LITHOCHOLYL INSULIN: A NEW GENERATION OF PROLONGED-ACTING INSULINS.==
-	===CRYSTALLOGRAPHIC AND SOLUTION STUDIES OF N-LITHOCHOLYL INSULIN: A NEW GENERATION OF PROLONGED-ACTING INSULINS.===	+	<StructureSection load='1uz9' size='340' side='right' caption='[[1uz9]], [[Resolution\|resolution]] 1.60Å' scene=''>
-	{~~{ABSTRACT_PUBMED_15147182}~~}	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[1uz9]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1UZ9 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1UZ9 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=CRS:M-CRESOL'>CRS</scene>, <scene name='pdbligand=UZ9:(2S)-2-AMINO-6-({(4R)-4-[(10R,13S)-10,13-DIMETHYL-3-OXOHEXADECAHYDRO-1H-CYCLOPENTA[A]PHENANTHREN-17-YL]PENTANOYL}AMINO)HEXANOIC+ACID'>UZ9</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">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1efe\|1efe]], [[1ev3\|1ev3]], [[1ev6\|1ev6]], [[1evr\|1evr]], [[1fu2\|1fu2]], [[1fub\|1fub]], [[1g7a\|1g7a]], [[1g7b\|1g7b]], [[1guj\|1guj]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1kmf\|1kmf]], [[1lkq\|1lkq]], [[1lnp\|1lnp]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1mso\|1mso]], [[1os3\|1os3]], [[1os4\|1os4]], [[1q4v\|1q4v]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</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=1uz9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1uz9 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1uz9 RCSB], [http://www.ebi.ac.uk/pdbsum/1uz9 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.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	The addition of specific bulky hydrophobic groups to the insulin molecule provides it with affinity for circulating serum albumin and enables it to form soluble macromolecular complexes at the site of subcutaneous injection, thereby securing slow absorption of the insulin analogue into the blood stream and prolonging its half-life once there. N-Lithocholic acid acylated insulin [Lys(B29)-lithocholyl des-(B30) human insulin] has been crystallized and the structure determined by X-ray crystallography at 1.6 A resolution to explore the molecular basis of its assembly. The unit cell in the crystal consists of an insulin hexamer containing two zinc ions, with two m-cresol molecules bound at each dimer-dimer interface stabilizing an R(6) conformation. Six covalently bound lithocholyl groups are arranged symmetrically around the outside of the hexamer. These form specific van der Waals and hydrogen-bonding interactions at the interfaces between neighboring hexamers, possibly representing the kinds of interactions which occur in the soluble aggregates at the site of injection. Comparison with an equivalent nonderivatized native insulin hexamer shows that the addition of the lithocholyl group disrupts neither the important conformational features of the insulin molecule nor its hexamer-forming ability. Indeed, binding studies show that the affinity of N-lithocholyl insulin for the human insulin receptor is not significantly diminished.

-	~~==Disease==~~	+	Crystallographic and solution studies of N-lithocholyl insulin: a new generation of prolonged-acting human insulins.,Whittingham JL, Jonassen I, Havelund S, Roberts SM, Dodson EJ, Verma CS, Wilkinson AJ, Dodson GG Biochemistry. 2004 May 25;43(20):5987-95. PMID:15147182<ref>PMID:15147182</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==~~	+
-	~~[[1uz9]] is a 2 chain structure~~. ~~Full crystallographic information is available from [http://oca~~.~~weizmann.ac.il~~/~~oca-bin/ocashort?id=1UZ9 OCA].~~	+

	==See Also==		==See Also==
	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]		*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:015147182</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
-	[[Category: Dodson, E J.]]	+	</StructureSection>
-	[[Category: Dodson, G G.]]	+	[[Category: Dodson, E J]]
-	[[Category: Havelund, S.]]	+	[[Category: Dodson, G G]]
-	[[Category: Jonassen, I.]]	+	[[Category: Havelund, S]]
-	[[Category: Roberts, S M.]]	+	[[Category: Jonassen, I]]
-	[[Category: Verma, C S.]]	+	[[Category: Roberts, S M]]
-	[[Category: Whittingham, J L.]]	+	[[Category: Verma, C S]]
-	[[Category: Wilkinson, A J.]]	+	[[Category: Whittingham, J L]]
		+	[[Category: Wilkinson, A J]]
	[[Category: Diabetes mellitus]]		[[Category: Diabetes mellitus]]
	[[Category: Hormone disease mutation]]		[[Category: Hormone disease mutation]]
	[[Category: Insulin]]		[[Category: Insulin]]
	[[Category: Insulin family]]		[[Category: Insulin family]]

OCA at 19:07, 24 March 2013

2013-03-24T19:07:34Z

←Older revision		Revision as of 19:07, 24 March 2013
Line 1:		Line 1:
-	[[Image:1uz9.png\|left\|200px]]
-
	{{STRUCTURE_1uz9\| PDB=1uz9 \| SCENE= }}		{{STRUCTURE_1uz9\| PDB=1uz9 \| SCENE= }}
-
	===CRYSTALLOGRAPHIC AND SOLUTION STUDIES OF N-LITHOCHOLYL INSULIN: A NEW GENERATION OF PROLONGED-ACTING INSULINS.===		===CRYSTALLOGRAPHIC AND SOLUTION STUDIES OF N-LITHOCHOLYL INSULIN: A NEW GENERATION OF PROLONGED-ACTING INSULINS.===
		+	{{ABSTRACT_PUBMED_15147182}}

-	~~{{ABSTRACT_PUBMED_15147182}}~~	+	==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:015147182</ref><references group="xtra"/>	+	<ref group="xtra">PMID:015147182</ref><references group="xtra"/><references/>
	[[Category: Dodson, E J.]]		[[Category: Dodson, E J.]]
	[[Category: Dodson, G G.]]		[[Category: Dodson, G G.]]

OCA at 19:28, 20 October 2012

2012-10-20T19:28:08Z

←Older revision		Revision as of 19:28, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[1uz9]] is a 2 chain structure ~~of [[Molecular Playground/Insulin]]~~. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1UZ9 OCA].	+	[[1uz9]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1UZ9 OCA].

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

OCA: Protected "1uz9" [edit=sysop:move=sysop]

2012-07-27T07:27:12Z

Protected "1uz9" [edit=sysop:move=sysop]

←Older revision

Revision as of 07:27, 27 July 2012

OCA at 07:27, 27 July 2012

2012-07-27T07:27:10Z

←Older revision		Revision as of 07:27, 27 July 2012
Line 1:		Line 1:
-	{{Seed}}
	[[Image:1uz9.png\|left\|200px]]		[[Image:1uz9.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_1uz9", 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_1uz9\| PDB=1uz9 \| SCENE= }}		{{STRUCTURE_1uz9\| PDB=1uz9 \| SCENE= }}

	===CRYSTALLOGRAPHIC AND SOLUTION STUDIES OF N-LITHOCHOLYL INSULIN: A NEW GENERATION OF PROLONGED-ACTING INSULINS.===		===CRYSTALLOGRAPHIC AND SOLUTION STUDIES OF N-LITHOCHOLYL INSULIN: A NEW GENERATION OF PROLONGED-ACTING INSULINS.===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_15147182}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 15147182 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_15147182}}		{{ABSTRACT_PUBMED_15147182}}

	==About this Structure==		==About this Structure==
-	~~1UZ9~~ is a [[~~Protein complex~~]] ~~structure~~. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1UZ9 OCA].	+	[[1uz9]] is a 2 chain structure of [[Molecular Playground/Insulin]]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1UZ9 OCA].
		+
		+	==See Also==
		+	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]

	==Reference==		==Reference==
-	Crystallographic and solution studies of N-lithocholyl insulin: a new generation of prolonged-acting human insulins., Whittingham JL, Jonassen I, Havelund S, Roberts SM, Dodson EJ, Verma CS, Wilkinson AJ, Dodson GG, Biochemistry. 2004 May 25;43(20):5987-95. PMID:~~[http:~~//~~www.ncbi.nlm.nih.gov/pubmed/15147182 15147182]~~	+	<ref group="xtra">PMID:015147182</ref><references group="xtra"/>
-	~~[[Category: Protein complex]]~~	+
	[[Category: Dodson, E J.]]		[[Category: Dodson, E J.]]
	[[Category: Dodson, G G.]]		[[Category: Dodson, G G.]]
Line 37:		Line 27:
	[[Category: Insulin]]		[[Category: Insulin]]
	[[Category: Insulin family]]		[[Category: Insulin family]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Tue Jul 29 07:36:11 2008''

←Older revision		Revision as of 06:21, 6 October 2021
Line 3:		Line 3:
	<StructureSection load='1uz9' size='340' side='right'caption='[[1uz9]], [[Resolution\|resolution]] 1.60Å' scene=''>		<StructureSection load='1uz9' size='340' side='right'caption='[[1uz9]], [[Resolution\|resolution]] 1.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1uz9]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1UZ9 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1UZ9 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1uz9]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1UZ9 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1UZ9 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=CRS:M-CRESOL'>CRS</scene>, <scene name='pdbligand=UZ9:(2S)-2-AMINO-6-({(4R)-4-[(10R,13S)-10,13-DIMETHYL-3-OXOHEXADECAHYDRO-1H-CYCLOPENTA[A]PHENANTHREN-17-YL]PENTANOYL}AMINO)HEXANOIC+ACID'>UZ9</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=CRS:M-CRESOL'>CRS</scene>, <scene name='pdbligand=UZ9:(2S)-2-AMINO-6-({(4R)-4-[(10R,13S)-10,13-DIMETHYL-3-OXOHEXADECAHYDRO-1H-CYCLOPENTA[A]PHENANTHREN-17-YL]PENTANOYL}AMINO)HEXANOIC+ACID'>UZ9</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">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1efe\|1efe]], [[1ev3\|1ev3]], [[1ev6\|1ev6]], [[1evr\|1evr]], [[1fu2\|1fu2]], [[1fub\|1fub]], [[1g7a\|1g7a]], [[1g7b\|1g7b]], [[1guj\|1guj]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1kmf\|1kmf]], [[1lkq\|1lkq]], [[1lnp\|1lnp]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1mso\|1mso]], [[1os3\|1os3]], [[1os4\|1os4]], [[1q4v\|1q4v]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1efe\|1efe]], [[1ev3\|1ev3]], [[1ev6\|1ev6]], [[1evr\|1evr]], [[1fu2\|1fu2]], [[1fub\|1fub]], [[1g7a\|1g7a]], [[1g7b\|1g7b]], [[1guj\|1guj]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1kmf\|1kmf]], [[1lkq\|1lkq]], [[1lnp\|1lnp]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1mso\|1mso]], [[1os3\|1os3]], [[1os4\|1os4]], [[1q4v\|1q4v]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</div></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=1uz9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1uz9 OCA], [~~http~~://pdbe.org/1uz9 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=1uz9 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/1uz9 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=1uz9 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=1uz9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1uz9 OCA], [https://pdbe.org/1uz9 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1uz9 RCSB], [https://www.ebi.ac.uk/pdbsum/1uz9 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1uz9 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.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==