6nwv - Revision history

OCA at 07:01, 11 October 2023

OCA — Wed, 11 Oct 2023 07:01:09 GMT

←Older revision		Revision as of 07:01, 11 October 2023
Line 3:		Line 3:
	<StructureSection load='6nwv' size='340' side='right'caption='[[6nwv]], [[Resolution\|resolution]] 1.60Å' scene=''>		<StructureSection load='6nwv' size='340' side='right'caption='[[6nwv]], [[Resolution\|resolution]] 1.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6nwv]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6NWV OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=6NWV FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6nwv]] is a 12 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=6NWV OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6NWV 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=GOL:GLYCEROL'>GOL</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]] 1.601Å</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=6nwv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6nwv OCA], [~~http~~://pdbe.org/6nwv PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6nwv RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6nwv PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6nwv ProSAT]</span></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=GOL:GLYCEROL'>GOL</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=6nwv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6nwv OCA], [https://pdbe.org/6nwv PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6nwv RCSB], [https://www.ebi.ac.uk/pdbsum/6nwv PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6nwv 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.
		+
		+	==See Also==
		+	*[[Insulin 3D Structures\|Insulin 3D Structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Cruz-Rangel, A]]	+	[[Category: Cruz-Rangel A]]
-	[[Category: Reyes-Grajeda~~, J P~~]]	+	[[Category: Reyes-Grajeda JP]]
-	[[Category: Romero, A]]	+	[[Category: Romero A]]
-	~~[[Category: Diabetes]]~~	+
-	~~[[Category: Hexameric]]~~	+
-	~~[[Category: Hormone]]~~	+
-	~~[[Category: Insulin analog~~]]	+

OCA at 04:17, 13 February 2020

OCA — Thu, 13 Feb 2020 04:17:11 GMT

←Older revision		Revision as of 04:17, 13 February 2020
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 6nwv is ~~ON HOLD until Feb~~ 12 ~~2021~~	+	==Insulin Lispro Analog==
-		+	<StructureSection load='6nwv' size='340' side='right'caption='[[6nwv]], [[Resolution\|resolution]] 1.60Å' scene=''>
-	~~Authors~~: ~~Cruz~~-~~Rangel~~, A., ~~Romero~~, A., ~~Reyes~~-~~Grajeda~~, J.P.	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[6nwv]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6NWV OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6NWV FirstGlance]. <br>
-	~~Description~~: Insulin ~~Lispro Analog~~	+	</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=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-	[[Category: ~~Unreleased~~ Structures]]	+	<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=6nwv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6nwv OCA], [http://pdbe.org/6nwv PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6nwv RCSB], [http://www.ebi.ac.uk/pdbsum/6nwv PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6nwv ProSAT]</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.
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Cruz-Rangel, A]]
		+	[[Category: Reyes-Grajeda, J P]]
	[[Category: Romero, A]]		[[Category: Romero, A]]
-	[[Category: ~~Cruz-Rangel, A~~]]	+	[[Category: Diabetes]]
-	[[Category: ~~Reyes-Grajeda, J.P~~]]	+	[[Category: Hexameric]]
		+	[[Category: Hormone]]
		+	[[Category: Insulin analog]]

OCA at 05:06, 6 November 2019

OCA — Wed, 06 Nov 2019 05:06:18 GMT

←Older revision		Revision as of 05:06, 6 November 2019
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 6nwv is ON HOLD until ~~Nov 06 2020~~	+	The entry 6nwv is ON HOLD until Feb 12 2021

	Authors: Cruz-Rangel, A., Romero, A., Reyes-Grajeda, J.P.		Authors: Cruz-Rangel, A., Romero, A., Reyes-Grajeda, J.P.

OCA at 04:13, 7 August 2019

OCA — Wed, 07 Aug 2019 04:13:41 GMT

←Older revision		Revision as of 04:13, 7 August 2019
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 6nwv is ON HOLD until ~~Aug 07~~ 2020	+	The entry 6nwv is ON HOLD until Nov 06 2020

	Authors: Cruz-Rangel, A., Romero, A., Reyes-Grajeda, J.P.		Authors: Cruz-Rangel, A., Romero, A., Reyes-Grajeda, J.P.

OCA at 05:10, 21 February 2019

OCA — Thu, 21 Feb 2019 05:10:20 GMT

←Older revision		Revision as of 05:10, 21 February 2019
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 6nwv is ON HOLD	+	The entry 6nwv is ON HOLD until Aug 07 2020

	Authors: Cruz-Rangel, A., Romero, A., Reyes-Grajeda, J.P.		Authors: Cruz-Rangel, A., Romero, A., Reyes-Grajeda, J.P.

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

OCA — Wed, 13 Feb 2019 07:54:01 GMT

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

←Older revision

Revision as of 07:54, 13 February 2019

OCA: New page: '''Unreleased structure''' The entry 6nwv is ON HOLD Authors: Cruz-Rangel, A., Romero, A., Reyes-Grajeda, J.P. Description: Insulin Lispro Analog Category: Unreleased Structures [[...

OCA — Wed, 13 Feb 2019 07:53:59 GMT

New page: '''Unreleased structure''' The entry 6nwv is ON HOLD Authors: Cruz-Rangel, A., Romero, A., Reyes-Grajeda, J.P. Description: Insulin Lispro Analog Category: Unreleased Structures [[...

New page

'''Unreleased structure'''

The entry 6nwv is ON HOLD

Authors: Cruz-Rangel, A., Romero, A., Reyes-Grajeda, J.P.

Description: Insulin Lispro Analog
[[Category: Unreleased Structures]]
[[Category: Romero, A]]
[[Category: Cruz-Rangel, A]]
[[Category: Reyes-Grajeda, J.P]]