1trz - Revision history

OCA at 11:25, 14 March 2024

OCA — Thu, 14 Mar 2024 11:25:09 GMT

←Older revision		Revision as of 11:25, 14 March 2024
Line 3:		Line 3:
	<StructureSection load='1trz' size='340' side='right'caption='[[1trz]], [[Resolution\|resolution]] 1.60Å' scene=''>		<StructureSection load='1trz' size='340' side='right'caption='[[1trz]], [[Resolution\|resolution]] 1.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [https://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [https://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. The February 2016 RCSB PDB [https://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Designer Insulins'' by David Goodsell is [https://dx.doi.org/10.2210/rcsb_pdb/mom_2016_2 10.2210/rcsb_pdb/mom_2016_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1TRZ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. The February 2001 RCSB PDB [https://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [https://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. The February 2016 RCSB PDB [https://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Designer Insulins'' by David Goodsell is [https://dx.doi.org/10.2210/rcsb_pdb/mom_2016_2 10.2210/rcsb_pdb/mom_2016_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1TRZ 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=NA:SODIUM+ION'>NA</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='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=NA:SODIUM+ION'>NA</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=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [https://pdbe.org/1trz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [https://www.ebi.ac.uk/pdbsum/1trz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1trz 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=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [https://pdbe.org/1trz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [https://www.ebi.ac.uk/pdbsum/1trz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1trz 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 21:		Line 22:
	</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=1trz 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=1trz ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
-	<div style="background-color:#fffaf0;">
-	== Publication Abstract from PubMed ==
-	The T3R3 human insulin hexamer (T and R referring to extended and alpha-helical conformations, respectively, of the first eight residues of the B-chain), complexed to two zinc ions, crystallizes in space group R3 with hexagonal cell constants a = 80.64 and c = 37.78 A. The structure has been refined to a residual of 0.172 using 9225 independent data to 1.6-A resolution. The asymmetric unit consists of a TR dimer, and the insulin hexamer is generated by the action of the crystallographic 3-fold axis. The conformation of one insulin trimer is nearly identical to that of the T6 hexamer, while the other trimer approximates that of the R6 hexamer, except for the three N-terminal B-chain residues that adopt an extended rather than an alpha-helical conformation. Each of the two zinc ions, which lie on the crystallographic 3-fold axis and exhibit two different, disordered coordination geometries, is coordinated by the imidazole groups of three symmetry-related B10 histidine residues. The coordination sphere of the zinc in the T3 trimer is either tetrahedral, with the fourth site filled by a chloride ion, or octahedral, completed by three water molecules. The coordination of the zinc in the 12-A narrow channel in the R3 trimer is tetrahedral, with either a second chloride ion or a water molecule completing the coordination sphere. The putative off-axial zinc binding sites that result from the T-->R transition of monomer II do not contain zinc ion, but instead are filled with clusters of ordered water molecules.(ABSTRACT TRUNCATED AT 250 WORDS)
-
-	Crystallographic evidence for dual coordination around zinc in the T3R3 human insulin hexamer.,Ciszak E, Smith GD Biochemistry. 1994 Feb 15;33(6):1512-7. PMID:8312271<ref>PMID:8312271</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 1trz" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 38:		Line 30:
	</StructureSection>		</StructureSection>
	[[Category: Designer Insulins]]		[[Category: Designer Insulins]]
		+	[[Category: Homo sapiens]]
	[[Category: Insulin]]		[[Category: Insulin]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: RCSB PDB Molecule of the Month]]		[[Category: RCSB PDB Molecule of the Month]]
-	[[Category: Ciszak, E]]	+	[[Category: Ciszak E]]
-	[[Category: Smith~~, G D]]~~	+	[[Category: Smith GD]]
-	~~[[Category: Hormone~~]]	+

OCA at 09:31, 29 September 2021

OCA — Wed, 29 Sep 2021 09:31:52 GMT

←Older revision		Revision as of 09:31, 29 September 2021
Line 3:		Line 3:
	<StructureSection load='1trz' size='340' side='right'caption='[[1trz]], [[Resolution\|resolution]] 1.60Å' scene=''>		<StructureSection load='1trz' size='340' side='right'caption='[[1trz]], [[Resolution\|resolution]] 1.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [~~http~~://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [~~http~~://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. The February 2016 RCSB PDB [~~http~~://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Designer Insulins'' by David Goodsell is [~~http~~://dx.doi.org/10.2210/rcsb_pdb/mom_2016_2 10.2210/rcsb_pdb/mom_2016_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1TRZ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [https://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [https://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. The February 2016 RCSB PDB [https://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Designer Insulins'' by David Goodsell is [https://dx.doi.org/10.2210/rcsb_pdb/mom_2016_2 10.2210/rcsb_pdb/mom_2016_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1TRZ 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=NA:SODIUM+ION'>NA</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=NA:SODIUM+ION'>NA</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'>[~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [~~http~~://pdbe.org/1trz PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/1trz PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=1trz 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=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [https://pdbe.org/1trz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [https://www.ebi.ac.uk/pdbsum/1trz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1trz 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]]

OCA at 14:01, 25 December 2019

OCA — Wed, 25 Dec 2019 14:01:30 GMT

←Older revision		Revision as of 14:01, 25 December 2019
Line 1:		Line 1:

	==CRYSTALLOGRAPHIC EVIDENCE FOR DUAL COORDINATION AROUND ZINC IN THE T3R3 HUMAN INSULIN HEXAMER==		==CRYSTALLOGRAPHIC EVIDENCE FOR DUAL COORDINATION AROUND ZINC IN THE T3R3 HUMAN INSULIN HEXAMER==
-	<StructureSection load='1trz' size='340' side='right' caption='[[1trz]], [[Resolution\|resolution]] 1.60Å' scene=''>	+	<StructureSection load='1trz' size='340' side='right'caption='[[1trz]], [[Resolution\|resolution]] 1.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. The February 2016 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Designer Insulins'' by David Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2016_2 10.2210/rcsb_pdb/mom_2016_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1TRZ FirstGlance]. <br>		<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. The February 2016 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Designer Insulins'' by David Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2016_2 10.2210/rcsb_pdb/mom_2016_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1TRZ FirstGlance]. <br>
Line 32:		Line 32:

	==See Also==		==See Also==
-	*[[~~Molecular Playground/~~Insulin\|~~Molecular Playground/~~Insulin]]	+	*[[Insulin 3D Structures\|Insulin 3D Structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 39:		Line 39:
	[[Category: Designer Insulins]]		[[Category: Designer Insulins]]
	[[Category: Insulin]]		[[Category: Insulin]]
		+	[[Category: Large Structures]]
	[[Category: RCSB PDB Molecule of the Month]]		[[Category: RCSB PDB Molecule of the Month]]
	[[Category: Ciszak, E]]		[[Category: Ciszak, E]]
	[[Category: Smith, G D]]		[[Category: Smith, G D]]
	[[Category: Hormone]]		[[Category: Hormone]]

OCA at 08:51, 21 March 2018

OCA — Wed, 21 Mar 2018 08:51:17 GMT

←Older revision		Revision as of 08:51, 21 March 2018
Line 1:		Line 1:
		+
	==CRYSTALLOGRAPHIC EVIDENCE FOR DUAL COORDINATION AROUND ZINC IN THE T3R3 HUMAN INSULIN HEXAMER==		==CRYSTALLOGRAPHIC EVIDENCE FOR DUAL COORDINATION AROUND ZINC IN THE T3R3 HUMAN INSULIN HEXAMER==
	<StructureSection load='1trz' size='340' side='right' caption='[[1trz]], [[Resolution\|resolution]] 1.60Å' scene=''>		<StructureSection load='1trz' size='340' side='right' caption='[[1trz]], [[Resolution\|resolution]] 1.60Å' scene=''>
Line 4:		Line 5:
	<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. The February 2016 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Designer Insulins'' by David Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2016_2 10.2210/rcsb_pdb/mom_2016_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1TRZ FirstGlance]. <br>		<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. The February 2016 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Designer Insulins'' by David Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2016_2 10.2210/rcsb_pdb/mom_2016_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1TRZ 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=NA:SODIUM+ION'>NA</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=NA:SODIUM+ION'>NA</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'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [http://pdbe.org/1trz PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [http://www.ebi.ac.uk/pdbsum/1trz 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=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [http://pdbe.org/1trz PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [http://www.ebi.ac.uk/pdbsum/1trz PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1trz ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 14:		Line 15:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/tr/1trz_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/tr/1trz_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 31:		Line 32:

	==See Also==		==See Also==
-	*[[Hormone\|Hormone]]
	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]		*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
	== References ==		== References ==

OCA at 11:26, 7 February 2016

OCA — Sun, 07 Feb 2016 11:26:29 GMT

←Older revision		Revision as of 11:26, 7 February 2016
Line 2:		Line 2:
	<StructureSection load='1trz' size='340' side='right' caption='[[1trz]], [[Resolution\|resolution]] 1.60Å' scene=''>		<StructureSection load='1trz' size='340' side='right' caption='[[1trz]], [[Resolution\|resolution]] 1.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1TRZ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. The February 2016 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Designer Insulins'' by David Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2016_2 10.2210/rcsb_pdb/mom_2016_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1TRZ 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=NA:SODIUM+ION'>NA</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=NA:SODIUM+ION'>NA</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'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [http://pdbe.org/1trz PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [http://www.ebi.ac.uk/pdbsum/1trz 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=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [http://pdbe.org/1trz PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [http://www.ebi.ac.uk/pdbsum/1trz PDBsum]</span></td></tr>
Line 18:		Line 18:
	<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=1trz ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 37:		Line 37:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Designer Insulins]]
	[[Category: Insulin]]		[[Category: Insulin]]
	[[Category: RCSB PDB Molecule of the Month]]		[[Category: RCSB PDB Molecule of the Month]]

OCA at 01:02, 10 September 2015

OCA — Thu, 10 Sep 2015 01:02:30 GMT

←Older revision		Revision as of 01:02, 10 September 2015
Line 4:		Line 4:
	<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1TRZ FirstGlance]. <br>		<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1TRZ 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=NA:SODIUM+ION'>NA</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=NA:SODIUM+ION'>NA</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'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [http://www.ebi.ac.uk/pdbsum/1trz 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=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [http://pdbe.org/1trz PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [http://www.ebi.ac.uk/pdbsum/1trz PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 28:		Line 28:
	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 1trz" style="background-color:#fffaf0;"></div>

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

OCA at 12:55, 6 January 2015

OCA — Tue, 06 Jan 2015 12:55:27 GMT

←Older revision		Revision as of 12:55, 6 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1TRZ FirstGlance]. <br>		<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1TRZ FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene><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=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [http://www.ebi.ac.uk/pdbsum/1trz 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=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [http://www.ebi.ac.uk/pdbsum/1trz PDBsum]</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>		[[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>
Line 38:		Line 38:
	[[Category: Insulin]]		[[Category: Insulin]]
	[[Category: RCSB PDB Molecule of the Month]]		[[Category: RCSB PDB Molecule of the Month]]
-	[[Category: Ciszak, E.]]	+	[[Category: Ciszak, E]]
-	[[Category: Smith, G D.]]	+	[[Category: Smith, G D]]
	[[Category: Hormone]]		[[Category: Hormone]]

OCA at 20:36, 29 September 2014

OCA — Mon, 29 Sep 2014 20:36:06 GMT

←Older revision		Revision as of 20:36, 29 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_1trz\| PDB=1trz \| SCENE= }}~~	+	==CRYSTALLOGRAPHIC EVIDENCE FOR DUAL COORDINATION AROUND ZINC IN THE T3R3 HUMAN INSULIN HEXAMER==
-	===CRYSTALLOGRAPHIC EVIDENCE FOR DUAL COORDINATION AROUND ZINC IN THE T3R3 HUMAN INSULIN HEXAMER===	+	<StructureSection load='1trz' size='340' side='right' caption='[[1trz]], [[Resolution\|resolution]] 1.60Å' scene=''>
-	~~{{ABSTRACT_PUBMED_8312271}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1TRZ FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene><br>
		+	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1trz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1trz OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1trz RCSB], [http://www.ebi.ac.uk/pdbsum/1trz 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/tr/1trz_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 ==
		+	The T3R3 human insulin hexamer (T and R referring to extended and alpha-helical conformations, respectively, of the first eight residues of the B-chain), complexed to two zinc ions, crystallizes in space group R3 with hexagonal cell constants a = 80.64 and c = 37.78 A. The structure has been refined to a residual of 0.172 using 9225 independent data to 1.6-A resolution. The asymmetric unit consists of a TR dimer, and the insulin hexamer is generated by the action of the crystallographic 3-fold axis. The conformation of one insulin trimer is nearly identical to that of the T6 hexamer, while the other trimer approximates that of the R6 hexamer, except for the three N-terminal B-chain residues that adopt an extended rather than an alpha-helical conformation. Each of the two zinc ions, which lie on the crystallographic 3-fold axis and exhibit two different, disordered coordination geometries, is coordinated by the imidazole groups of three symmetry-related B10 histidine residues. The coordination sphere of the zinc in the T3 trimer is either tetrahedral, with the fourth site filled by a chloride ion, or octahedral, completed by three water molecules. The coordination of the zinc in the 12-A narrow channel in the R3 trimer is tetrahedral, with either a second chloride ion or a water molecule completing the coordination sphere. The putative off-axial zinc binding sites that result from the T-->R transition of monomer II do not contain zinc ion, but instead are filled with clusters of ordered water molecules.(ABSTRACT TRUNCATED AT 250 WORDS)

-	~~==Disease==~~	+	Crystallographic evidence for dual coordination around zinc in the T3R3 human insulin hexamer.,Ciszak E, Smith GD Biochemistry. 1994 Feb 15;33(6):1512-7. PMID:8312271<ref>PMID:8312271</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==~~	+
-	~~[[1trz]] is~~ a ~~4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule~~ of the ~~Month] feature on ''Insulin'' by David~~ S. ~~Goodsell is [http://dx~~.~~doi.org~~/~~10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA].~~	+

	==See Also==		==See Also==
	*[[Hormone\|Hormone]]		*[[Hormone\|Hormone]]
	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]		*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:008312271</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Insulin]]		[[Category: Insulin]]
	[[Category: RCSB PDB Molecule of the Month]]		[[Category: RCSB PDB Molecule of the Month]]

OCA at 18:52, 24 March 2013

OCA — Sun, 24 Mar 2013 18:52:47 GMT

←Older revision		Revision as of 18:52, 24 March 2013
Line 1:		Line 1:
-	[[Image:1trz.png\|left\|200px]]
-
	{{STRUCTURE_1trz\| PDB=1trz \| SCENE= }}		{{STRUCTURE_1trz\| PDB=1trz \| SCENE= }}
-
	===CRYSTALLOGRAPHIC EVIDENCE FOR DUAL COORDINATION AROUND ZINC IN THE T3R3 HUMAN INSULIN HEXAMER===		===CRYSTALLOGRAPHIC EVIDENCE FOR DUAL COORDINATION AROUND ZINC IN THE T3R3 HUMAN INSULIN HEXAMER===
		+	{{ABSTRACT_PUBMED_8312271}}

-	~~{{ABSTRACT_PUBMED_8312271}}~~	+	==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 15:		Line 17:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:008312271</ref><references group="xtra"/>	+	<ref group="xtra">PMID:008312271</ref><references group="xtra"/><references/>
	[[Category: Insulin]]		[[Category: Insulin]]
	[[Category: RCSB PDB Molecule of the Month]]		[[Category: RCSB PDB Molecule of the Month]]

OCA at 06:29, 20 October 2012

OCA — Sat, 20 Oct 2012 06:29:52 GMT

←Older revision		Revision as of 06:29, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[1trz]] is a 4 chain structure ~~of [[Hormone]] and [[Molecular Playground/Insulin]]~~. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA].	+	[[1trz]] is a 4 chain structure. The February 2001 RCSB PDB [http://pdb.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/index.html Molecule of the Month] feature on ''Insulin'' by David S. Goodsell is [http://dx.doi.org/10.2210/rcsb_pdb/mom_2001_2 10.2210/rcsb_pdb/mom_2001_2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TRZ OCA].

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