2c8q: Difference between revisions

No edit summary
No edit summary
 
(5 intermediate revisions by the same user not shown)
Line 1: Line 1:
{{STRUCTURE_2c8q|  PDB=2c8q  |  SCENE=  }}
===INSULINE(1SEC) AND UV LASER EXCITED FLUORESCENCE===
{{ABSTRACT_PUBMED_16510972}}


==Disease==
==insuline(1sec) and UV laser excited fluorescence==
[[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>  
<StructureSection load='2c8q' size='340' side='right'caption='[[2c8q]], [[Resolution|resolution]] 1.95&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[2c8q]] 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=2C8Q OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2C8Q FirstGlance]. <br>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.95&#8491;</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=2c8q FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2c8q OCA], [https://pdbe.org/2c8q PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2c8q RCSB], [https://www.ebi.ac.uk/pdbsum/2c8q PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2c8q ProSAT]</span></td></tr>
</table>
== 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>  
== 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.
<div style="background-color:#fffaf0;">
== Publication Abstract from PubMed ==
Structural proteomics has promoted the rapid development of automated protein structure determination using X-ray crystallography. Robotics are now routinely used along the pipeline from genes to protein structures. However, a bottleneck still remains. At synchrotron beamlines, the success rate of automated sample alignment along the X-ray beam is limited by difficulties in visualization of protein crystals, especially when they are small and embedded in mother liquor. Despite considerable improvement in optical microscopes, the use of visible light transmitted or reflected by the sample may result in poor or misleading contrast. Here, the endogenous fluorescence from aromatic amino acids has been used to identify even tiny or weakly fluorescent crystals with a high success rate. The use of a compact laser at 266 nm in combination with non-fluorescent sample holders provides an efficient solution to collect high-contrast fluorescence images in a few milliseconds and using standard camera optics. The best image quality was obtained with direct illumination through a viewing system coaxial with the UV beam. Crystallographic data suggest that the employed UV exposures do not generate detectable structural damage.


==Function==
UV laser-excited fluorescence as a tool for the visualization of protein crystals mounted in loops.,Vernede X, Lavault B, Ohana J, Nurizzo D, Joly J, Jacquamet L, Felisaz F, Cipriani F, Bourgeois D Acta Crystallogr D Biol Crystallogr. 2006 Mar;62(Pt 3):253-61. Epub 2006, Feb 22. PMID:16510972<ref>PMID:16510972</ref>
[[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==
From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
[[2c8q]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2C8Q OCA].
</div>
<div class="pdbe-citations 2c8q" style="background-color:#fffaf0;"></div>


==See Also==
==See Also==
*[[Molecular Playground/Insulin|Molecular Playground/Insulin]]
*[[Insulin 3D Structures|Insulin 3D Structures]]
 
== References ==
==Reference==
<references/>
<ref group="xtra">PMID:016510972</ref><references group="xtra"/><references/>
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Bourgeois, D.]]
[[Category: Large Structures]]
[[Category: Cipriani, F.]]
[[Category: Bourgeois D]]
[[Category: Felisaz, F.]]
[[Category: Cipriani F]]
[[Category: Jacquamet, L.]]
[[Category: Felisaz F]]
[[Category: Joly, J.]]
[[Category: Jacquamet L]]
[[Category: Lavault, B.]]
[[Category: Joly J]]
[[Category: Nurizzo, D.]]
[[Category: Lavault B]]
[[Category: Ohana, J.]]
[[Category: Nurizzo D]]
[[Category: Vernede, X.]]
[[Category: Ohana J]]
[[Category: Carbohydrate metabolism]]
[[Category: Vernede X]]
[[Category: Diabetes mellitus]]
[[Category: Glucose metabolism]]
[[Category: Hormone]]
[[Category: Laser]]
[[Category: Uv]]

Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

OCA