3v1g: Difference between revisions

Jump to navigation Jump to search
No edit summary
No edit summary
 
(7 intermediate revisions by the same user not shown)
Line 1: Line 1:
'''Unreleased structure'''


The entry 3v1g is ON HOLD  until Dec 12 2013
==Forestalling insulin fibrillation by insertion of a chiral clamp mechanism-based application of protein engineering to global health==
<StructureSection load='3v1g' size='340' side='right'caption='[[3v1g]], [[Resolution|resolution]] 2.20&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[3v1g]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3V1G OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3V1G 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]] 2.2&#8491;</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=DGL:D-GLUTAMIC+ACID'>DGL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3v1g FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3v1g OCA], [https://pdbe.org/3v1g PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3v1g RCSB], [https://www.ebi.ac.uk/pdbsum/3v1g PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3v1g 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.


Authors: Wan, Z.L., Hua, Q.X., Wickramasinghe, N.P., Huang, K., Petkova, A.T., Hu, S.Q., Phillips, N.B., Yeh, I.J., Whittake, J., Ismail-Beigi, F., Katsoyyannis, P.G., Tycko, R., Weiss, M.A.
==See Also==
 
*[[Insulin 3D Structures|Insulin 3D Structures]]
Description: Forestalling insulin fibrillation by insertion of a chiral clamp mechanism-based application of protein engineering to global health
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Hu SQ]]
[[Category: Hua QX]]
[[Category: Huang K]]
[[Category: Ismail-Beigi F]]
[[Category: Katsoyyannis PG]]
[[Category: Petkova AT]]
[[Category: Phillips NB]]
[[Category: Tycko R]]
[[Category: Wan ZL]]
[[Category: Weiss MA]]
[[Category: Whittake J]]
[[Category: Wickramasinghe NP]]
[[Category: Yeh IJ]]

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

OCA