8pi6 - Revision history

OCA at 05:35, 17 April 2024

OCA — Wed, 17 Apr 2024 05:35:03 GMT

←Older revision		Revision as of 05:35, 17 April 2024
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	== 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;">
-	== Publication Abstract from PubMed ==
-	Since the first administration of insulin to a person with diabetes in 1922, scientific contributions from academia and industry have improved insulin therapy and access. The pharmaceutical need for insulin is now more than 40 tons annually, half of which is produced by recombinant secretory expression in Saccharomyces cerevisiae. We discuss how, in this yeast species, adaptation of insulin precursors by removable structural elements is pivotal for efficient secretory expression. The technologies reviewed have been implemented at industrial scale and are seminal for the supply of human insulin and insulin analogues to people with diabetes now and in the future. Engineering of a target protein with removable structural elements may provide a general approach to yield optimisation.
-
-	Molecular engineering of insulin for recombinant expression in yeast.,Kjeldsen T, Andersen AS, Hubalek F, Johansson E, Kreiner FF, Schluckebier G, Kurtzhals P Trends Biotechnol. 2023 Oct 24:S0167-7799(23)00286-X. doi: , 10.1016/j.tibtech.2023.09.012. PMID:37880066<ref>PMID:37880066</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 8pi6" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>

OCA at 12:03, 8 November 2023

OCA — Wed, 08 Nov 2023 12:03:29 GMT

←Older revision		Revision as of 12:03, 8 November 2023
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-	'''Unreleased structure'''

-	~~The entry~~ 8pi6 is ~~ON HOLD until Paper~~ Publication	+	==Crystal structure of the monomeric zinc free human insulin A22K, B3E, B26E, B29R, desB30 precursor with a Ser-Glu-Asp-Trp-Trp-Arg C-peptide and a Glu-Glu-Gly-Glu-Pro-Arg N-terminal extension==
		+	<StructureSection load='8pi6' size='340' side='right'caption='[[8pi6]], [[Resolution\|resolution]] 2.14Å' scene=''>
		+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[8pi6]] is a 5 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=8PI6 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8PI6 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]] 2.14Å</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=8pi6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8pi6 OCA], [https://pdbe.org/8pi6 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8pi6 RCSB], [https://www.ebi.ac.uk/pdbsum/8pi6 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8pi6 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 ==
		+	Since the first administration of insulin to a person with diabetes in 1922, scientific contributions from academia and industry have improved insulin therapy and access. The pharmaceutical need for insulin is now more than 40 tons annually, half of which is produced by recombinant secretory expression in Saccharomyces cerevisiae. We discuss how, in this yeast species, adaptation of insulin precursors by removable structural elements is pivotal for efficient secretory expression. The technologies reviewed have been implemented at industrial scale and are seminal for the supply of human insulin and insulin analogues to people with diabetes now and in the future. Engineering of a target protein with removable structural elements may provide a general approach to yield optimisation.

-	~~Authors~~:	+	Molecular engineering of insulin for recombinant expression in yeast.,Kjeldsen T, Andersen AS, Hubalek F, Johansson E, Kreiner FF, Schluckebier G, Kurtzhals P Trends Biotechnol. 2023 Oct 24:S0167-7799(23)00286-X. doi: , 10.1016/j.tibtech.2023.09.012. PMID:37880066<ref>PMID:37880066</ref>

-	~~Description~~:	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	[[Category: ~~Unreleased~~ Structures]]	+	</div>
		+	<div class="pdbe-citations 8pi6" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Homo sapiens]]
		+	[[Category: Large Structures]]
		+	[[Category: Johansson E]]
		+	[[Category: Schluckebier G]]

OCA at 09:02, 2 August 2023

OCA — Wed, 02 Aug 2023 09:02:59 GMT

←Older revision		Revision as of 09:02, 2 August 2023
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	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 8pi6 is ON HOLD	+	The entry 8pi6 is ON HOLD until Paper Publication

	Authors:		Authors:

OCA at 04:12, 5 July 2023

OCA — Wed, 05 Jul 2023 04:12:01 GMT

←Older revision		Revision as of 04:12, 5 July 2023
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	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 8pi6 is ON HOLD ~~until sometime in the future~~	+	The entry 8pi6 is ON HOLD

	Authors:		Authors:

OCA: Protected "8pi6" [edit=sysop:move=sysop]

OCA — Wed, 28 Jun 2023 19:53:40 GMT

Protected "8pi6" [edit=sysop:move=sysop]

←Older revision

Revision as of 19:53, 28 June 2023

OCA: New page: '''Unreleased structure''' The entry 8pi6 is ON HOLD until sometime in the future Authors: Description: Category: Unreleased Structures

OCA — Wed, 28 Jun 2023 19:53:39 GMT

New page: '''Unreleased structure''' The entry 8pi6 is ON HOLD until sometime in the future Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 8pi6 is ON HOLD until sometime in the future

Authors:

Description:
[[Category: Unreleased Structures]]