5m3x: Difference between revisions

From Proteopedia
Jump to navigationJump to search
OCA (talk | contribs)
m Protected "5m3x" [edit=sysop:move=sysop]
OCA (talk | contribs)
No edit summary
Line 1: Line 1:
'''Unreleased structure'''


The entry 5m3x is ON HOLD  until Paper Publication
==Crystal structure of human angiotensin I-deleted angiotensinogen==
 
<StructureSection load='5m3x' size='340' side='right' caption='[[5m3x]], [[Resolution|resolution]] 2.63&Aring;' scene=''>
Authors: Yan, Y., Read, R.J.
== Structural highlights ==
 
<table><tr><td colspan='2'>[[5m3x]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5M3X OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5M3X FirstGlance]. <br>
Description: Crystal structure of human angiotensin I-deleted angiotensinogen
</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=5m3x FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5m3x OCA], [http://pdbe.org/5m3x PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5m3x RCSB], [http://www.ebi.ac.uk/pdbsum/5m3x PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5m3x ProSAT]</span></td></tr>
[[Category: Unreleased Structures]]
</table>
[[Category: Read, R.J]]
== Disease ==
[[http://www.uniprot.org/uniprot/ANGT_HUMAN ANGT_HUMAN]] Genetic variations in AGT are a cause of susceptibility to essential hypertension (EHT) [MIM:[http://omim.org/entry/145500 145500]]. Essential hypertension is a condition in which blood pressure is consistently higher than normal with no identifiable cause.  Defects in AGT are a cause of renal tubular dysgenesis (RTD) [MIM:[http://omim.org/entry/267430 267430]]. RTD is an autosomal recessive severe disorder of renal tubular development characterized by persistent fetal anuria and perinatal death, probably due to pulmonary hypoplasia from early-onset oligohydramnios (the Potter phenotype).<ref>PMID:16116425</ref> 
== Function ==
[[http://www.uniprot.org/uniprot/ANGT_HUMAN ANGT_HUMAN]] Essential component of the renin-angiotensin system (RAS), a potent regulator of blood pressure, body fluid and electrolyte homeostasis.<ref>PMID:1132082</ref> <ref>PMID:10619573</ref> <ref>PMID:17138938</ref>  Angiotensin-2: acts directly on vascular smooth muscle as a potent vasoconstrictor, affects cardiac contractility and heart rate through its action on the sympathetic nervous system, and alters renal sodium and water absorption through its ability to stimulate the zona glomerulosa cells of the adrenal cortex to synthesize and secrete aldosterone.<ref>PMID:1132082</ref> <ref>PMID:10619573</ref> <ref>PMID:17138938</ref>  Angiotensin-3: stimulates aldosterone release.<ref>PMID:1132082</ref> <ref>PMID:10619573</ref> <ref>PMID:17138938</ref>  Angiotensin 1-7: is a ligand for the G-protein coupled receptor MAS1 (By similarity). Has vasodilator and antidiuretic effects (By similarity). Has an antithrombotic effect that involves MAS1-mediated release of nitric oxide from platelets (By similarity).<ref>PMID:1132082</ref> <ref>PMID:10619573</ref> <ref>PMID:17138938</ref> 
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Read, R J]]
[[Category: Yan, Y]]
[[Category: Yan, Y]]
[[Category: Angiotensin i-deleted angiotensinogen]]
[[Category: Serine protease inhibitor]]
[[Category: Spent angiotensinogen]]