2jp8

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{{STRUCTURE_2jp8| PDB=2jp8 | SCENE= }}
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==Angiotensin 1-7==
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===Angiotensin 1-7===
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<StructureSection load='2jp8' size='340' side='right' caption='[[2jp8]], [[NMR_Ensembles_of_Models | 10 NMR models]]' scene=''>
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{{ABSTRACT_PUBMED_17904691}}
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== Structural highlights ==
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<table><tr><td colspan='2'>[[2jp8]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JP8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2JP8 FirstGlance]. <br>
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</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=2jp8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jp8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2jp8 RCSB], [http://www.ebi.ac.uk/pdbsum/2jp8 PDBsum]</span></td></tr>
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</table>
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== Disease ==
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[[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>
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== Function ==
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[[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>
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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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We report the complete sequence-specific hydrogen NMR assignments of vasoactive peptide angiotensin-(1-7) (Ang-(1-7)). Assignments of the majority of the resonances were accomplished by COSY, TOCSY, and ROESY peak coordinates at 400MHz and 600MHz. Long-side-chain amino acid spin system identification was facilitated by long-range coherence transfer experiments (TOCSY). Problems with overlapped resonance signals were solved by analysis of heteronuclear 2D experiments (HSQC and HMBC). Nuclear Overhauser effects (NOE) results were used to probe peptide conformation. We show that the inclusion of the angiotensin-(1-7) tyrosine residue is favored in inclusion complexes with beta-cyclodextrin. QM/MM simulations at the DFTB/UFF level confirm the experimental NMR findings and provide detailed structural information on these compounds in aqueous solution.
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==Disease==
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Study of angiotensin-(1-7) vasoactive peptide and its beta-cyclodextrin inclusion complexes: complete sequence-specific NMR assignments and structural studies.,Lula I, Denadai AL, Resende JM, de Sousa FB, de Lima GF, Pilo-Veloso D, Heine T, Duarte HA, Santos RA, Sinisterra RD Peptides. 2007 Nov;28(11):2199-210. Epub 2007 Aug 19. PMID:17904691<ref>PMID:17904691</ref>
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[[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>
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==Function==
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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[[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>
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</div>
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==About this Structure==
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[[2jp8]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JP8 OCA].
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==See Also==
==See Also==
*[[Serpin|Serpin]]
*[[Serpin|Serpin]]
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== References ==
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==Reference==
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<references/>
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<references group="xtra"/><references/>
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__TOC__
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[[Category: Denadai, A L.]]
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</StructureSection>
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[[Category: Duarte, H A.]]
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[[Category: Denadai, A L]]
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[[Category: Heine, T.]]
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[[Category: Duarte, H A]]
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[[Category: Lima, G F.de.]]
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[[Category: Heine, T]]
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[[Category: Lula, I.]]
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[[Category: Lima, G F.de]]
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[[Category: Pilo-Veloso, D.]]
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[[Category: Lula, I]]
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[[Category: Resende, J M.]]
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[[Category: Pilo-Veloso, D]]
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[[Category: Santos, R A.S.]]
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[[Category: Resende, J M]]
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[[Category: Sinesterra, R D.]]
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[[Category: Santos, R A.S]]
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[[Category: Souza, F B.de.]]
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[[Category: Sinesterra, R D]]
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[[Category: Souza, F B.de]]
[[Category: Bend]]
[[Category: Bend]]
[[Category: Signaling protein]]
[[Category: Signaling protein]]

Revision as of 12:01, 18 December 2014

Angiotensin 1-7

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