6f3w: Difference between revisions
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==Backbone structure of free bradykinin (BK) in DDM/CHS detergent micelle determined by MAS SSNMR== | |||
<StructureSection load='6f3w' size='340' side='right' caption='[[6f3w]], [[NMR_Ensembles_of_Models | 10 NMR models]]' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[6f3w]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6F3W OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6F3W FirstGlance]. <br> | |||
</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[6f3v|6f3v]], [[6f27|6f27]]</td></tr> | |||
[[Category: | <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=6f3w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6f3w OCA], [http://pdbe.org/6f3w PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6f3w RCSB], [http://www.ebi.ac.uk/pdbsum/6f3w PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6f3w ProSAT]</span></td></tr> | ||
[[Category: | </table> | ||
== Disease == | |||
[[http://www.uniprot.org/uniprot/KNG1_HUMAN KNG1_HUMAN]] Congenital high-molecular-weight kininogen deficiency. The disease is caused by mutations affecting the gene represented in this entry. | |||
== Function == | |||
[[http://www.uniprot.org/uniprot/KNG1_HUMAN KNG1_HUMAN]] (1) Kininogens are inhibitors of thiol proteases; (2) HMW-kininogen plays an important role in blood coagulation by helping to position optimally prekallikrein and factor XI next to factor XII; (3) HMW-kininogen inhibits the thrombin- and plasmin-induced aggregation of thrombocytes; (4) the active peptide bradykinin that is released from HMW-kininogen shows a variety of physiological effects: (4A) influence in smooth muscle contraction, (4B) induction of hypotension, (4C) natriuresis and diuresis, (4D) decrease in blood glucose level, (4E) it is a mediator of inflammation and causes (4E1) increase in vascular permeability, (4E2) stimulation of nociceptors (4E3) release of other mediators of inflammation (e.g. prostaglandins), (4F) it has a cardioprotective effect (directly via bradykinin action, indirectly via endothelium-derived relaxing factor action); (5) LMW-kininogen inhibits the aggregation of thrombocytes; (6) LMW-kininogen is in contrast to HMW-kininogen not involved in blood clotting. | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Glaubitz, C]] | |||
[[Category: Kuenze, G]] | |||
[[Category: Lopez, J J]] | |||
[[Category: Mao, J]] | |||
[[Category: Meiler, J]] | [[Category: Meiler, J]] | ||
[[Category: Michel, H]] | [[Category: Michel, H]] | ||
[[Category: Schwalbe, H]] | [[Category: Schwalbe, H]] | ||
[[Category: | [[Category: Shukla, A K]] | ||
[[Category: Dnp]] | |||
[[Category: Gpcr]] | |||
[[Category: Membrane protein]] | |||
Revision as of 11:35, 10 January 2018
Backbone structure of free bradykinin (BK) in DDM/CHS detergent micelle determined by MAS SSNMRBackbone structure of free bradykinin (BK) in DDM/CHS detergent micelle determined by MAS SSNMR
Structural highlights
Disease[KNG1_HUMAN] Congenital high-molecular-weight kininogen deficiency. The disease is caused by mutations affecting the gene represented in this entry. Function[KNG1_HUMAN] (1) Kininogens are inhibitors of thiol proteases; (2) HMW-kininogen plays an important role in blood coagulation by helping to position optimally prekallikrein and factor XI next to factor XII; (3) HMW-kininogen inhibits the thrombin- and plasmin-induced aggregation of thrombocytes; (4) the active peptide bradykinin that is released from HMW-kininogen shows a variety of physiological effects: (4A) influence in smooth muscle contraction, (4B) induction of hypotension, (4C) natriuresis and diuresis, (4D) decrease in blood glucose level, (4E) it is a mediator of inflammation and causes (4E1) increase in vascular permeability, (4E2) stimulation of nociceptors (4E3) release of other mediators of inflammation (e.g. prostaglandins), (4F) it has a cardioprotective effect (directly via bradykinin action, indirectly via endothelium-derived relaxing factor action); (5) LMW-kininogen inhibits the aggregation of thrombocytes; (6) LMW-kininogen is in contrast to HMW-kininogen not involved in blood clotting. |
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