1o0d: Difference between revisions

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-[[Image:1o0d.jpg|left|200px]]
-<!--
+==Human Thrombin complexed with a d-Phe-Pro-Arg-type Inhibitor and a C-terminal Hirudin derived exo-site inhibitor==
-The line below this paragraph, containing "STRUCTURE_1o0d", creates the "Structure Box" on the page.
+<StructureSection load='1o0d' size='340' side='right'caption='[[1o0d]], [[Resolution|resolution]] 2.44&Aring;' scene=''>
-You may change the PDB parameter (which sets the PDB file loaded into the applet)
+== Structural highlights ==
-or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
+<table><tr><td colspan='2'>[[1o0d]] is a 3 chain structure with sequence from [https://en.wikipedia.org/wiki/Hirudo_medicinalis Hirudo medicinalis] and [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1O0D OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1O0D FirstGlance]. <br>
-or leave the SCENE parameter empty for the default display.
+</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.44&#8491;</td></tr>
--->
+<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=163:(2-{2-[(5-CARBAMIMIDOYL-1-METHYL-1H-PYRROL-2-YLMETHYL)-CARBAMOYL]-PYRROL-1-YL}-+1-CYCLOHEXYLMETHYL-2-OXO-ETHYLAMINO)-ACETIC+ACID'>163</scene>, <scene name='pdbligand=ALC:2-AMINO-3-CYCLOHEXYL-PROPIONIC+ACID'>ALC</scene>, <scene name='pdbligand=HYP:4-HYDROXYPROLINE'>HYP</scene>, <scene name='pdbligand=SIN:SUCCINIC+ACID'>SIN</scene>, <scene name='pdbligand=SMF:4-SULFOMETHYL-L-PHENYLALANINE'>SMF</scene></td></tr>
-{{STRUCTURE_1o0d|  PDB=1o0d  |  SCENE=  }}
+<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1o0d FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1o0d OCA], [https://pdbe.org/1o0d PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1o0d RCSB], [https://www.ebi.ac.uk/pdbsum/1o0d PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1o0d ProSAT]</span></td></tr>
+</table>
+== Disease ==
+[https://www.uniprot.org/uniprot/THRB_HUMAN THRB_HUMAN] Defects in F2 are the cause of factor II deficiency (FA2D) [MIM:[https://omim.org/entry/613679 613679]. It is a very rare blood coagulation disorder characterized by mucocutaneous bleeding symptoms. The severity of the bleeding manifestations correlates with blood factor II levels.<ref>PMID:14962227</ref> <ref>PMID:6405779</ref> <ref>PMID:3771562</ref> <ref>PMID:3567158</ref> <ref>PMID:3801671</ref> <ref>PMID:3242619</ref> <ref>PMID:2719946</ref> <ref>PMID:1354985</ref> <ref>PMID:1421398</ref> <ref>PMID:1349838</ref> <ref>PMID:7865694</ref> <ref>PMID:7792730</ref>   Genetic variations in F2 may be a cause of susceptibility to ischemic stroke (ISCHSTR) [MIM:[https://omim.org/entry/601367 601367]; also known as cerebrovascular accident or cerebral infarction. A stroke is an acute neurologic event leading to death of neural tissue of the brain and resulting in loss of motor, sensory and/or cognitive function. Ischemic strokes, resulting from vascular occlusion, is considered to be a highly complex disease consisting of a group of heterogeneous disorders with multiple genetic and environmental risk factors.<ref>PMID:15534175</ref>   Defects in F2 are the cause of thrombophilia due to thrombin defect (THPH1) [MIM:[https://omim.org/entry/188050 188050]. It is a multifactorial disorder of hemostasis characterized by abnormal platelet aggregation in response to various agents and recurrent thrombi formation. Note=A common genetic variation in the 3-prime untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increased risk of venous thrombosis.  Defects in F2 are associated with susceptibility to pregnancy loss, recurrent, type 2 (RPRGL2) [MIM:[https://omim.org/entry/614390 614390]. A common complication of pregnancy, resulting in spontaneous abortion before the fetus has reached viability. The term includes all miscarriages from the time of conception until 24 weeks of gestation. Recurrent pregnancy loss is defined as 3 or more consecutive spontaneous abortions.<ref>PMID:11506076</ref>
+== Function ==
+[https://www.uniprot.org/uniprot/THRB_HUMAN THRB_HUMAN] Thrombin, which cleaves bonds after Arg and Lys, converts fibrinogen to fibrin and activates factors V, VII, VIII, XIII, and, in complex with thrombomodulin, protein C. Functions in blood homeostasis, inflammation and wound healing.<ref>PMID:2856554</ref>
+== Evolutionary Conservation ==
+[[Image:Consurf_key_small.gif|200px|right]]
+Check<jmol>
+  <jmolCheckbox>
+    <scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/o0/1o0d_consurf.spt"</scriptWhenChecked>
+    <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
+    <text>to colour the structure by Evolutionary Conservation</text>
+  </jmolCheckbox>
+</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1o0d ConSurf].
+<div style="clear:both"></div>
-'''Human Thrombin complexed with a d-Phe-Pro-Arg-type Inhibitor and a C-terminal Hirudin derived exo-site inhibitor'''
+==See Also==
+*[[Hirudin 3D structures|Hirudin 3D structures]]
+*[[Thrombin 3D Structures|Thrombin 3D Structures]]
-==Overview==
+== References ==
-Synthesis of thrombin inhibitors and their binding mode to thrombin is described. Modification of the P1 moiety leads to an increased selectivity versus trypsin. The observed selectivity is discussed in view of their thrombin-inhibitor complex X-ray structures.
+<references/>
+__TOC__
-==Disease==
+</StructureSection>
-Known disease associated with this structure: Dysprothrombinemia OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176930 176930]], Hyperprothrombinemia OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176930 176930]], Hypoprothrombinemia OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176930 176930]]
+[[Category: Hirudo medicinalis]]
-==About this Structure==
-O0D is a [[Protein complex]] structure of sequences from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1O0D OCA].
-==Reference==
-D-Phe-Pro-Arg type thrombin inhibitors: unexpected selectivity by modification of the P1 moiety., Lange UE, Baucke D, Hornberger W, Mack H, Seitz W, Hoffken HW, Bioorg Med Chem Lett. 2003 Jun 16;13(12):2029-33. PMID:[http://www.ncbi.nlm.nih.gov/pubmed/12781189 12781189]
 [[Category: Homo sapiens]]
-[[Category: Protein complex]]
+[[Category: Large Structures]]
-[[Category: Thrombin]]
+[[Category: Bauke D]]
-[[Category: Bauke, D.]]
+[[Category: Hoeffken HW]]
-[[Category: Hoeffken, H W.]]
+[[Category: Hornberger W]]
-[[Category: Hornberger, W.]]
+[[Category: Lange UE]]
-[[Category: Lange, U E.]]
+[[Category: Mack H]]
-[[Category: Mack, H.]]
+[[Category: Seitz W]]
-[[Category: Seitz, W.]]
-[[Category: Ternary complex]]
-[[Category: Thrombin/active-site inhibitor/exo-site inhibitor]]
-''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Sat May  3 03:12:27 2008''