1gen: Difference between revisions

<table><tr><td colspan='2'>[[1gen]] is a 1 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=1GEN OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1GEN 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]] 2.15&#8491;</td></tr>

<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></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=1gen FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1gen OCA], [https://pdbe.org/1gen PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1gen RCSB], [https://www.ebi.ac.uk/pdbsum/1gen PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1gen ProSAT]</span></td></tr>

[https://www.uniprot.org/uniprot/MMP2_HUMAN MMP2_HUMAN] Defects in MMP2 are the cause of Torg-Winchester syndrome (TWS) [MIM:[https://omim.org/entry/259600 259600]; also known as multicentric osteolysis nodulosis and arthropathy (MONA). TWS is an autosomal recessive osteolysis syndrome. It is severe with generalized osteolysis and osteopenia. Subcutaneous nodules are usually absent. Torg-Winchester syndrome has been associated with a number of additional features including coarse face, corneal opacities, patches of thickened, hyperpigmented skin, hypertrichosis and gum hypertrophy. However, these features are not always present and have occasionally been observed in other osteolysis syndromes.<ref>PMID:11431697</ref> <ref>PMID:15691365</ref> <ref>PMID:16542393</ref>  

[https://www.uniprot.org/uniprot/MMP2_HUMAN MMP2_HUMAN] Ubiquitinous metalloproteinase that is involved in diverse functions such as remodeling of the vasculature, angiogenesis, tissue repair, tumor invasion, inflammation, and atherosclerotic plaque rupture. As well as degrading extracellular matrix proteins, can also act on several nonmatrix proteins such as big endothelial 1 and beta-type CGRP promoting vasoconstriction. Also cleaves KISS at a Gly-|-Leu bond. Appears to have a role in myocardial cell death pathways. Contributes to myocardial oxidative stress by regulating the activity of GSK3beta. Cleaves GSK3beta in vitro.<ref>PMID:9476898</ref> <ref>PMID:10559137</ref> <ref>PMID:11029402</ref> <ref>PMID:11751392</ref> <ref>PMID:11710594</ref> <ref>PMID:19493954</ref> <ref>PMID:22509276</ref>  PEX, the C-terminal non-catalytic fragment of MMP2, posseses anti-angiogenic and anti-tumor properties and inhibits cell migration and cell adhesion to FGF2 and vitronectin. Ligand for integrinv/beta3 on the surface of blood vessels.<ref>PMID:9476898</ref> <ref>PMID:10559137</ref> <ref>PMID:11029402</ref> <ref>PMID:11751392</ref> <ref>PMID:11710594</ref> <ref>PMID:19493954</ref> <ref>PMID:22509276</ref>  Isoform 2: Mediates the proteolysis of CHUK/IKKA and initiates a primary innate immune response by inducing mitochondrial-nuclear stress signaling with activation of the pro-inflammatory NF-kappaB, NFAT and IRF transcriptional pathways.<ref>PMID:9476898</ref> <ref>PMID:10559137</ref> <ref>PMID:11029402</ref> <ref>PMID:11751392</ref> <ref>PMID:11710594</ref> <ref>PMID:19493954</ref> <ref>PMID:22509276</ref>  

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[[Category: Homo sapiens]]

[[Category: Collier IE]]

[[Category: Gittis AG]]

[[Category: Goldberg GG]]

[[Category: Lattman EE]]

[[Category: Libson AM]]

[[Category: Marmer BL]]