2le9
From Proteopedia
(Difference between revisions)
| (8 intermediate revisions not shown.) | |||
| Line 1: | Line 1: | ||
| + | |||
==RAGEC2-S100A13 tetrameric complex== | ==RAGEC2-S100A13 tetrameric complex== | ||
| - | <StructureSection load='2le9' size='340' side='right' caption='[[2le9 | + | <StructureSection load='2le9' size='340' side='right'caption='[[2le9]]' scene=''> |
== Structural highlights == | == Structural highlights == | ||
| - | [[2le9]] is a 4 chain structure with sequence from [ | + | <table><tr><td colspan='2'>[[2le9]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE9 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2LE9 FirstGlance]. <br> |
| - | <b> | + | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR, 1 model</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=2le9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le9 OCA], [https://pdbe.org/2le9 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2le9 RCSB], [https://www.ebi.ac.uk/pdbsum/2le9 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2le9 ProSAT]</span></td></tr> | ||
| + | </table> | ||
| + | == Function == | ||
| + | [https://www.uniprot.org/uniprot/RAGE_HUMAN RAGE_HUMAN] Mediates interactions of advanced glycosylation end products (AGE). These are nonenzymatically glycosylated proteins which accumulate in vascular tissue in aging and at an accelerated rate in diabetes. Acts as a mediator of both acute and chronic vascular inflammation in conditions such as atherosclerosis and in particular as a complication of diabetes. AGE/RAGE signaling plays an important role in regulating the production/expression of TNF-alpha, oxidative stress, and endothelial dysfunction in type 2 diabetes. Interaction with S100A12 on endothelium, mononuclear phagocytes, and lymphocytes triggers cellular activation, with generation of key proinflammatory mediators. Interaction with S100B after myocardial infarction may play a role in myocyte apoptosis by activating ERK1/2 and p53/TP53 signaling (By similarity). Receptor for amyloid beta peptide. Contributes to the translocation of amyloid-beta peptide (ABPP) across the cell membrane from the extracellular to the intracellular space in cortical neurons. ABPP-initiated RAGE signaling, especially stimulation of p38 mitogen-activated protein kinase (MAPK), has the capacity to drive a transport system delivering ABPP as a complex with RAGE to the intraneuronal space.<ref>PMID:19906677</ref> | ||
| + | |||
| + | ==See Also== | ||
| + | *[[S100 proteins 3D structures|S100 proteins 3D structures]] | ||
== References == | == References == | ||
<references/> | <references/> | ||
| Line 9: | Line 17: | ||
</StructureSection> | </StructureSection> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
| - | [[Category: | + | [[Category: Large Structures]] |
| - | [[Category: | + | [[Category: Mohan SK]] |
| - | [[Category: | + | [[Category: Rani SG]] |
| - | [[Category: | + | [[Category: Yu C]] |
| - | + | ||
| - | + | ||
| - | + | ||
Current revision
RAGEC2-S100A13 tetrameric complex
| |||||||||||
