3oq9: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
No edit summary |
||
| (5 intermediate revisions by the same user not shown) | |||
| Line 1: | Line 1: | ||
< | ==Structure of the FAS/FADD death domain assembly== | ||
<StructureSection load='3oq9' size='340' side='right'caption='[[3oq9]], [[Resolution|resolution]] 6.80Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[3oq9]] is a 10 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3OQ9 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3OQ9 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]] 6.8Å</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=3oq9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3oq9 OCA], [https://pdbe.org/3oq9 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3oq9 RCSB], [https://www.ebi.ac.uk/pdbsum/3oq9 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3oq9 ProSAT]</span></td></tr> | ||
</table> | |||
== Disease == | |||
[https://www.uniprot.org/uniprot/TNR6_MOUSE TNR6_MOUSE] Note=Defects in Fas are the cause of the lymphoproliferation phenotype (lpr). Lpr mice show lymphadenopathy and autoantibody production. | |||
== Function == | |||
[https://www.uniprot.org/uniprot/TNR6_MOUSE TNR6_MOUSE] Receptor for TNFSF6/FASLG. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both (By similarity). | |||
== | ==See Also== | ||
*[[Tumor necrosis factor receptor 3D structures|Tumor necrosis factor receptor 3D structures]] | |||
__TOC__ | |||
</StructureSection> | |||
< | |||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Large Structures]] | |||
[[Category: Mus musculus]] | [[Category: Mus musculus]] | ||
[[Category: Kabaleeswaran | [[Category: Kabaleeswaran V]] | ||
[[Category: Wu | [[Category: Wu H]] | ||
Latest revision as of 13:35, 21 February 2024
Structure of the FAS/FADD death domain assemblyStructure of the FAS/FADD death domain assembly
Structural highlights
DiseaseTNR6_MOUSE Note=Defects in Fas are the cause of the lymphoproliferation phenotype (lpr). Lpr mice show lymphadenopathy and autoantibody production. FunctionTNR6_MOUSE Receptor for TNFSF6/FASLG. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both (By similarity). See Also |
| ||||||||||||||||