2yt0: Difference between revisions

<StructureSection load='2yt0' size='340' side='right'caption='[[2yt0]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''>

<table><tr><td colspan='2'>[[2yt0]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Lk3_transgenic_mice Lk3 transgenic mice]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2YT0 OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=2YT0 FirstGlance]. <br>

</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=2yt0 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2yt0 OCA], [http://pdbe.org/2yt0 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2yt0 RCSB], [http://www.ebi.ac.uk/pdbsum/2yt0 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2yt0 ProSAT], [http://www.topsan.org/Proteins/RSGI/2yt0 TOPSAN]</span></td></tr>

[[http://www.uniprot.org/uniprot/A4_MOUSE A4_MOUSE]] Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibit Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(O) and JIP. Inhibits G(o) alpha ATPase activity (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. May be involved in copper homeostasis/oxidative stress through copper ion reduction. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV (By similarity). The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons (By similarity). Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1.<ref>PMID:15677459</ref>  Beta-amyloid peptides are lipophilic metal chelators with metal-reducing activity. Binds transient metals such as copper, zinc and iron. Rat and mouse beta-amyloid peptides bind only weakly transient metals and have little reducing activity due to substitutions of transient metal chelating residues. Beta-APP42 may activate mononuclear phagocytes in the brain and elicit inflammatory responses. Promotes both tau aggregation and TPK II-mediated phosphorylation. Also bind GPC1 in lipid rafts (By similarity).<ref>PMID:15677459</ref>  The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis.<ref>PMID:15677459</ref>  N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6) (By similarity).<ref>PMID:15677459</ref> 

[[Category: Lk3 transgenic mice]]

[[Category: Harada, T]]

[[Category: Kigawa, T]]

[[Category: Koshiba, S]]

[[Category: Li, H]]

[[Category: Structural genomic]]

[[Category: Tochio, N]]

[[Category: Watanabe, S]]

[[Category: Yokoyama, S]]

[[Category: Rsgi]]