5t2q: Difference between revisions
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==Unliganded Human HVEM at 1.9A in P 1 21 1== | |||
<StructureSection load='5t2q' size='340' side='right' caption='[[5t2q]], [[Resolution|resolution]] 1.90Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[5t2q]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5T2Q OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5T2Q FirstGlance]. <br> | |||
</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5t2q FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5t2q OCA], [http://pdbe.org/5t2q PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5t2q RCSB], [http://www.ebi.ac.uk/pdbsum/5t2q PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5t2q ProSAT]</span></td></tr> | |||
[[Category: | </table> | ||
== Function == | |||
[[http://www.uniprot.org/uniprot/TNR14_HUMAN TNR14_HUMAN]] Receptor for BTLA. Receptor for TNFSF14/LIGHT and homotrimeric TNFSF1/lymphotoxin-alpha. Involved in lymphocyte activation. Plays an important role in HSV pathogenesis because it enhanced the entry of several wild-type HSV strains of both serotypes into CHO cells, and mediated HSV entry into activated human T-cells.<ref>PMID:8898196</ref> | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Nemcovicova, I]] | |||
[[Category: Zajonc, D M]] | |||
[[Category: Herpesvirus entry mediator]] | |||
[[Category: Human hvem]] | |||
[[Category: Immune system]] | |||
[[Category: Unliganded]] |
Revision as of 08:43, 24 October 2018
Unliganded Human HVEM at 1.9A in P 1 21 1Unliganded Human HVEM at 1.9A in P 1 21 1
Structural highlights
Function[TNR14_HUMAN] Receptor for BTLA. Receptor for TNFSF14/LIGHT and homotrimeric TNFSF1/lymphotoxin-alpha. Involved in lymphocyte activation. Plays an important role in HSV pathogenesis because it enhanced the entry of several wild-type HSV strains of both serotypes into CHO cells, and mediated HSV entry into activated human T-cells.[1] References |
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