CD69: Difference between revisions

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<StructureSection load='3hup' size='350' side='right' caption='Structure of human CD69 C-type lectin-like domain dimer complex with Cl- (green) and Na+ (purple) ions (PDB entry [[3hup]])' scene='55/552187/Cv/1'>
<StructureSection load='3hup' size='350' side='right' caption='Structure of human CD69 extracellular domain dimer complex with Cl- (green) and Na+ (purple) ions (PDB entry [[3hup]])' scene='55/552187/Cv/1'>
    
    
'''CD69''' ('''Cluster of Differentiation 69''') is a human transmembrane calcium-dependent lectin protein.  CD69 functions as a signal-transmitting receptor in lymphocytes natural killer cells and platelets.  CD69 expression is induced upon activation of T-cell lymphocytes. <ref>PMID:11101293</ref> <scene name='55/552187/Cv/2'>Na ion binding site</scene> of CD69 C-type lectin-like domain dimer complex.<ref>PMID:20054122</ref>
'''CD69''' ('''Cluster of Differentiation 69''') is a human transmembrane calcium-dependent lectin protein.  CD69 functions as a signal-transmitting receptor in lymphocytes natural killer cells and platelets.  CD69 expression is induced upon activation of T-cell lymphocytes. <ref>PMID:11101293</ref> <scene name='55/552187/Cv/3'>Na ion coordination site</scene> of CD69 extracellular domain dimer complex.<ref>PMID:20054122</ref> Water molecules are shown as red spheres.
</StructureSection>
==3D structures of CD69==
==3D structures of CD69==


Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}


[[1e87]], [[1e8i]], [[1fm5]], [[3cck]], [[3hup]] – hCD69 C-type lectin-like domain – human <br />
[[1e87]], [[1e8i]], [[1fm5]], [[3cck]], [[3hup]] – hCD69 extracellular domain 70-199 – human <br />
[[8g94]] – hCD69 + S1PR1 + Gi proteins + ScfV – Cryo EM<br />
== References ==
== References ==
<references/>
<references/>
[[Category: Topic Page]]
[[Category: Topic Page]]

Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

Michal Harel, Alexander Berchansky