7s5a

<table><tr><td colspan='2'>[[7s5a]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7S5A OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7S5A FirstGlance]. <br>

</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=7s5a FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7s5a OCA], [https://pdbe.org/7s5a PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7s5a RCSB], [https://www.ebi.ac.uk/pdbsum/7s5a PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7s5a ProSAT]</span></td></tr>

== Function ==

[[https://www.uniprot.org/uniprot/CCL8_HUMAN CCL8_HUMAN]] Chemotactic factor that attracts monocytes, lymphocytes, basophils and eosinophils. May play a role in neoplasia and inflammatory host responses. This protein can bind heparin. The processed form MCP-2(6-76) does not show monocyte chemotactic activity, but inhibits the chemotactic effect most predominantly of CCL7, and also of CCL2 and CCL5 and CCL8.<ref>PMID:9558113</ref>

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== Publication Abstract from PubMed ==

As natural chemokine inhibitors, evasin proteins produced in tick saliva are potential therapeutic agents for numerous inflammatory diseases. Engineering evasins to block the desired chemokines and avoid off-target side effects requires structural understanding of their target selectivity. Structures of the class A evasin EVA-P974 bound to human CC chemokine ligands 7 and 17 (CCL7 and CCL17) and to a CCL8-CCL7 chimera reveal that the specificity of class A evasins for chemokines of the CC subfamily is defined by conserved, rigid backbone-backbone interactions, whereas the preference for a subset of CC chemokines is controlled by side-chain interactions at four hotspots in flexible structural elements. Hotspot mutations alter target preference, enabling inhibition of selected chemokines. The structure of an engineered EVA-P974 bound to CCL2 reveals an underlying molecular mechanism of EVA-P974 target preference. These results provide a structure-based framework for engineering evasins as targeted antiinflammatory therapeutics.

 

== References ==

[[Category: Aryal, P]]

[[Category: Bhusal, R P]]

[[Category: Devkota, S R]]

[[Category: Stone, M J]]

[[Category: Wilce, M C.J]]

[[Category: Cytokine]]