2l4n: Difference between revisions
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== Function == | == Function == | ||
[[http://www.uniprot.org/uniprot/CCL21_HUMAN CCL21_HUMAN]] Inhibits hemopoiesis and stimulates chemotaxis. Chemotactic in vitro for thymocytes and activated T-cells, but not for B-cells, macrophages, or neutrophils. Shows preferential activity towards naive T-cells. May play a role in mediating homing of lymphocytes to secondary lymphoid organs. Binds to atypical chemokine receptor ACKR4 and mediates the recruitment of beta-arrestin (ARRB1/2) to ACKR4. | [[http://www.uniprot.org/uniprot/CCL21_HUMAN CCL21_HUMAN]] Inhibits hemopoiesis and stimulates chemotaxis. Chemotactic in vitro for thymocytes and activated T-cells, but not for B-cells, macrophages, or neutrophils. Shows preferential activity towards naive T-cells. May play a role in mediating homing of lymphocytes to secondary lymphoid organs. Binds to atypical chemokine receptor ACKR4 and mediates the recruitment of beta-arrestin (ARRB1/2) to ACKR4. | ||
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== Publication Abstract from PubMed == | |||
CCL21 is a human chemokine that recruits normal immune cells and metastasizing tumor cells to lymph nodes through activation of the G protein-coupled receptor CCR7. The CCL21 structure solved by NMR contains a conserved chemokine domain followed by an extended, unstructured C-terminus that is not typical of most other chemokines. A sedimentation equilibrium study showed CCL21 to be monomeric. Chemical shift mapping indicates that the CCR7 N-terminus binds to the N-loop and third beta-strand of CCL21's chemokine domain. Details of CCL21-receptor recognition may enable structure-based drug discovery of novel antimetastatic agents. | |||
Solution structure of CCL21 and identification of a putative CCR7 binding site.,Love M, Sandberg JL, Ziarek JJ, Gerarden KP, Rode RR, Jensen DR, McCaslin DR, Peterson FC, Veldkamp CT Biochemistry. 2012 Jan 24;51(3):733-5. Epub 2012 Jan 17. PMID:22221265<ref>PMID:22221265</ref> | |||
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | |||
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== References == | |||
<references/> | |||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
