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Sci. Signal., 30 April 2013
Vol. 6, Issue 273, p. pc11
[DOI: 10.1126/scisignal.2004231]


Science Signaling Podcast: 30 April 2013

Elena M. Borroni1, Raffaella Bonecchi1,2, and Annalisa M. VanHook3

1 Department of Medical Biotechnologies and Translational Medicine, University of Milan, 20089 Rozzano (Milan), Italy.
2 Humanitas Clinical and Research Center, 20089 Rozzano (Milan), Italy.
3 Web Editor, Science Signaling, American Association for the Advancement of Science, 1200 New York Avenue NW, Washington, DC 20005, USA.

Abstract: This Podcast features an interview with Elena M. Borroni and Raffaella Bonecchi, authors of a Research Article that appears in the 30 April 2013 issue of Science Signaling. Chemokines recruit leukocytes to sites of infection and inflammation by binding to chemokine receptors, which are members of the G protein–coupled receptor superfamily, present on the surface of leukocytes. Whereas activation of typical chemokine receptors leads to G protein–dependent signaling that promotes cell migration toward the chemokine source, activation of atypical chemokine receptors does not promote cell migration. Instead, signaling initiated by atypical chemokine receptors contributes to the immune response in other ways. The atypical chemokine receptor D6 is a scavenger that alters the chemokine gradient by binding to and degrading chemokines. Borroni and Bonecchi found that activation of a β-arrestin–dependent signaling pathway was necessary for D6 to act as a chemokine scavenger.

Citation: E. M. Borroni, R. Bonecchi, A. M. VanHook, Science Signaling Podcast: 30 April 2013. Sci. Signal. 6, pc11 (2013).

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