Abstract:
:The atypical chemokine receptor 3 (ACKR3) plays a pivotal role in directing the migration of various cellular populations and its over-expression in tumors promotes cell proliferation and invasiveness. The intracellular signaling pathways transducing ACKR3-dependent effects remain poorly characterized, an issue we addressed by identifying the interactome of ACKR3. Here, we report that recombinant ACKR3 expressed in HEK293T cells recruits the gap junction protein Connexin 43 (Cx43). Cx43 and ACKR3 are co-expressed in mouse brain astrocytes and human glioblastoma cells and form a complex in embryonic mouse brain. Functional in vitro studies show enhanced ACKR3 interaction with Cx43 upon ACKR3 agonist stimulation. Furthermore, ACKR3 activation promotes β-arrestin2- and dynamin-dependent Cx43 internalization to inhibit gap junctional intercellular communication in primary astrocytes. These results demonstrate a functional link between ACKR3 and gap junctions that might be of pathophysiological relevance.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Fumagalli A,Heuninck J,Pizzoccaro A,Moutin E,Koenen J,Séveno M,Durroux T,Junier MP,Schlecht-Louf G,Bachelerie F,Schütz D,Stumm R,Smit MJ,Guérineau NC,Chaumont-Dubel S,Marin Pdoi
10.1038/s41467-020-18634-ysubject
Has Abstractpub_date
2020-09-25 00:00:00pages
4855issue
1issn
2041-1723pii
10.1038/s41467-020-18634-yjournal_volume
11pub_type
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