β-Arrestin recruitment and G protein signaling by the atypical human chemokine decoy receptor CCX-CKR

A.O. Watts; F. Verkaar; M.M.C. van der Lee; C.A.W. Timmerman; M. Kuijer; J. van Offenbeek; L.H.J.C. van Lith; M.J. Smit; R. Leurs; G.J.R. Zaman; H.F. Vischer

doi:10.1074/jbc.M112.406108

β-Arrestin recruitment and G protein signaling by the atypical human chemokine decoy receptor CCX-CKR

A.O. Watts
, F. Verkaar
, M.M.C. van der Lee
, C.A.W. Timmerman
, M. Kuijer
, J. van Offenbeek
, L.H.J.C. van Lith
, M.J. Smit
, R. Leurs
, G.J.R. Zaman
, H.F. Vischer

AIMMS

Research output: Contribution to Journal › Article › Academic › peer-review

Abstract

Background: CCX-CKR is considered to be a chemokine decoy receptor that is unable to signal. Results: Chemokines induce β-arrestin recruitment to CCX-CKR and pertussis toxin (PTX)-dependent CRE activity. Conclusion: PTX-sensitive G proteins hinder CCX-CKR coupling to other G proteins and consequently keep receptors silent. Significance: Recruitment of β-arrestin to CCX-CKR requests re-evaluation of the signaling capacity of this atypical receptor. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.

Original language	English
Pages (from-to)	7169-7181
Journal	Journal of Biological Chemistry
Volume	288
Issue number	10
DOIs	https://doi.org/10.1074/jbc.M112.406108
Publication status	Published - 2013

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This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

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10.1074/jbc.M112.406108

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Watts, A. O., Verkaar, F., van der Lee, M. M. C., Timmerman, C. A. W., Kuijer, M., van Offenbeek, J., van Lith, L. H. J. C., Smit, M. J., Leurs, R., Zaman, G. J. R., & Vischer, H. F. (2013). β-Arrestin recruitment and G protein signaling by the atypical human chemokine decoy receptor CCX-CKR. Journal of Biological Chemistry, 288(10), 7169-7181. https://doi.org/10.1074/jbc.M112.406108

@article{d2ad544382eb4ccd98c4e60875664cce,

title = "β-Arrestin recruitment and G protein signaling by the atypical human chemokine decoy receptor CCX-CKR",

abstract = "Background: CCX-CKR is considered to be a chemokine decoy receptor that is unable to signal. Results: Chemokines induce β-arrestin recruitment to CCX-CKR and pertussis toxin (PTX)-dependent CRE activity. Conclusion: PTX-sensitive G proteins hinder CCX-CKR coupling to other G proteins and consequently keep receptors silent. Significance: Recruitment of β-arrestin to CCX-CKR requests re-evaluation of the signaling capacity of this atypical receptor. {\textcopyright} 2013 by The American Society for Biochemistry and Molecular Biology, Inc.",

author = "A.O. Watts and F. Verkaar and \{van der Lee\}, M.M.C. and C.A.W. Timmerman and M. Kuijer and \{van Offenbeek\}, J. and \{van Lith\}, L.H.J.C. and M.J. Smit and R. Leurs and G.J.R. Zaman and H.F. Vischer",

year = "2013",

doi = "10.1074/jbc.M112.406108",

language = "English",

volume = "288",

pages = "7169--7181",

journal = "Journal of Biological Chemistry",

issn = "0021-9258",

publisher = "American Society for Biochemistry and Molecular Biology Inc.",

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}

TY - JOUR

T1 - β-Arrestin recruitment and G protein signaling by the atypical human chemokine decoy receptor CCX-CKR

AU - Watts, A.O.

AU - Verkaar, F.

AU - van der Lee, M.M.C.

AU - Timmerman, C.A.W.

AU - Kuijer, M.

AU - van Offenbeek, J.

AU - van Lith, L.H.J.C.

AU - Smit, M.J.

AU - Leurs, R.

AU - Zaman, G.J.R.

AU - Vischer, H.F.

PY - 2013

Y1 - 2013

N2 - Background: CCX-CKR is considered to be a chemokine decoy receptor that is unable to signal. Results: Chemokines induce β-arrestin recruitment to CCX-CKR and pertussis toxin (PTX)-dependent CRE activity. Conclusion: PTX-sensitive G proteins hinder CCX-CKR coupling to other G proteins and consequently keep receptors silent. Significance: Recruitment of β-arrestin to CCX-CKR requests re-evaluation of the signaling capacity of this atypical receptor. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.

AB - Background: CCX-CKR is considered to be a chemokine decoy receptor that is unable to signal. Results: Chemokines induce β-arrestin recruitment to CCX-CKR and pertussis toxin (PTX)-dependent CRE activity. Conclusion: PTX-sensitive G proteins hinder CCX-CKR coupling to other G proteins and consequently keep receptors silent. Significance: Recruitment of β-arrestin to CCX-CKR requests re-evaluation of the signaling capacity of this atypical receptor. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.

U2 - 10.1074/jbc.M112.406108

DO - 10.1074/jbc.M112.406108

M3 - Article

SN - 0021-9258

VL - 288

SP - 7169

EP - 7181

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

IS - 10

ER -

β-Arrestin recruitment and G protein signaling by the atypical human chemokine decoy receptor CCX-CKR

Abstract

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