The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Functional antagonism of different G protein-coupled receptor kinases for β-arrestin-mediated angiotensin II receptor signaling
Open accessAbstract
β-arrestins bind to G protein-coupled receptor kinase (GRK)-phosphorylated seven transmembrane receptors, desensitizing their activation of G proteins, while concurrently mediating receptor endocytosis, and some aspects of receptor signaling. We have used RNA interference to assess the roles of the four widely expressed isoforms of GRKs (GRK 2, 3, 5, and 6) in regulating β-arrestin-mediated signaling to the mitogen-activated protein kinase, extracellular signal-regulated kinase (ERK) 1/2 by the angiotensin II type 1A receptor. Angiotensin II-stimulated receptor phosphorylation, β-arrestin recruitment, and receptor endocytosis are all mediated primarily by GRK2/3. In contrast, inhibiting GRK 5 or 6 expression abolishes β-arrestin-mediated ERK activation, whereas lowering GRK 2 or 3 leads to an increase in this signaling. Consistent with these findings, β-arrestin-mediated ERK activation is enhanced by overexpression of GRK 5 and 6, and reciprocally diminished by GRK 2 and 3. These findings indicate distinct functional capabilities of β-arrestins bound to receptors phosphorylated by different classes of GRKs.
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Cites
Duplexes of 21-nucleotide RNAs mediate RNA interference in cultured mammalian cells
Elbashir, S. M., Harborth, J., Lendeckel, W., Yalcin, A., Weber, K., & Tuschl, T. (2001) · Nature · doi:10.1038/35078107 · Cited by 9,456
Pierce, K. L., Premont, R. T., & Lefkowitz, R. J. (2002) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm908 · Cited by 2,701
Self-citationInternational Union of Pharmacology. XXIII. The Angiotensin II Receptors
de Gasparo, M., Catt, K. J., Inagami, T., Wright, J. W., & Unger, T. (2000) · Pharmacological Reviews · doi:10.1016/s0031-6997(24)01458-3 · Cited by 2,132
β-Arrestin-Dependent Formation of β 2 Adrenergic Receptor-Src Protein Kinase Complexes
Luttrell, L. M., Ferguson, S. S. G., Daaka, Y., Miller, W. E., Maudsley, S., Della Rocca, G. J., Lin, F.-T., Kawakatsu, H., Owada, K., Luttrell, D. K., et al. (1999) · Science · doi:10.1126/science.283.5402.655 · Cited by 1,475
Self-citationβ-Arrestin acts as a clathrin adaptor in endocytosis of the β2-adrenergic receptor
Goodman, O. B., Krupnick, J. G., Santini, F., Gurevich, V. V., Penn, R. B., Gagnon, A. W., Keen, J. H., & Benovic, J. L. (1996) · Nature · doi:10.1038/383447a0 · Cited by 1,384
G PROTEIN–COUPLED RECEPTOR KINASES
Pitcher, J. A., Freedman, N. J., & Lefkowitz, R. J. (1998) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.67.1.653 · Cited by 1,361
Self-citationTHE ROLE OF RECEPTOR KINASES AND ARRESTINS IN G PROTEIN–COUPLED RECEPTOR REGULATION
Krupnick, J. G., & Benovic, J. L. (1998) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pharmtox.38.1.289 · Cited by 1,103
Lefkowitz, R. J. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.30.18677 · Cited by 1,044
Self-citationOakley, R. H., Laporte, S. A., Holt, J. A., Caron, M. G., & Barak, L. S. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.m910348199 · Cited by 882
Activation and targeting of extracellular signal-regulated kinases by β-arrestin scaffolds
Luttrell, L. M., Roudabush, F. L., Choy, E. W., Miller, W. E., Field, M. E., Pierce, K. L., & Lefkowitz, R. J. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.041604898 · Cited by 831
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Cited by
Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system
Mehta, P. K., & Griendling, K. K. (2007) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00287.2006 · Cited by 1,924
β-Arrestin-dependent, G Protein-independent ERK1/2 Activation by the β2 Adrenergic Receptor
Shenoy, S. K., Drake, M. T., Nelson, C. D., Houtz, D. A., Xiao, K., Madabushi, S., Reiter, E., Premont, R. T., Lichtarge, O., & Lefkowitz, R. J. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m506576200 · Cited by 759
Self-citationGRKs and β-arrestins: roles in receptor silencing, trafficking and signaling
Reiter, E., & Lefkowitz, R. J. (2006) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2006.03.008 · Cited by 666
Self-citationKenakin, T., & Miller, L. J. (2010) · Pharmacological Reviews · doi:10.1124/pr.108.000992 · Cited by 573
Emerging paradigms of β-arrestin-dependent seven transmembrane receptor signaling
Shukla, A. K., Xiao, K., & Lefkowitz, R. J. (2011) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2011.06.003 · Cited by 418
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Metadata
- Authors
- Kim, J., Ahn, S., Ren, X.-R., Whalen, E. J., Reiter, E., Wei, H., & Lefkowitz, R. J.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2005-01-25
- Volume
- 102
- Issue
- 5
- Pages
- 1442-1447
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2006268283
- Cited by
- 349
- References
- 34
- FWCI
- 7.49
- Type
- journal article
- Language
- en
- Open access
- green
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