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Papers In Press, published online ahead of print March 19, 2004
Molecular Neurobiology, Physiological Sciences, Lund 22184
Corresponding Author: fredrik.leeb-lundberg{at}mphy.lu.se
B1 bradykinin (BK) receptor (B1R) induction is critical in the adaptation of the kinin-mediated inflammatory response from a B2 BK receptor (B2R) subtype to a B1R subtype that occurs during chronic insult. Here, we show that B1R spontaneously forms of a proteolytic plasma membrane complex with B2R along with increased receptor signaling capacity. Co-expression of HA-tagged B2R with FLAG-tagged B1R in HEK293 cells resulted in degradation of B2R as determined by the diminution of the intact 65-kDa B2R species and the appearance of proteolytic B2R products at 30-40-kDa and by the reduction in B2R bradykinin binding sites. On the other hand, the 35-kDa B1R remained intact. Receptor co-expression also led to an increase in constitutive and agonist-stimulated receptor signaling. Selective immunoprecipitation with epitope-specific antibodies revealed a spontaneously formed heterologous receptor complex, which was composed of the intact 35-kDa B1R and the B2R degradation products. Cellular fractionation, cell surface biotinylation, and immunoelectron microscopy showed that B2R/B1R complexes were present on the cell surface. This is the first evidence that a heterologous G protein-coupled receptor complex in the plasma membrane is linked to proteolytic degradation of a participating receptor, and this mechanism may contribute to the adaptation of the kinin response from a B2-type to a B1-type during chronic insult.
J. Biol. Chem, 10.1074/jbc.M402572200
Submitted on March 8, 2004
Revised on March 19, 2004
Accepted on March 19, 2004
Spontaneous formation of a proteolytic B1 and B2 Bradykinin receptor complex with enhanced signaling capacity
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