Fig. 3.

A schematic representation of BDKRB1 and BDKRB2 signaling mechanisms mediated by bradykinin. A Stress, inflammation and tissue injury lead to the expression of BDKRB1, which gets stimulated upon binding with Des-Arg9-BK and triggers downstream signaling cascades. In the absence of agonist stimulation, BDKRB1 gets internalized for breakdown by lysosomal degradation. B BDKRB2 receptor is activated upon the binding of Bradykinin and subsequent phosphorylation. Arrestin mediated internalization occurs through clathrin-coated vesicles. BDKRB2 is secluded into the lysosome for degradation if exposed to kinin for the long term. Short-term exposure with bradykinin results in dephosphorylation followed by receptor recycling back to the surface