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Coexpression of this variant with GRK2 in COS-7 cells resulted in a significantly decreased GRK-mediated phosphorylation and a complete attenuation of short-term desensitization (Small et al., 2001)

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In both in vitro and in vivo rodent studies, BPC-157 induces early expression of EGR-1 and its corepressor NAB2, forming a regulatory feedback loop that modulates the duration and amplitude of angiogenic gene transcription during wound healing, which suggests BPC-157 may engage feedback mechanisms to prevent excessive angiogenic signaling [56]