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Both of these conundrums can be explained by a model where IMiDs behave as a switch to block ubiquitination of natural substrates of CRL4 CRBN , but promote ubiquitination of neo-substrates, such as IKZF1 and IKZF3 (Figure 4B)
The timing and stability of these proteins are tightly controlled by post-translational mechanisms, including ubiquitin-mediated degradation
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When administered subcutaneously, BPC-157 achieves peak concentrations within minutes and begins working through multiple interconnected signaling pathways
