Figure 2.

The activation of CREB3L1 by RIP and its transcriptionally regulated downstream target genes. Upon the chronic simulation of TGF-β, CREB3L1 can bind to Smad4 and translocate to the nuclei to activate the transcription of Col1α1, while receiving the signal of ER stress, such as treatment with BMP2, tunicamycin, thapsigargin, or suffered from fluid deprivation or salt loading, CREB3L1 on ER can be transferred to the Golgi apparatus and sequentially cleaved by S1P and S2P, then the liberated active form of CREB3L1 translocates to the nuclei to regulate the expressions of genes, for instance AVP, Gcm1, VEGFA, and Col5 by itself or interaction with other proteins.