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. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Pharmacol Ther. 2017 Jan 27;173:19–33. doi: 10.1016/j.pharmthera.2017.01.004

Fig. 2.

Fig. 2

Apo-CRBP1 enables mobilization of RE. a) Kinetics of apo-CRBP1 inhibiting LRAT and stimulating endogenous RE hydrolysis (Herr & Ong, 1992; Boerman & Napoli, 1991). b) Model relating actions of apo-CRBP1 to cellular retinoid homeostasis. Apo-CRBP1 acts as a sink to draw retinol into cells from the serum BP, RBP4, and also signals cell retinoid status. In the absence of apo-CRBP1, CRBP1 directs retinol into RE formation, while maintaining atRA biosynthesis. As apo-CRBP1 increases, inhibition of LRAT preserves remaining holo-CRBP1 to support atRA biosynthesis.