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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. 3.

Fig. 3

Contribution of CRBP1 to atRA homeostasis. a) Crosslinking with holo-CRBP1 identified RDH as members of the short-chain dehydrogenase/reductase gene family (SDR) by radio-iodinating this CRBP1 target enzyme (Boerman & Napoli, 1995). b) Michaelis-Menten kinetics confirmed ability of holo-CRBP1 to deliver retinol to RDH. The lack of change in Km or Vm with differences in the ratio CRBP1/retinol further confirmed direct interaction between holo-CRBP1 and RDH (Posch et al., 1991). c) Illustration of CRBP1’s impact on the amount of “free” retinol, calculated using a kd value of 2 nM. d) Kinetics of the reductase DHRS4 with free retinal or CRBP1-retinal (Lei et al., 2003). e) Inhibition of the DHRS4 reaction by apo-CRBP1, illustrating the mechanism of a decreased Vm with CRBP1-retinal as substrate shown in d. The filled blue symbols show that partial sequestration of retinal does not lower the reaction rate, indicating that both free and bound retinal are available as substrate. The red symbol shows the impact of equimolar amounts of BP and retinal, indicating ability of apo-CRBP1 to inhibit DHRS4.