DossierPhysiological occurrence, biosynthesis and metabolism of retinoic acid: evidence for roles of Cellular Retinol-Binding Protein (CRBP) and Cellular Retinoic Acid-Binding Protein (CRABP) in the pathway of retinoic acid homeostasis
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Cited by (112)
17β-hydroxysteroid dehydrogenases in the progression of nonalcoholic fatty liver disease
2023, Pharmacology and TherapeuticsP450 oxidoreductase regulates barrier maturation by mediating retinoic acid metabolism in a model of the human BBB
2022, Stem Cell ReportsCitation Excerpt :RA-generating cells release RA, which is taken up by neighboring cells. Within target cells, RA is transported into the nucleus by CRABP1 and CRABP2, which facilitate RA ligation to RA receptors (RARs) (Majumdar et al., 2011; Napoli et al., 1991). Thus, RA controls gene transcriptional programs through activating nuclear RARs that bind to RA response elements (RAREs) (Maden, 1982; Petkovich et al., 1987).
Retinoid signaling in skeletal development: Scoping the system for predictive toxicology
2021, Reproductive ToxicologyBiochemical and physiological importance of the CYP26 retinoic acid hydroxylases
2019, Pharmacology and TherapeuticsCitation Excerpt :It has been shown that atRA and 4-oxo-atRA both have high affinities to cellular retinoic acid binding proteins (CRABPs), CRABP I and II (Kd < 20 nM; (Fiorella & Napoli, 1991, 1994). In addition, before the CYP26 enzymes were identified, it was shown that the CRABPs interact with the microsomal enzymes that metabolize atRA in rat testis microsomes and impact the metabolite formation and atRA clearance (Fiorella & Napoli, 1991, 1994; Napoli, Posch, Fiorella, & Boerman, 1991). Based on current knowledge of the enzymes expressed in the testis and hydroxylating atRA, it is likely that these early findings were characterizing the interactions between CRABPs and CYP26 enzymes.
Retinoic acid induction of CD1d expression primes chronic lymphocytic leukemia B cells for killing by CD8<sup>+</sup> invariant natural killer T cells
2017, Clinical ImmunologyCitation Excerpt :Magnetic bead sorted CD19+ B cells from CLL patients were treated with either ATRA or AM580 and analysed by flow cytometry for CD1d cell surface expression (Fig. 4A). As little as 1 nM of ATRA (Fig. 4B) or AM580 (Fig. 4C) were sufficient to upregulate CD1d expression on CLL B cells, a concentration within the physiological range of RA in humans [45]. Furthermore, 48 h of treatment with RA was enough to observe CD1d upregulation on CLL B cells (Fig. 4D).