Cellular Retinoid-Binding Proteins

Ong, David E.

doi:10.1001/archderm.1987.01660360140026

Cited by 69 publications

(12 citation statements)

References 115 publications

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“…In contrast, retinol binds RAR 35 times less potently than ATRA (Repa et al, 1993), and 1000 times more retinol is required for RAR activity (Giguere et al, 1987). Although the circulating retinol in human plasma (2 gM) may seem more than adequate for RAR induction (Miller et al, 1984), its effective concentration may be limited by retinol-binding proteins such as CRBPII (Ong, 1987). The RAR activators from the acidified ether extracts of serum described here may support both ATRA and retinol as circulating effectors ( Figure 2B).…”

Section: Phytol Metabolites As Transcriptional Signalsmentioning

confidence: 91%

Phytol metabolites are circulating dietary factors that activate the nuclear receptor RXR.

Kitareewan

Burka

Tomer

et al. 1996

MBoC

179

135

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RXR is a nuclear receptor that plays a central role in cell signaling by pairing with a host of other receptors. Previously, 9-cis-retinoic acid (9cRA) was defined as a potent RXR activator. Here we describe a unique RXR effector identified from organic extracts of bovine serum by following RXR-dependent transcriptional activity. Structural analyses of material in active fractions pointed to the saturated diterpenoid phytanic acid, which induced RXR-dependent transcription at concentrations between 4 and 64 ,uM. Although 200 times more potent than phytanic acid, 9cRA was undetectable in equivalent amounts of extract and cannot be present at a concentration that could account for the activity. Phytenic acid, another phytol metabolite, was synthesized and stimulated RXR with a potency and efficacy similar to phytanic acid. These metabolites specifically displaced[3H]-9cRA from RXR with Ki values of 4 ,uM, indicating that their transcriptional effects are mediated by direct receptor interactions. Phytol metabolites are compelling candidates for physiological effectors, because their RXR binding affinities and activation potencies match their micromolar circulating concentrations. Given their exclusive dietary origin, these chlorophyll metabolites may represent essential nutrients that coordinate cellular metabolism through RXR-dependent signaling pathways.

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Section: Phytol Metabolites As Transcriptional Signalsmentioning

confidence: 91%

Phytol metabolites are circulating dietary factors that activate the nuclear receptor RXR.

Kitareewan

Burka

Tomer

et al. 1996

MBoC

179

135

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“…An inducer of CYP1A1 (β-naphthoflavone) induced the metabolism of all-trans-RA in human intestinal epithelial cells (Lampen et al 2000). CYP1A1 is upregulated by TCDD (Portier et al 1993), suggesting the linkage between TCDD and genes in the RAR-signaling pathway such as RARB, NCOA2, and CRABP, a specific carrier protein for vitamin A that influences metabolism of RA and increases the sensitivity of a cell to vitamin A signaling (Boylan and Gudas 1992;Ong 1987). The CRABP promoter contains an enhancer region through which RA inhibits CRABP transcription (Means et al 2000).…”

Section: ) Acox1 (Acox Palmcox)mentioning

confidence: 99%

Gene Interaction Network Suggests Dioxin Induces a Significant Linkage between Aryl Hydrocarbon Receptor and Retinoic Acid Receptor Beta

Toyoshiba¹,

Yamanaka²,

Sone³

et al. 2004

Environ Health Perspect

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Gene expression arrays (gene chips) have enabled researchers to roughly quantify the level of mRNA expression for a large number of genes in a single sample. Several methods have been developed for the analysis of gene array data including clustering, outlier detection, and correlation studies. Most of these analyses are aimed at a qualitative identification of what is different between two samples and/or the relationship between two genes. We propose a quantitative, statistically sound methodology for the analysis of gene regulatory networks using gene expression data sets. The method is based on Bayesian networks for direct quantification of gene expression networks. Using the gene expression changes in HPL1A lung airway epithelial cells after exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin at levels of 0.1, 1.0, and 10.0 nM for 24 hr, a gene expression network was hypothesized and analyzed. The method clearly demonstrates support for the assumed network and the hypothesis linking the usual dioxin expression changes to the retinoic acid receptor system. Simulation studies demonstrated the method works well, even for small samples.

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“…Retinal is further irreversibly oxidized to RA by retinal dehydrogenases 1-3 (ALDH1A1-3) (Napoli, 1999). RA binds cellular retinoic acid binding proteins (CRABPs) that transport RA throughout the cell (Ong, 1987). CRABP2bound RA is transported into the nucleus and delivered to retinoic acid receptors (RARA, RARB, and RARG) (Dong et al, 1999;Sessler and Noy, 2005).…”

Section: Introductionmentioning

confidence: 99%

Dietary Vitamin A Impacts Refractory Telogen

Suo

VanBuren

Hovland

et al. 2021

Front. Cell Dev. Biol.

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Hair follicles cycle through periods of growth (anagen), regression (catagen), rest (telogen), and release (exogen). Telogen is further divided into refractory and competent telogen based on expression of bone morphogenetic protein 4 (BMP4) and wingless-related MMTV integration site 7A (WNT7A). During refractory telogen hair follicle stem cells (HFSC) are inhibited. Retinoic acid synthesis proteins localized to the hair follicle and this localization pattern changed throughout the hair cycle. In addition, excess retinyl esters arrested hair follicles in telogen. The purpose of this study was to further define these hair cycle changes. BMP4 and WNT7A expression was also used to distinguish refractory from competent telogen in C57BL/6J mice fed different levels of retinyl esters from two previous studies. These two studies produced opposite results; and differed in the amount of retinyl esters the dams consumed and the age of the mice when the different diet began. There were a greater percentage of hair follicles in refractory telogen both when mice were bred on an unpurified diet containing copious levels of retinyl esters (study 1) and consumed excess levels of retinyl esters starting at 12 weeks of age, as well as when mice were bred on a purified diet containing adequate levels of retinyl esters (study 2) and remained on this diet at 6 weeks of age. WNT7A expression was consistent with these results. Next, the localization of vitamin A metabolism proteins in the two stages of telogen was examined. Keratin 6 (KRT6) and cellular retinoic acid binding protein 2 (CRABP2) localized almost exclusively to refractory telogen hair follicles in study 1. However, KRT6 and CRABP2 localized to both competent and refractory telogen hair follicles in mice fed adequate and high levels of retinyl esters in study 2. In mice bred and fed an unpurified diet retinol dehydrogenase SDR16C5, retinal dehydrogenase 2 (ALDH1A2), and cytochrome p450 26B1 (CYP26B1), enzymes and proteins involved in RA metabolism, localized to BMP4 positive refractory telogen hair follicles. This suggests that vitamin A may contribute to the inhibition of HFSC during refractory telogen in a dose dependent manner.

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Cellular Retinoid-Binding Proteins

Cited by 69 publications

References 115 publications

Phytol metabolites are circulating dietary factors that activate the nuclear receptor RXR.

Phytol metabolites are circulating dietary factors that activate the nuclear receptor RXR.

Gene Interaction Network Suggests Dioxin Induces a Significant Linkage between Aryl Hydrocarbon Receptor and Retinoic Acid Receptor Beta

Dietary Vitamin A Impacts Refractory Telogen

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