A sustained elevation in retinoic acid receptor-β2 mRNA and protein occurs during retinoic acid-induced fetal dysmorphogenesis

Soprano, Dianne Robert; Gyda, Michael; Jiang, Heng; Harnish, Douglas C.; Ugen, K E; Satre, Michael; Chen, Lan; Soprano, Kenneth J.; Kochhar, D. M.

doi:10.1016/0925-4773(94)90011-6

Cited by 31 publications

(11 citation statements)

References 45 publications

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“…In mouse embryos, all‐trans RA has been shown to produce severe limb defects and craniofacial malformations when treatment occurs between gestation days (GD) 11 and 14.5 (Kwasigroch and Kochhar, 1980; Kochhar et al, 1996; Hansen et al, 2001). A single 100 mg/kg dose of all‐trans RA to GD 11 mice has been shown to result in 92% (Creech Kraft et al, 1989) and 100% (Soprano et al, 1994; Kochhar et al, 1996) malformed fetuses. At 10 mg/kg, all‐trans RA exposure resulted in 23–39% of the fetuses being malformed (Soprano et al, 1994; Kochhar et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Dose‐response for retinoic acid‐induced forelimb malformations and cleft palate: A comparison of computerized image analysis and visual inspection

Campbell

Smith

Fisher

et al. 2004

Birth Defects Research Pt B

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Section: Introductionmentioning

confidence: 99%

Dose‐response for retinoic acid‐induced forelimb malformations and cleft palate: A comparison of computerized image analysis and visual inspection

Campbell

Smith

Fisher

et al. 2004

Birth Defects Research Pt B

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“…Retinoid binding assays were performed as described previously (22,37) with the following exceptions: the total protein concentration in each assay was 6 -12 g, and both 9-cis-RA and all-trans-retinol binding were determined exactly as described for all-trans-RA using either Western Blot Analysis-The levels of wild type and mutant RAR␣ protein were determined by Western blot analysis using CV-1 cells transfected with the indicated expression construct essentially as described previously (17,39).…”

Section: Methodsmentioning

confidence: 99%

Differential Role of Homologous Positively Charged Amino Acid Residues for Ligand Binding in Retinoic Acid Receptor α Compared with Retinoic Acid Receptor β

Scafonas

Wolfgang²,

Gabriel

et al. 1997

Journal of Biological Chemistry

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The diverse biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARs) and retinoid X receptors. Although it has been suggested that the ligand binding domains (LBDs) of RARs share the same novel folding pattern, many RAR subtype-specific agonists and antagonists have been synthesized demonstrating that the LBD of each RAR subtype has unique features. We have examined the role of several positively charged amino acid residues located in the LBD of RAR␣ in RA binding. These results are compared with previously published data for the homologous mutations in RAR␤.

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“…In many of these systems ligands that activate particular subsets of RARs have proven to be particularly efficacious. Apoptosis of tracheal epithelial cells is preferentially induced by RARa agonists (Zhang et al, 1995), apoptosis of thymic lymphocytes responds best to RARg ligands (Szondy et al, 1997), co-stimulation of RARa and RARg induces apoptosis in neuroblastoma cells (Melino et al, 1997), and ligand activation of RARb may play a particularly important role in limb teratogenesis (Soprano et al, 1994). We have recently shown that RXR ligands can also be very effective inducers of apoptosis in myeloid leukemia cells (Nagy et al, 1996b;Nagy et al, 1995).…”

Section: Retinoid Receptors and Apoptosismentioning

confidence: 99%

Retinoid-induced apoptosis in normal and neoplastic tissues

Thomázy²,

et al. 1998

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Vitamin A and its derivatives (collectively referred to as retinoids) are required for many fundamental life processes, including vision, reproduction, metabolism, cellular differentiation, hematopoesis, bone development, and pattern formation during embryogenesis. There is also considerable evidence to suggest that natural and synthetic retinoids have therapeutical effects due to their antiproliferative and apoptosis-inducing effectsin human diseases such ascancer. Therefore it is not surprising that a significant amount of research was dedicated to probe the molecular and cellular mechanisms of retinoid action during the past decade. One of the cellular mechanisms retinoids have been implicated in is the initiation and modulation of apoptosis in normal development and disease. This review provides a brief overview of the molecular basis of retinoid signaling, and focuses on the retinoid-regulation of apoptotic cell death and gene expression during normal development and in pathological conditions in vivo and in various tumor cell lines in vitro.Keywords: retinoic acid; retinoic acid receptor; RAR; RXR; apoptosis; tissue transglutaminase; gene expression Abbreviations: ATRA, All-trans retinoic acid; 9-cis RA, 9-cis retinoic acid; PG-J 2 , 15-deoxy-D 12,14 PGJ 2 ; RAR, retinoic acid receptor; RXR, retinoid X receptor; Tgase, tissue transglutaminase; SMRT, silencing mediator of retinoid and thyroid receptors; N-CoR, nuclear receptor corepressor; CREB, creb binding protein; HDAC-1, histone deacetylase-1 Retinoids are modulators of transcriptionThe retinoid's mechanism of action in both normal and pathological conditions has been the subject of more than a decade of intense research. The cloning and discovery of the retinoic acid receptor (RAR), which belongs to the superfamily of ligand-activated transcription factors (nuclear receptors) revolutionized our understanding as to how retinoids exert their pleiotropic effects (for reviews see Chambon (1996);Mangelsdorf et al (1994)). Members of the nuclear receptor superfamily mediate the biological effects of many hormones, vitamins and drugs (i.e. steroid hormones, thyroid hormones, vitamin D, prostaglandin-J 2 (PG-J 2 ) and drugs that activate peroxisomal proliferation). There are two families of retinoid receptors, Retinoid X Receptors (RXRs) that bind 9-cis retinoic acid (9-cis RA) and Retinoic Acid Receptors (RARs) that bind both 9-cis RA and all-trans retinoic acid (ATRA) (for reviews see Chambon 1996;Mangelsdorf et al, 1994)). Each of these receptor families includes at least three distinct genes, (RARa,b and g; RXRa,b and g) that through differential promoter usage and alternative splicing, give rise to a large number of distinct retinoid receptor proteins (for reviews see

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A sustained elevation in retinoic acid receptor-β2 mRNA and protein occurs during retinoic acid-induced fetal dysmorphogenesis

Cited by 31 publications

References 45 publications

Dose‐response for retinoic acid‐induced forelimb malformations and cleft palate: A comparison of computerized image analysis and visual inspection

Dose‐response for retinoic acid‐induced forelimb malformations and cleft palate: A comparison of computerized image analysis and visual inspection

Differential Role of Homologous Positively Charged Amino Acid Residues for Ligand Binding in Retinoic Acid Receptor α Compared with Retinoic Acid Receptor β

Retinoid-induced apoptosis in normal and neoplastic tissues

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