Stimulation of the myelin basic protein gene expression by 9-cis-retinoic acid and thyroid hormone: activation in the context of its native promoter

Pombo, Pilar M.G; Barettino, Domingo; Ibarrola, Nieves; Vega, Sonia; Rodrı́guez-Peña, Angeles

doi:10.1016/s0169-328x(98)00311-8

Cited by 63 publications

(30 citation statements)

References 37 publications

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“…Although examinations in the present study clearly show that the levels of prestin mRNA and protein were reduced severely in the absence of TH during the first postnatal week, prestin gene expression eventually achieved the levels in controls at the end of the fourth postnatal week as do other TH-regulated genes (16,25). This phenomenon might be attributed either to transcription factors (25) or local compensation of T3 levels by type 2 deiodinase (38).…”

Section: Discussioncontrasting

confidence: 56%

“…This phenomenon might be attributed either to transcription factors (25) or local compensation of T3 levels by type 2 deiodinase (38). The absence of TH for more than 3 weeks, however, still was associated with an immature prestin protein distribution across the entire plasma membrane.…”

Section: Discussionmentioning

confidence: 96%

“…Interestingly, additional putative TREs are located also within the first 600 bp of the homologous intron of the human prestin gene. Although most of the reported TREs exert a positive or negative effect at various positions upstream of the transcriptional start site (23)(24)(25)(26), the number of TREs found in introns currently is increasing. Examples have been described for RGH (27) The TRE Prest detected in the prestin gene contains two half-sites that have been reported as having been recognized by TR and related receptors of the steroid hormone receptor family (20,32).…”

Section: Discussionmentioning

confidence: 99%

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Thyroid hormone is a critical determinant for the regulation of the cochlear motor protein prestin

Weber

Zimmermann

Winter

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

107

112

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CorrectionsBIOCHEMISTRY. For the article ''Differential effects of a centrally acting fatty acid synthase inhibitor in lean and obese mice,'' by Monica V. Kumar, Teruhiko Shimokawa, Tim R. Nagy, and M. Daniel Lane, which appeared in number 4, February 19, 2002, of Proc. Natl. Acad. Sci. USA (99, 1921-1925, the authors note the following. ''Under a licensing agreement between FASgen, Inc., and The Johns Hopkins University, Dr. Lane is entitled to a share of royalty received by the University on sales of products that embody the technology described in this article. (98, 10687-10691; First Published August 28, 2001; 10.1073͞pnas.181354398), the authors note the following. In the Introduction and Discussion of our paper, we failed to reference a recent article by Rousseau et al.(1), which demonstrated that single point mutations can significantly perturb the equilibrium between monomeric and domain-swapped dimeric p13suc1. Rational methods were used to redesign p13suc1 from a fully monomeric protein (dissociation constant of Ϸ900 mM) to a fully dimeric protein (dissociation constant of Ϸ100 nM). Fig. 3 appeared incorrectly. The correct version of the figure and its legend appear below.

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Section: Discussioncontrasting

confidence: 56%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

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Thyroid hormone is a critical determinant for the regulation of the cochlear motor protein prestin

Weber

Zimmermann

Winter

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

107

112

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“…T 3 concentration in the brain reaches a peak approximately 2 weeks after birth, which correlates with an increase in TR␤1 expression and in the activity of type II iodothyronine deiodinase, the enzyme responsible for the conversion of T 4 to T 3 in the brain. Expression of myelin protein-encoding genes in the rodent brain, including the myelin-basic-protein gene in which the presence of a TRE has been demonstrated (Pombo et al, 1999) and of genes encoding the peroxisomal ␤-oxidation enzymes, reaches its highest point during the postnatal period. ABCD2 expression, which progressively increases after birth and reaches a maximum level at approximately days 15 to 21 in the brain of rat ) and mouse , seems to match the local T 3 bioavailability.…”

Section: Discussionmentioning

confidence: 99%

Thyroid Hormone Induction of the Adrenoleukodystrophy-Related Gene (ABCD2)

et al. 2003

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X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VL-CFA) ␤-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3Ј-tri-iodothyronine (T 3 ) receptor (TR␤) as a heterodimer and mediating T 3 responsiveness of ABCD2 in its promoter context. After a T 3 treatment, an induction of the ABCD2 gene was observed in the liver of normal rats but not that of TR␤Ϫ/Ϫ mice. ABCD2 was not induced in the brain of the T 3 -treated rats. However, we report for the first time that induction of the ABCD2 redundant gene is feasible in myelin-producing cells (differentiated CG4 oligodendrocytes). The induction was specific for this cell type because it did not occur in astrocytes. Furthermore, we observed T 3 induction of ABCD2 in human and mouse ABCD1-deficient fibroblasts, which was correlated with normalization of the VLCFA ␤-oxidation. Finally, ABCD3 (PMP70), a close homolog of ABCD2, was also induced by T 3 in the liver of control rats, but not that of TR␤Ϫ/Ϫ mice, and in CG4 oligodendrocytes.

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“…For instance, Western blotting and immunofluoresent staining studies have shown that CG-4 and primary OL both have similar expression of neural cell adhesion molecules, cadherins and betacatenin (Hughson et al, 1998). Both OL and CG-4 also express functional ionotropic glutamate receptors of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and kainate sub-types, and both cell types express thyroid receptors (Baas et al, 1994;Pende et al, 1994;Yoshioka et al, 1995Yoshioka et al, , 1996Meucci et al, 1996;Pombo et al, 1999). As well, the developmental expression of the krox-24 differentiation regulator protein is similar in both CG-4 and primary OL (Sock et al, 1997).…”

Section: A Comparison Of Primary Ol and Cg-4mentioning

confidence: 99%

Mitogen‐activated protein kinase signalling in oligodendrocytes: a comparison of primary cultures and CG‐4

Stariha¹,

Kim²

2001

Intl J of Devlp Neuroscience

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Oligodendrocytes play a significant role in the central nervous system, as these cells are responsible for myelinating axons and allowing for the efficient conduction of nerve impulses. Therefore, any understanding we can gain about the functional biology of oligodendrocytes will give us important insights into demyelinating diseases such as multiple sclerosis, where oligodendrocytes and myelin are damaged or destroyed. Currently, much attention has focussed on the role of a family of mitogen-activated protein kinases in OL. This kinase family includes the extracellular signal-regulated protein kinases (ERKs), the stress-activated c-Jun N-terminal kinase (JNK), and the 38 kDa high osmolarity glycerol response kinase (p38). The actions of mitogen-activated protein kinases in oligodendrocytes appear to range from proliferation and cell survival to differentiation and cell death. In the past, studies on oligodendrocytes have been hampered by the difficulties inherent in producing large enough quantities of these cells for experimentation. This problem arises in large part due to the post-mitotic nature of mature oligodendrocytes. Over the years, a cell line known as Central Glia-4 (CG-4) has become a popular oligodendrocyte model due to its potentially unlimited capacity for self-renewal. In this review, we will look at the suitability of the Central Glia-4 cell line as an oligodendrocyte model, specifically in respect to studies on mitogen-activated protein kinase signalling in oligodendrocytes.

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Stimulation of the myelin basic protein gene expression by 9-cis-retinoic acid and thyroid hormone: activation in the context of its native promoter

Cited by 63 publications

References 37 publications

Thyroid hormone is a critical determinant for the regulation of the cochlear motor protein prestin

Thyroid hormone is a critical determinant for the regulation of the cochlear motor protein prestin

Thyroid Hormone Induction of the Adrenoleukodystrophy-Related Gene (ABCD2)

Mitogen‐activated protein kinase signalling in oligodendrocytes: a comparison of primary cultures and CG‐4

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