cDNA cloning, tissue expression, and chromosome mapping of human homolog of SOX18

Abe, Takanori; Seki, Naohiko; Yoshikawa, Tsutomu; Masuho, Yasuhiko; Muramatsu, Masaaki

doi:10.1007/s100380050210

Cited by 15 publications

(11 citation statements)

References 15 publications

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“…Other studies have shown a critical role for Sox proteins in sex determination (Jennifer and Marshall, 1998), as well as in the proper development of the central and/or peripheral nervous system (Connor et al, 1995;Tani et al, 1997;Pevny and Lovell-Badge, 1997). Evidence of the expression of Sox18 in the brain (Azuma et al, 2000), as well as Sry in midbrain (Wegner, 1999), makes it plausible that Sox18 regulation could mediate known sex differences in mor expression. Therefore, it is tempting to propose that dual promoters could be a mechanism for sexually dimorphic gene regulation by Sox factors, to provide sex differences in pain responses and in the effectiveness of various analgesic agents that act on opioid receptors.…”

Section: Discussionmentioning

confidence: 95%

“…Sox proteins have critical roles in the regulation of numerous developmental pathways, such as those of epithelium-derived tissues, including the nervous system (Connor et al, 1995;Lefebvre et al, 1997;Tani et al, 1997;Wegner, 1999), T-cell differentiation (Van de Wetering et al, 1993;Wotton et al, 1995), and bone formation and gonadogenesis (Lefebvre et al, 1997;Pevny and Lovell-Badge, 1997;Wegner, 1999). Recently, the expression of Sox18 in the CNS has been reported (Azuma et al, 2000), although its role in regulating particular CNS genes has hitherto been unknown. Therefore, the mor gene is, to the best of our knowledge, the first reported Sox18 target gene expressed in brain.…”

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confidence: 99%

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Transcriptional Modulation of Mouse μ-Opioid Receptor Distal Promoter Activity by Sox18

Smirnov

Yuhi

et al. 2001

Mol Pharmacol

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Previously, we reported the presence of dual promoters, referred to as distal (DP) and proximal, with a negative regulatory element between them in the mouse -opioid receptor (mor) gene. Here we have identified a positive regulatory element influencing mor DP transcription, which contains multiple consensus binding motifs for Sox factors (sex-determining Sry-like high mobility group box-containing genes). In gel supershift assays, the Sox family member Sox18 bound directly to the multiple Sox consensus binding motifs of the mor DP enhancer. Overexpression of Sox18 cDNA increased luciferase activity regulated by the mor DP, and did so in a Sox18 concentrationdependent manner. In contrast, overexpression of another Sox member, Sox5, triggered no such trans-activation of mor DPdriven luciferase activity or DNA-protein binding activity. These results suggest that Sox18 directly and specifically stimulates mor gene expression, by trans-activating the mor DP enhancer.

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Section: Discussionmentioning

confidence: 95%

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confidence: 99%

Transcriptional Modulation of Mouse μ-Opioid Receptor Distal Promoter Activity by Sox18

Smirnov

Yuhi

et al. 2001

Mol Pharmacol

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“…Cloning of these SOX proteins from the adult mouse brain cDNA library indicates that the expression of these SOX genes is not only restricted to early central nervous system development (31)(32)(33)(34), but these genes are also expressed in the adult mouse brain. Although none of these proteins is strictly expressed in the central nervous system (31-34), the co-existence of SOXes and MOR in the central nervous system provides the Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Several papers have reported a critical role for SOX proteins in sex determination (49) as well as in the proper development of the central and/or peripheral nervous system (12,32,50). In addition, Sox18 is expressed in fetal brain (34) and also expressed weakly in adult brain (33). The Sox21 gene is highly conserved and specifically expressed in the brain (51,52).…”

Section: Discussionmentioning

confidence: 99%

Mouse μ Opioid Receptor Distal Promoter Transcriptional Regulation by SOX Proteins

Hwang

Wang

et al. 2003

Journal of Biological Chemistry

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We have identified transcription factors that bind to specific sequences in 5 -distal promoter regulatory sequences of the mouse opioid receptor (mor) promoter using the yeast one-hybrid system. The sequence between ؊746 and ؊707 in mor distal promoter was used as the bait because it acts as a functional promoter element and binds several DNA-binding proteins. From an adult mouse brain cDNA library, five cDNA clones encoding three Sox gene family (Sry like high mobility group (HMG) box gene) transcriptional factors, mSOX18, mSOX21, and mSOX6, were isolated. Electrophoretic mobility shift assays confirmed the presence of a binding site for SOX proteins in the ؊731/؊725 region. Additionally, we have also established that the flanking regions outside the core Sox-binding site play an essential role in high affinity binding. DNase I footprint analysis indicates that proteins from mouse brain interact with the Sox-binding site within the mor distal promoter. Finally, we demonstrated that overexpression of mSOX18 and/or mSOX21 was able to up-regulate mouse mor distal promoter activity in mor-expressing neuronal cells (NMB). These data indicate that SOX proteins might contribute to the transcriptional activity of the mor gene and suggest that opioid receptor could mediate some of the developmental processes in which SOX proteins are included.Opioids have many pharmacological and physiological effects, including analgesia, sedation, euphoria, and respiratory depression and also induce tolerance and physical dependence when administered chronically. Pharmacological, physiological, receptor binding, and molecular cloning studies (1) have revealed that opioids interact with three major types of opioid receptors in the mammalian central nervous system and peripheral tissues, , ␦, and . All three types of receptors belong to the superfamily of G-protein-coupled receptors (2), and the opioid receptor (mor) 1 is known to play the essential role in morphine-induced analgesia, tolerance, and dependence as indicated from pharmacological studies. This has also been confirmed by additional in vivo pharmacological analyses of mice where mor was deleted by homologous recombination (3).Mor is expressed mainly in the central nervous system, where it exhibits distinct temporal and spatial patterns of distribution (1). Recently, in situ hybridization studies and other methods (e.g. RPA (RNase protection assay) and reverse transcriptase-PCR) indicate that expression of mor mRNA is regulated at the transcriptional level, especially during embryonic development (4 -7). The molecular mechanisms underlying this regulation are not completely understood, but analysis of the 5Ј-upstream sequences from the translation initiation sites of the mor gene has shown that expression of mor is driven by two promoters, a distal and a proximal promoter (8). Both promoters exhibit characteristics of housekeeping genes lacking a TATA box (9, 10), with the proximal promoter regulating mor transcription from four major initiation sites located in a region 291-...

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“…7 These include 10 genes encoding crystallins (CRYAA, CRYAB, CRYBA1/ A3, CRYBA, CRYBB1, CRYBB2, CRYBB3, CRYGC, CRYGD, CRYGs), three encoding membrane transport proteins (MIP, GJA3, GJA8), two encoding a cytoskeletal protein (BSFP2, BFSP1), three encoding transcription factors (HSF4, MAF, PITX3), one encoding a lens intrinsic membrane protein (Lim2), one encoding a chromatin modifying protein (CHMP4B), one encoding a protein-tyrosine kinase protein (EPHA2) and other genes forkhead box E3(FOXE3), eyes absent homolog 1(EYA1). [7][8][9][10][11][12][13] The crystallin genes encode more than 90% of the water-soluble structural proteins present in the vertebrate crystallin lens and clearly represent compelling candidate genes for congenital cataracts.…”

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confidence: 99%

Autosomal Dominant Congenital Nuclear Cataracts Caused by a CRYAA Gene Mutation

Li¹,

Yang²,

Ma³

et al. 2010

Current Eye Research

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This study identified a mutation in the CRYAA gene causing autosomal dominant nuclear cataracts and some patients show nystagmus or small blepharophimosis clinical features. These results provide evidence that CRYAA is a pathogenic gene for congenital cataracts, congenital cataracts are a clinically and genetically heterogeneous lens condition; at the same time, demonstrates a possible mechanism of action for the mutant gene.

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cDNA cloning, tissue expression, and chromosome mapping of human homolog of SOX18

Cited by 15 publications

References 15 publications

Transcriptional Modulation of Mouse μ-Opioid Receptor Distal Promoter Activity by Sox18

Transcriptional Modulation of Mouse μ-Opioid Receptor Distal Promoter Activity by Sox18

Mouse μ Opioid Receptor Distal Promoter Transcriptional Regulation by SOX Proteins

Autosomal Dominant Congenital Nuclear Cataracts Caused by a CRYAA Gene Mutation

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