Genomic Organization and Expression of a Human Gene for Myc-associated Zinc Finger Protein (MAZ)

Song, Jun; Murakami, Hisashi; Tsutsui, Hatsumi; Tang, Xiaoou; Matsumura, Masatoshi; Itakura, Keiichi; Kanazawa, I.; Sun, Kun; Yokoyama, Kazunari K.

doi:10.1074/jbc.273.32.20603

Cited by 61 publications

(59 citation statements)

References 47 publications

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“…Amplification by polymerase chain reaction and ligation into the HindIII site of pSV00CAT generated pMAZCAT3-m1-pMAZCAT3-m8. pCMV-MAZ was constructed as described previously (22). pCMV-Sp1 and pCMV-DNMT1 were provided by R. Chiu and R. Raenish, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…Immunoprecipitation-Western Blotting Analysis-ImmunoprecipitationWestern blotting analysis was performed as described previously (22).…”

Section: Methodsmentioning

confidence: 99%

“…It is a zinc finger protein with six C2H2-type zinc fingers at the carboxyl terminus, a proline-rich region, and three alanine repeats. It is expressed ubiquitously, albeit at different levels in different human tissues (22). It can regulate the expression of numerous genes, such as c-myc (19,20,23,24), genes for insulin I and II (25), the gene for CD4 (26), the gene for the serotonin receptor (27), and the gene for nitric-oxide synthase (28).…”

mentioning

confidence: 99%

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Independent Repression of a GC-rich Housekeeping Gene by Sp1 and MAZ Involves the Same cis-Elements

Song

Ugai²,

Kanazawa

et al. 2001

Journal of Biological Chemistry

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The transcription factors Sp1 and MAZ (Myc-associated zinc finger protein) contain several zinc finger motifs, and each functions as both a positive and a negative regulator of gene expression. In this study, we characterized the extremely GC-rich promoter of the human gene for MAZ, which is known as a housekeeping gene. Unique symmetrical motifs in the promoter region (nucleotides ؊383 to ؊334) were essential for the expression of the gene for MAZ, whereas an upstream silencer element (nucleotides ؊784 to ؊612) was found to act in a position-dependent but orientation-independent manner. Sp1 and MAZ bound to the same cis-elements in the GC-rich promoter, apparently sharing DNA-binding sites. The relative extent of binding of Sp1 and MAZ to these cis-elements corresponded to the extent of negative regulation of the expression of the gene for MAZ in various lines of cells. Furthermore, novel repressive domains in both Sp1 (amino acids 622-788) and MAZ (amino acids 127-292) were identified. Suppression by Sp1 and suppression by MAZ were independent phenomena; histone deacetylases were involved in the autorepression by MAZ itself, whereas DNA methyltransferase 1 was associated with suppression by Sp1. Our results indicate that both deacetylation and methylation might be involved in the regulation of expression of a single gene via the actions of different zinc finger proteins that bind to the same cis-elements.

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Section: Methodsmentioning

confidence: 99%

“…Immunoprecipitation-Western Blotting Analysis-ImmunoprecipitationWestern blotting analysis was performed as described previously (22).…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Independent Repression of a GC-rich Housekeeping Gene by Sp1 and MAZ Involves the Same cis-Elements

Song

Ugai²,

Kanazawa

et al. 2001

Journal of Biological Chemistry

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“…After correction for the bound oligonucleotide, the predicted molecular mass of each protein was 75, 35, and 27 kDa, respectively. The molecular mass of MAZ was estimated at 60 kDa (20). These results suggest that the active c-myc promoter element binds a transcription factor that is distinct from MAZ, but which recognizes a core sequence with great similarity to that of MAZ.…”

Section: Emsa Scanning Mutagenesis Identifies a Protein Binding Site mentioning

confidence: 76%

A Myc-associated Zinc Finger Protein-related Factor Binding Site Is Required for the Deregulation of c-mycExpression by the Immunoglobulin Heavy Chain Gene Enhancers in Burkitt's Lymphoma

Arcinas

Boxer

2002

Journal of Biological Chemistry

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The deregulation of expression of the c-myc gene in Burkitt's lymphoma results from the translocation that links one c-myc allele to one of the immunoglobulin genes. This physical linkage promotes interactions between c-myc and immunoglobulin gene regulatory elements that affect c-myc transcription initiation and elongation. We have located a region in the c-myc promoter that is required for the complete activation by the immunoglobulin heavy chain gene enhancer. This regulatory element contains a core sequence, GGGAGG, similar to the GA box recognized by the transcription factor Myc-associated zinc finger protein (MAZ). UV cross-link analysis indicated that the mass of this protein did not correspond to that of MAZ, suggesting that a protein related to but distinct from MAZ bound to this site. Mutation of this regulatory element resulted in a loss of promoter activity induced by the immunoglobulin heavy chain gene enhancer. This site was also required for the c-myc promoter shift from P2 to P1. In vivo footprinting revealed that this site was occupied on the translocated c-myc allele but not on the untranslocated allele. Taken together, these findings suggest that this regulatory element is required for the full activation of c-myc promoter activity by the immunoglobulin heavy chain gene enhancer.Burkitt's lymphoma is characterized by specific chromosomal translocations that juxtapose the proto-oncogene c-myc on chromosome 8 to one of the Ig loci on chromosome 2, 14, or 22. The most common form of the translocation is t(8;14) where the c-myc gene is covalently linked to the immunoglobulin heavy chain gene (IgH)1 . The translocated c-myc gene is highly expressed, whereas the normal allele is silent. Furthermore, the transcripts initiated from the c-myc P1 promoter, which normally contribute to a minor (10 -20%) population of c-myc mRNA, increase to a level greater than the transcripts initiated from the P2 promoter, a phenomenon known as promoter shift (1-3). It is assumed that the physical linkage of the c-myc gene to one of the immunoglobulin loci promotes the interactions between c-myc and Ig regulatory elements that affect c-myc transcriptional initiation and elongation. In support of this view, it has been demonstrated that linkage of the murine IgH 3Ј enhancer region, MHS1234, to a 2.3-kb region of the human c-myc promoter in an episomal vector is sufficient to reproduce the activation of c-myc transcription and the promoter shift in stably transfected Raji cells (4). Similar results have been obtained with the Ig (5) and Ig (6) light chain enhancers. Despite these findings, most of the cis-acting enhancer and promoter elements that contribute to the deregulation of expression of the c-myc gene remain unidentified.We have shown previously that an NF-B site in the MHS4 region of the IgH enhancer is required for the transcriptional activation of the translocated c-myc gene and is involved in inducing the c-myc promoter shift from P2 to P1 (7). Others have found that NF-B and PU.1 sites are critical for the d...

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“…It is expressed ubiquitously in different tissues, albeit at varied levels. 61 It can regulate the expression of numerous genes, such as c-myc, [61][62][63] genes for insulin I and II, 64 the gene for CD4, 65 the gene for the serotonin receptor, 57 and the gene for nitric oxide synthase. 60 The human telomerase promoter, a TATA-less promoter, possesses 2 Sp1 and 3 MAZ sites.…”

Section: Discussionmentioning

confidence: 99%

X protein of hepatitis B virus functions as a transcriptional corepressor on the human telomerase promoter†

Su¹,

Lai

Lan

et al. 2007

Hepatology

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The X protein of hepatitis B virus (HBx) is essential for transactivation of hepatitis B viral and host cellular genes. It has been specifically implicated in the development of hepatocellular carcinoma; however, the molecular mechanism remains unknown. Telomeres, the DNA-protein complexes at the ends of eukaryotic chromosomes, protect chromosomes from degradation at the terminal regions, fusion with a broken DNA end, and inappropriate recombination. The shortening of telomeres that occurs during hepatocellular carcinogenesis has been well studied. In the present study, we isolated an HBx isoform that resulted in telomere shortening in hepatoma cell lines. We found that this HBx isoform down-regulated the expression of human telomerase by transcriptionally repressing its promoter. To further determine the molecular mechanism, we examined human telomerase promoter and identified myc-associated zinc finger protein (MAZ) as a transcriptional repressor of the promoter. We found that the HBx isoform achieved transcriptional suppression of human telomerase by enhancing MAZ binding to its consensus sequence in the promoter through physical association with MAZ. Conclusion: The data suggest that HBx can induce telomere shortening by acting as a transcriptional corepressor of MAZ on the human telomerase promoter. (HEPATOLOGY 2007;46:402-413.)

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Genomic Organization and Expression of a Human Gene for Myc-associated Zinc Finger Protein (MAZ)

Cited by 61 publications

References 47 publications

Independent Repression of a GC-rich Housekeeping Gene by Sp1 and MAZ Involves the Same cis-Elements

Independent Repression of a GC-rich Housekeeping Gene by Sp1 and MAZ Involves the Same cis-Elements

A Myc-associated Zinc Finger Protein-related Factor Binding Site Is Required for the Deregulation of c-mycExpression by the Immunoglobulin Heavy Chain Gene Enhancers in Burkitt's Lymphoma

X protein of hepatitis B virus functions as a transcriptional corepressor on the human telomerase promoter†

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