Regulation of Major Histocompatibility Complex Class I Gene Expression in Thyroid Cells
The major histocompatibility complex (MHC) class I gene cAMP response element (CRE)-like site, −107 to −100 base pairs, is a critical component of a previously unrecognized silencer, −127 to −90 bp, important for thyrotropin (TSH)/cAMP-mediated repression in thyrocytes. TSH/cAMP induced-silencer act...
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Published in | The Journal of biological chemistry Vol. 272; no. 32; pp. 20096 - 20107 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Elsevier Inc
08.08.1997
American Society for Biochemistry and Molecular Biology |
Online Access | Get full text |
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Abstract | The major histocompatibility complex (MHC) class I gene cAMP response element (CRE)-like site, −107 to −100 base pairs, is a critical component of a previously unrecognized silencer, −127 to −90 bp, important for thyrotropin (TSH)/cAMP-mediated repression in thyrocytes. TSH/cAMP induced-silencer activity is associated with the formation of novel complexes with the 38-base pair silencer, whose appearance requires the CRE and involves ubiquitous and thyroid-specific proteins as follows: the CRE-binding protein, a Y-box protein termed thyrotropin receptor (TSHR) suppressor element protein-1 (TSEP-1); thyroid transcription factor-1 (TTF-1); and Pax-8. TTF-1 is an enhancer of class I promoter activity; Pax-8 and TSEP-1 are suppressors. TSH/cAMP decreases TTF-1 complex formation with the silencer, thereby decreasing maximal class I expression; TSH/cAMP enhance TSEP-1 and Pax-8 complex formation in association with their repressive actions. Oligonucleotides that bind TSEP-1, not Pax-8, prevent formation of the TSH/cAMP-induced complexes associated with TSH-induced class I suppression, i.e. TSEP-1 appears to be the dominant repressor factor associated with TSH/cAMP-decreased class I activity and formation of the novel complexes. TSEP-1, TTF-1, and/or Pax-8 are involved in TSH/cAMP-induced negative regulation of the TSH receptor gene in thyrocytes, suppression of MHC class II, and up-regulation of thyroglobulin. TSH/cAMP coordinate regulation of common transcription factors may, therefore, be the basis for self-tolerance and the absence of autoimmunity in the face of TSHR-mediated increases in gene products that are important for thyroid growth and function but are able to act as autoantigens. |
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AbstractList | The major histocompatibility complex (MHC) class I gene cAMP response element (CRE)-like site, −107 to −100 base pairs, is a critical component of a previously unrecognized silencer, −127 to −90 bp, important for thyrotropin (TSH)/cAMP-mediated repression in thyrocytes. TSH/cAMP induced-silencer activity is associated with the formation of novel complexes with the 38-base pair silencer, whose appearance requires the CRE and involves ubiquitous and thyroid-specific proteins as follows: the CRE-binding protein, a Y-box protein termed thyrotropin receptor (TSHR) suppressor element protein-1 (TSEP-1); thyroid transcription factor-1 (TTF-1); and Pax-8. TTF-1 is an enhancer of class I promoter activity; Pax-8 and TSEP-1 are suppressors. TSH/cAMP decreases TTF-1 complex formation with the silencer, thereby decreasing maximal class I expression; TSH/cAMP enhance TSEP-1 and Pax-8 complex formation in association with their repressive actions. Oligonucleotides that bind TSEP-1, not Pax-8, prevent formation of the TSH/cAMP-induced complexes associated with TSH-induced class I suppression, i.e. TSEP-1 appears to be the dominant repressor factor associated with TSH/cAMP-decreased class I activity and formation of the novel complexes. TSEP-1, TTF-1, and/or Pax-8 are involved in TSH/cAMP-induced negative regulation of the TSH receptor gene in thyrocytes, suppression of MHC class II, and up-regulation of thyroglobulin. TSH/cAMP coordinate regulation of common transcription factors may, therefore, be the basis for self-tolerance and the absence of autoimmunity in the face of TSHR-mediated increases in gene products that are important for thyroid growth and function but are able to act as autoantigens. The major histocompatibility complex (MHC) class I gene cAMP response element (CRE)-like site, â107 to â100 base pairs, is a critical component of a previously unrecognized silencer, â127 to â90 bp, important for thyrotropin (TSH)/cAMP-mediated repression in thyrocytes. TSH/cAMP induced-silencer activity is associated with the formation of novel complexes with the 38-base pair silencer, whose appearance requires the CRE and involves ubiquitous and thyroid-specific proteins as follows: the CRE-binding protein, a Y-box protein termed thyrotropin receptor (TSHR) suppressor element protein-1 (TSEP-1); thyroid transcription factor-1 (TTF-1); and Pax-8. TTF-1 is an enhancer of class I promoter activity; Pax-8 and TSEP-1 are suppressors. TSH/cAMP decreases TTF-1 complex formation with the silencer, thereby decreasing maximal class I expression; TSH/cAMP enhance TSEP-1 and Pax-8 complex formation in association with their repressive actions. Oligonucleotides that bind TSEP-1, not Pax-8, prevent formation of the TSH/cAMP-induced complexes associated with TSH-induced class I suppression, i.e. TSEP-1 appears to be the dominant repressor factor associated with TSH/cAMP-decreased class I activity and formation of the novel complexes. TSEP-1, TTF-1, and/or Pax-8 are involved in TSH/cAMP-induced negative regulation of the TSH receptor gene in thyrocytes, suppression of MHC class II, and up-regulation of thyroglobulin. TSH/cAMP coordinate regulation of common transcription factors may, therefore, be the basis for self-tolerance and the absence of autoimmunity in the face of TSHR-mediated increases in gene products that are important for thyroid growth and function but are able to act as autoantigens. |
Author | Napolitano, Giorgio Kohn, Leonard D. Saji, Motoyasu Giuliani, Cesidio Shong, Minho Kirshner, Susan L. Singer, Dinah S. Ohta, Masanori Palmer, Lisa A. Taniguchi, Shin-Ichi Ohmori, Masayuki Suzuki, Koichi |
Author_xml | – sequence: 1 givenname: Motoyasu surname: Saji fullname: Saji, Motoyasu organization: Cell Regulation Section, Metabolic Diseases Branch, NIDDKD, Bethesda, Maryland 20892 – sequence: 2 givenname: Minho surname: Shong fullname: Shong, Minho organization: Cell Regulation Section, Metabolic Diseases Branch, NIDDKD, Bethesda, Maryland 20892 – sequence: 3 givenname: Giorgio surname: Napolitano fullname: Napolitano, Giorgio organization: Cell Regulation Section, Metabolic Diseases Branch, NIDDKD, Bethesda, Maryland 20892 – sequence: 4 givenname: Lisa A. surname: Palmer fullname: Palmer, Lisa A. organization: Experimental Immunology Branch, NCI, National Institutes of Health, Bethesda, Maryland 20892 – sequence: 5 givenname: Shin-Ichi surname: Taniguchi fullname: Taniguchi, Shin-Ichi organization: Cell Regulation Section, Metabolic Diseases Branch, NIDDKD, Bethesda, Maryland 20892 – sequence: 6 givenname: Masayuki surname: Ohmori fullname: Ohmori, Masayuki organization: Cell Regulation Section, Metabolic Diseases Branch, NIDDKD, Bethesda, Maryland 20892 – sequence: 7 givenname: Masanori surname: Ohta fullname: Ohta, Masanori organization: Cell Regulation Section, Metabolic Diseases Branch, NIDDKD, Bethesda, Maryland 20892 – sequence: 8 givenname: Koichi surname: Suzuki fullname: Suzuki, Koichi organization: Cell Regulation Section, Metabolic Diseases Branch, NIDDKD, Bethesda, Maryland 20892 – sequence: 9 givenname: Susan L. surname: Kirshner fullname: Kirshner, Susan L. organization: Experimental Immunology Branch, NCI, National Institutes of Health, Bethesda, Maryland 20892 – sequence: 10 givenname: Cesidio surname: Giuliani fullname: Giuliani, Cesidio organization: Cell Regulation Section, Metabolic Diseases Branch, NIDDKD, Bethesda, Maryland 20892 – sequence: 11 givenname: Dinah S. surname: Singer fullname: Singer, Dinah S. organization: Experimental Immunology Branch, NCI, National Institutes of Health, Bethesda, Maryland 20892 – sequence: 12 givenname: Leonard D. surname: Kohn fullname: Kohn, Leonard D. email: lenk@bdg10.niddk.nih.gov organization: Cell Regulation Section, Metabolic Diseases Branch, NIDDKD, Bethesda, Maryland 20892 |
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Snippet | The major histocompatibility complex (MHC) class I gene cAMP response element (CRE)-like site, −107 to −100 base pairs, is a critical component of a previously... The major histocompatibility complex (MHC) class I gene cAMP response element (CRE)-like site, â107 to â100 base pairs, is a critical component of a... |
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Title | Regulation of Major Histocompatibility Complex Class I Gene Expression in Thyroid Cells |
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