Novel regulation of keratin gene expression by thyroid hormone and retinoid receptors
Апстракт
Expression of keratin proteins, markers of epidermal differentiation and pathology, is uniquely regulated by the nuclear receptors for retinoic acid (RAR) and thyroid hormone (T3R) and their ligands: it is constitutively activated by unliganded T3R, but it is suppressed by ligand-occupied T3R or RAR. This regulation was studied using gel mobility shift assays with purified receptors and transient transfection assays with vectors expressing various receptor mutants. Regulation of keratin gene expression by RAR and T3R occurs through direct binding of these receptors to receptor response elements of the keratin gene promoters. The DNA binding C domain of these receptors is essential for both ligand-dependent and -independent regulation. However, the NH2-terminal A/B domain of T3R is not required for either mode of regulation of keratin gene expression. Furthermore, v-ErbA, an oncogenic derivative of cT3R, also activates keratin gene expression. In contrast to the previously described mec...hanism of gene regulation by T3R, heterodimerization with the retinoid X receptor is not essential for activation of keratin gene expression by unliganded T3R. These findings indicate that the mechanism of regulation of keratin genes by RAR and T3R differs significantly from the mechanisms described for other genes modulated by these receptors.
Извор:
Journal of Biological Chemistry, 1996, 271, 3, 1416-1423Финансирање / пројекти:
- NIAMS NIH HHS [AR39176, AR30682, AR40522]
DOI: 10.1074/jbc.271.3.1416
ISSN: 0021-9258
PubMed: 8576132
WoS: A1996TQ52500028
Scopus: 2-s2.0-0030030298
Колекције
Институција/група
VinčaTY - JOUR AU - Tomić-Canić, Marjana AU - Day, D AU - Samuels, HH AU - Freedberg, IM AU - Blumenberg, M PY - 1996 UR - https://vinar.vin.bg.ac.rs/handle/123456789/1958 AB - Expression of keratin proteins, markers of epidermal differentiation and pathology, is uniquely regulated by the nuclear receptors for retinoic acid (RAR) and thyroid hormone (T3R) and their ligands: it is constitutively activated by unliganded T3R, but it is suppressed by ligand-occupied T3R or RAR. This regulation was studied using gel mobility shift assays with purified receptors and transient transfection assays with vectors expressing various receptor mutants. Regulation of keratin gene expression by RAR and T3R occurs through direct binding of these receptors to receptor response elements of the keratin gene promoters. The DNA binding C domain of these receptors is essential for both ligand-dependent and -independent regulation. However, the NH2-terminal A/B domain of T3R is not required for either mode of regulation of keratin gene expression. Furthermore, v-ErbA, an oncogenic derivative of cT3R, also activates keratin gene expression. In contrast to the previously described mechanism of gene regulation by T3R, heterodimerization with the retinoid X receptor is not essential for activation of keratin gene expression by unliganded T3R. These findings indicate that the mechanism of regulation of keratin genes by RAR and T3R differs significantly from the mechanisms described for other genes modulated by these receptors. T2 - Journal of Biological Chemistry T1 - Novel regulation of keratin gene expression by thyroid hormone and retinoid receptors VL - 271 IS - 3 SP - 1416 EP - 1423 DO - 10.1074/jbc.271.3.1416 ER -
@article{ author = "Tomić-Canić, Marjana and Day, D and Samuels, HH and Freedberg, IM and Blumenberg, M", year = "1996", abstract = "Expression of keratin proteins, markers of epidermal differentiation and pathology, is uniquely regulated by the nuclear receptors for retinoic acid (RAR) and thyroid hormone (T3R) and their ligands: it is constitutively activated by unliganded T3R, but it is suppressed by ligand-occupied T3R or RAR. This regulation was studied using gel mobility shift assays with purified receptors and transient transfection assays with vectors expressing various receptor mutants. Regulation of keratin gene expression by RAR and T3R occurs through direct binding of these receptors to receptor response elements of the keratin gene promoters. The DNA binding C domain of these receptors is essential for both ligand-dependent and -independent regulation. However, the NH2-terminal A/B domain of T3R is not required for either mode of regulation of keratin gene expression. Furthermore, v-ErbA, an oncogenic derivative of cT3R, also activates keratin gene expression. In contrast to the previously described mechanism of gene regulation by T3R, heterodimerization with the retinoid X receptor is not essential for activation of keratin gene expression by unliganded T3R. These findings indicate that the mechanism of regulation of keratin genes by RAR and T3R differs significantly from the mechanisms described for other genes modulated by these receptors.", journal = "Journal of Biological Chemistry", title = "Novel regulation of keratin gene expression by thyroid hormone and retinoid receptors", volume = "271", number = "3", pages = "1416-1423", doi = "10.1074/jbc.271.3.1416" }
Tomić-Canić, M., Day, D., Samuels, H., Freedberg, I.,& Blumenberg, M.. (1996). Novel regulation of keratin gene expression by thyroid hormone and retinoid receptors. in Journal of Biological Chemistry, 271(3), 1416-1423. https://doi.org/10.1074/jbc.271.3.1416
Tomić-Canić M, Day D, Samuels H, Freedberg I, Blumenberg M. Novel regulation of keratin gene expression by thyroid hormone and retinoid receptors. in Journal of Biological Chemistry. 1996;271(3):1416-1423. doi:10.1074/jbc.271.3.1416 .
Tomić-Canić, Marjana, Day, D, Samuels, HH, Freedberg, IM, Blumenberg, M, "Novel regulation of keratin gene expression by thyroid hormone and retinoid receptors" in Journal of Biological Chemistry, 271, no. 3 (1996):1416-1423, https://doi.org/10.1074/jbc.271.3.1416 . .