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• W2058446342 abstract "The expression of A-type lamins, subdivided into lamin A and C, is developmentally regulated. Retinoic acid (RA)-induced differentiation of P19 embryonic carcinoma cells, in which A-type lamins are absent, increases the expression of lamin A/C. We previously showed, using P19 cells as a model system, that the lamin A/C promoter has a retinoic acid-responsive element (L-RARE), and that Sp1 and Sp3 bind the CACCC box of the L-RARE. In this study, we report that Sp1, Sp3, and c-Jun increase transactivation of the L-RARE during RA treatment. Sp1 and Sp3 regulate the lamin A/C promoter in Sp1-deficient SL2 cells and contribute to RA-dependent activation in GAL4-based transcriptional assays. Overexpression of c-Jun causes transactivation of a chimeric promoter consisting of four tandem L-RARE repeats fused with the luciferase gene in P19 cells. c-Jun also transactivates a reporter construct with five tandem GAL4-binding sites, only when co-expressed with either GAL4-Sp1 or Sp3 fusion proteins. Furthermore, we detect a physiological interaction between c-Jun with Sp1/Sp3 in RA-treated cells. Our data suggest that Sp1, Sp3, and c-Jun play an important role in gene expression through the L-RARE during RA treatment." @default.
• W2058446342 created "2016-06-24" @default.
• W2058446342 creator A5028226663 @default.
• W2058446342 creator A5083284492 @default.
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• W2058446342 date "2004-07-01" @default.
• W2058446342 modified "2023-09-25" @default.
• W2058446342 title "c-Jun and Sp1 family are critical for retinoic acid induction of the lamin A/C retinoic acid-responsive element" @default.
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• W2058446342 doi "https://doi.org/10.1016/j.bbrc.2004.05.191" @default.
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