Cell
ArticleJun-Fos and receptors for vitamins A and D recognize a common response element in the human osteocalcin gene
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2017, Comprehensive Biomaterials IIRetinoic acid induces two osteocalcin isoforms and inhibits markers of osteoclast activity in Atlantic cod (Gadus morhua) ex vivo cultured craniofacial tissues
2012, Comparative Biochemistry and Physiology - A Molecular and Integrative PhysiologyVitamin D effects on differentiation and cell cycle
2011, Vitamin D: Two-Volume SetOpposite regulation of the human apolipoprotein M gene by hepatocyte nuclear factor 1 and Jun transcription factors
2011, Journal of Biological ChemistryCitation Excerpt :The inability of Jun proteins to activate the apoM promoter could be either due to the absence of cooperating factors in the vicinity of the AP-1 element or due to the deviation of the apoM AP-1 element from the consensus sequence (Fig. 5A). Transcriptional repression by Jun and other AP-1 proteins has been reported in many cases including the genes encoding for c-Fos, osteocalcin, adipocyte P2, creatinine kinase, myoD, major histocompatibility class I, chorionic gonadotropin α and β, apoC-III, and insulin (36, 54–61). However, in the majority of the above cases, the molecular mechanisms by which AP-1 proteins inhibit transcription are not understood.
Folate deficiency regulates expression of DNA polymerase β in response to oxidative stress
2011, Free Radical Biology and MedicineCitation Excerpt :In addition, Lamph et al. have demonstrated that CREB, the CRE binding protein, can act as an activator when phosphorylated and can also act as a repressor in the dephosphorylated state [52]. Further, the CRE consensus sequence has similarities to the AP-1 binding site (TGACTCA) [52,53] and the AP-1 complex can act as both an activator and a repressor [54–56]. It has also been shown that AP-1 can bind to the CRE site and act as a repressor in the expression of MyoD1 involved in muscle cell differentiation [57].