The proliferative effects of estrogen stimulation arise in part through the estrogen-dependent activation of key cell cycle regulators such as Cyclin D1, encoded by the CCND1 gene. Although there is not a classical estrogen response element (ERE) in the proximal CCND1 promoter, estrogen-responsive transcription is mediated through recruitment of hormone-bound ESR1 by other DNA-binding proteins (reviewed in Guo et al, 2011; Klein and Assoian, 2008). A heterodimer of JUN:FOS binds to an estrogen-responsive G1 element (ERGE) between nucleotides -948 and -925 and is responsible for recruitment of ESR1 and estrogen to this site. OCT1 may facilitate this binding by diplacing a YY1:HDAC1 repressive complex that occupies an adjacent site in unstimulated cells (Albanese et al, 1995; Cicatiello et al, 2004; Shen et al, 2007). Binding of ATF2:JUN heterodimers to a cyclic AMP response element (CRE) located 52 nucleotides upstream of the transcriptional start site may also contribute to estrogen-responsive signaling (Sabbah et al, 1999; Castro-Rivera at al, 2001).
Yang, F, Hao, XH, Jiang, XL, Tan, FF, Shang, LM, Guo, ZY, Pei, X
Uray, IP, Li, Y, Strecker, TE, Brown, PH, Kim, HT, Krisko, TI, Shen, Q
Caristi, S, Perillo, B, Borgo, R, Addeo, R, Altucci, L, Scafoglio, C, Caporali, S, Cancemi, M, Teti, D, Sasso, A, Cicatiello, L, Weisz, A, Petrizzi, VB, Bresciani, F
Albanese, C, Arnold, A, Pestell, RG, Vu, D, Johnson, J, Eklund, N, Watanabe, G
Castro-Rivera, E, Samudio, I, Safe, S
Courilleau, D, Sabbah, M, Redeuilh, G, Mester, J
Klein, EA, Assoian, RK
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