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).
Shen, Q, Uray, IP, Li, Y, Krisko, TI, Strecker, TE, Kim, HT, Brown, PH
Guo, ZY, Hao, XH, Tan, FF, Pei, X, Shang, LM, Jiang, XL, Yang, F
Cicatiello, L, Addeo, R, Sasso, A, Altucci, L, Petrizzi, VB, Borgo, R, Cancemi, M, Caporali, S, Caristi, S, Scafoglio, C, Teti, D, Bresciani, F, Perillo, B, Weisz, A
Albanese, C, Johnson, J, Watanabe, G, Eklund, N, Vu, D, Arnold, A, Pestell, RG
Castro-Rivera, E, Samudio, I, Safe, S
Sabbah, M, Courilleau, D, Mester, J, Redeuilh, G
Klein, EA, Assoian, RK
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