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Spl transcription factor

The transcription factor Spl plays the predominant role in the expression of ADH5 [31, 33]. There is a pair of Spl sites flanking the transcription start site, and a minimal promoter containing these sites is a strong promoter in several different cell types [31]. This region of the promoter is essentially inactive in Drosophila cells that lack Spl, and are strongly activated by coexpression of Spl [33]. [Pg.426]

The ubiquitous transcription factor Spl is critical for both basal and Tat-induced transcription of the HIV-1 LTR (Kamine and Chinnadurai, 1992 Sune and Garcia-Bianco, 1995 Yedavalli et al, 2003). Spl could also play an important role in nuc-1-dependent HIV-1 regulation. Indeed, Spl has been demonstrated to interact with the acetyltransferase p300 and to act as a co-activator for Spl-mediated transcriptional activation (Billon et al, 1999 Suzuki et al, 2000 Xiao et al, 2000). Spl... [Pg.380]

Fig. 12.3 The +294T/C polymorphic site in PPARD influences the binding of transcription factor Spl (24). Electromobihty shift assays (EMSAs) of nnclear extract derived from hnman monocytic U937 cells using double-stranded 25-mer oligonucleotides corresponding to the sequence from position -1-281 to -1-305 of the common T allele and the rare C allele. Arrow refers to the -I-294C allele-predominant factor. F denotes free DNA. Lane 1, without extract lanes 2 to 4,12, with 10 ag nuclear extract in the absence of competitor lanes 5 to 7,13 to 15, with 10 ag nuclear extract in the presence of 150-fold excess of unlabeled DNA as competitor. Competitors used were -I-294C probe (lanes 5, 13 indicated with C) -I-294T probe (lanes 6, 14 indicated with T) and a nonspecific probe (lanes 7, 15 indicated with X). Spl complex. Lanes 8 to 11, with lOng nuclear extract in the presence of antibodies directed against Spl, p50, p65, and c-Rel, respectively... Fig. 12.3 The +294T/C polymorphic site in PPARD influences the binding of transcription factor Spl (24). Electromobihty shift assays (EMSAs) of nnclear extract derived from hnman monocytic U937 cells using double-stranded 25-mer oligonucleotides corresponding to the sequence from position -1-281 to -1-305 of the common T allele and the rare C allele. Arrow refers to the -I-294C allele-predominant factor. F denotes free DNA. Lane 1, without extract lanes 2 to 4,12, with 10 ag nuclear extract in the absence of competitor lanes 5 to 7,13 to 15, with 10 ag nuclear extract in the presence of 150-fold excess of unlabeled DNA as competitor. Competitors used were -I-294C probe (lanes 5, 13 indicated with C) -I-294T probe (lanes 6, 14 indicated with T) and a nonspecific probe (lanes 7, 15 indicated with X). Spl complex. Lanes 8 to 11, with lOng nuclear extract in the presence of antibodies directed against Spl, p50, p65, and c-Rel, respectively...
Examples for other trans-activating domains are the glutamine rich domains of the transcription factor Spl and the prohne rich domain of the transcription factor CTF/ NFl, which contains 20 % prohne residues. [Pg.48]

The transcription and therefore production of the integrin av and 33 subunits are each regulated by a promoter specific transcription factor Spl. This binds to guanine-rich promoter regions, which are found in many genes including those for both av and 33, IGF-I, and FGF. [Pg.437]

Courey, A.J., Holtzman, D.A., Jackson, S.P. Tjian, R. (1989). Synergistic activation by the glutamine-rich domains of human transcription factor Spl. Cell 59, 827-36. [Pg.302]

Porter, W., Saville, B., Hoivik, D., and Safe, S. 1997. Functional synergy between the transcription factor Spl and the estrogen receptor. Mol. Endocrinol. 11 1569-1580. [Pg.336]

Lee J, Kosaras B, Aleyasin H, Han JA, Park DS, et al. 2006. Role of cyclooxygenase-2 induction by transcription factor Spl and Sp3 in neuronal oxidative and DNA damage response. FASEB J 20 E1657-E1669. [Pg.230]

Glutamine-rich transcription factor Spl is readily cross-linked by TG 2 (Han and Park, 2000). Inasmuch as some TG 2 is present in the nucleus, and Qn domains are excellent substrates, it is possible that TGs may modulate the activity of at least some transcription factors in vivo. Because TG activity is increased in HD brain, and because the expanded Qn domain of Htt is an excellent TG substrate, the possibility exists that TGs play a critical role in altered transcription level and properties in Q -expansion diseases. [Pg.339]

Han JA, Park SC (2000) Transglutaminase-dependent modulation of transcription factor Spl activity. Mol Cells 10 612-618... [Pg.351]

Kadonaga, J. T., Carrier, K. R., Fasiar F- R and Tjian, R. (1987). Isolation of cDNA encoding transcription factor Spl and functional analysis of the DNA binding domain. Cell 51, 1079-1090. [Pg.870]

Narayan, V, Kriwacki, R., and Caradonna, J. P. (1997). Structures of zinc finger domains from transcription factor Spl. /. Biol. Chem. 272,7801-7809. [Pg.870]

Muangmoonchai R, Smirlis D, Wong SC, et al. Xenobiotic induction of cytochrome P450 2B1 (CYP2B1) is mediated by the orphan nuclear receptor constitutive androstane receptor (CAR) and requires steroid co-activator 1 (SRC-1) and the transcription factor Spl. Biochem J 2001 355 71-78. [Pg.96]

Fig. 10.2. The promoter region of a hormone-sensitive eukaryote gene, showing the transcriptional (actors that interact with different elements of the promoter. TF, transcription factor Spl, general initiation factor. Fig. 10.2. The promoter region of a hormone-sensitive eukaryote gene, showing the transcriptional (actors that interact with different elements of the promoter. TF, transcription factor Spl, general initiation factor.
Sun, J.-M., Penner, C.G. Davie, J.R. (1993). Repression of histone H5-gene expression in mature erythrocytes is correlated with reduced DNA-binding activities of transcription factors spl and GATA-1. FEBS Lett., 331,141-4. [Pg.260]


See other pages where Spl transcription factor is mentioned: [Pg.1129]    [Pg.1157]    [Pg.392]    [Pg.313]    [Pg.372]    [Pg.202]    [Pg.95]    [Pg.49]    [Pg.133]    [Pg.1129]    [Pg.1157]    [Pg.133]    [Pg.316]    [Pg.806]    [Pg.806]    [Pg.202]    [Pg.1681]    [Pg.1682]    [Pg.2423]    [Pg.21]    [Pg.39]    [Pg.328]    [Pg.539]    [Pg.715]    [Pg.445]    [Pg.825]    [Pg.694]    [Pg.318]    [Pg.149]    [Pg.157]   
See also in sourсe #XX -- [ Pg.39 ]

See also in sourсe #XX -- [ Pg.11 , Pg.151 ]




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