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Dependent Transcription

Key elements of o °-dependent promoters are the TATA box with the consensus sequence TATAAT10 bp upstream from the transcription initiation site (pos. -10), and the sequence TTGACA at the position -35 (Fig. 1.28). Both sequences are necessary [Pg.36]

The more than 1000 currently known promoters in E. coli display a significant graduation in efficiency of transcription initiation. There are strong and weak promoters depending upon their deviation from the optimal promoter. In bacteria part of the variability in the efficiency of transcription initiation can be explained at the level of the different promoter sequences. Some promoters do not possess any of the above mentioned structural characteristics. [Pg.37]

An important aspect of o -dependent promoters is the fact that the holoenzyme is capable of initiating a weak transcription even without accessory proteins. In this way, the containing holoenzyme can independently carry out all necessary steps, e.g. melting of the DNA, so that a constitutive transcription without the participation of regulatory proteins is possible. In this case, the extent of transcription depends on the affinity of the holoenzyme for the promoter and, thus, depends indirectly on the promoter sequence. [Pg.37]

The recognition sequences of regulatory proteins may overlap not only the promotor site, but can also be found in the immediate vicinity of the a promoter. The sequence elements are relatively simple and often include only one binding site for regulatory proteins. [Pg.37]

Transcriptional activity is controlled mainly according to two mechanisms  [Pg.37]


Rho-dependent transcription termination signals in E coll also appear to have a distinct consensus sequence, as shown in Figure 37—6. The conserved consensus sequence, which is about 40 nucleotide pairs in length, can be seen to contain a hyphenated or interrupted inverted repeat followed by a series of AT base pairs. As transcription proceeds through the hyphenated, inverted repeat, the generated transcript can form the intramolecular hairpin structure, also depicted in Figure 37-6. [Pg.346]

Norris J, Fan D, Aleman C et al. Identification of a new subclass of Alu DNA repeats which can function as estrogen receptor-dependent transcriptional enhancers. J Biol Chem 1995 270[39] 22777-22782. [Pg.34]

Puga, A., et. al., Aromatic hydrocarbon receptor interaction with the retinoblastoma protein potentiates repression of E2F-dependent transcription and cell cycle arrest, J. Biol. Chem., 275, 2943, 2000. [Pg.251]

Nelson There are three separate roles for Ca2+ waves. First, delivering Ca2+ for contraction. Second, modulating Ca2+ dependent ion channels that control the membrane potentials. Depending on the tissue this can involve BK channels, SK channels or Ca2+-activated Cl- channels. Third, controlling Ca2+-dependent transcription factors. There is quite clear evidence that the frequency and the amplitude components of the Ca2+ signals can determine which Ca2+-dependent transcription factors are activated. This can encode both short and long-term information to control smooth muscle function. [Pg.272]

Gibson, G.G., Plant, N.J., Swales, K.E., Ayrton, A. and El-Sankary, W. (2002) Receptor-dependent transcriptional activation of cytochrome P4503A genes induction mechanisms, species differences and interindividual variation in man. Xenobiotica, 32 (3), 165-206. [Pg.236]

Mirnezami, a. H., et ah, Hdm2 recruits a hypoxia-sensitive corepressor to negatively regulate p5 3-dependent transcription. Curr Biol, 2003, 13(14), 1234-9. [Pg.97]

Mayo, M. W., et al., PTEN blocks tumor necrosis factor-induced NE-kappa B-dependent transcription by inhibiting the transactivation potential of the p65 subunit. J Biol Chem, 2002, 277(13), 11116-25. [Pg.99]

Several mechanisms have been shown to regulate the activity of the SCF complex. The expression of F-box proteins such as Skp2 is regulated by cell-cycle-dependent transcription [4]. The expression of Skp2 is high in late Gl, S, and G2/M phase but... [Pg.149]

REGULATION OF CHROMATIN STRUCTURE AND CHROMATIN-DEPENDENT TRANSCRIPTION BY POLY(ADP-RIBOSE) POLYMERASE-1... [Pg.45]

The Role of PARP-1 as a Specific Nucleosome-Binding Factor Effects on Chromatin Compaction and Chromatin-dependent Transcription... [Pg.51]

Angelov D, Verdel A, An W, Bondarenko V, Hans F, Doyen CM, Studitsky VM, Hamiche A, Roeder RG, Bouvet P, Dimitrov S (2004) SWI/SNF remodeling and p300-dependent transcription of histone variant H2ABbd nucleosomal arrays. Embo J 23 3815-3824... [Pg.84]

Lu Q, Hutchins AE, Doyle CM, Lundblad JR, Kwok RP (2003) Acetylation of CAMP-responsive element-binding protein (CREB) by CREB-binding protein enhances (REB-dependent Transcription. J Biol Chem. 278(18) 15727-15734... [Pg.210]

Janknecht R, Nordheim A (1996) MAP kinase-dependent transcriptional coactivation by Elk-1 and its cofactor CBP. Biochem Biophys Res Commun 228 831-837 Jason LJ, Moore SC, Lewis JD, Lindsey G, Ausio J (2002) Histone ubiquitination a tagging tail unfolds Bioessays 24, 166-174... [Pg.256]

Figure 4. Therapeutic strategies to counteract CBP loss of function. CBP loss of function leads to a decrease in histone acetylation levels as well as a decrease in CBP-dependent transcription. Two main approaches can be tested to reverse diis process either resetting HAT functionality or resetting global acetylation levels widi die use of HDAC inhibitors. Whereas both strategies would increase histone acetylation levels, HDAC inhibition would act on a broad range of genes, while CBP activation (overexpression or by a pharmacological approach) would specifically target bodi CBP-dependent histone acetylation and transcription. The structure of some of the HDACi that have been tested in different models, such as small fatty acids and hydroxamic acids, are represented in the boxes... Figure 4. Therapeutic strategies to counteract CBP loss of function. CBP loss of function leads to a decrease in histone acetylation levels as well as a decrease in CBP-dependent transcription. Two main approaches can be tested to reverse diis process either resetting HAT functionality or resetting global acetylation levels widi die use of HDAC inhibitors. Whereas both strategies would increase histone acetylation levels, HDAC inhibition would act on a broad range of genes, while CBP activation (overexpression or by a pharmacological approach) would specifically target bodi CBP-dependent histone acetylation and transcription. The structure of some of the HDACi that have been tested in different models, such as small fatty acids and hydroxamic acids, are represented in the boxes...
Cai Y, Jin J, Tomomori-Sato C, Sato S, Sorokina 1, Parmely TJ, Conaway RC, Conaway JW (2003) Identification of new subunits of the multiprotein maimnalian TRRAP/TIP60-containing histone acetyltransferase complex. J Biol Chem 278 42733 2736 Cao X, Sudhof TC (2001) A transcriptionally [correction of transcriptively] active complex of APP with Fe65 and histone acetyltransferase Tip60. Science 293 115-120 Cao X, Sudhof TC (2004) Dissection of amyloid-beta precursor protein-dependent transcriptional transactivation. J Biol Chem 279 24601-24611... [Pg.311]


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