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Transcription development

Vazquez, M., Moore, L., and Kennison, J.A. (1999) The trithorax group gene osa encodes an ARID-domain protein that genetically interacts with the brahma chromatin-remodeling factor to regulate transcription. Development 126, 733-742. [Pg.456]

Christians, E., Campion, E., Thompson, E.M., and Renard, J.-P. (1995). Expression of the HSP 70.1 gene, a landmark of early zygotic activity in the mouse embryo, is restricted to the first burst of transcription. Development 727 113-122. [Pg.160]

Our discussion shows that the Ising model, lattice gas and binary alloy are related and present one and the same statistical mechanical problem. The solution to one provides, by means of the transcription tables, the solution to the others. Flistorically, however, they were developed independently before the analogy between the models was recognized. [Pg.529]

The specific role of vitamin A in tissue differentiation has been an active area of research. The current thinking, developed in 1979, involves initial dehvery of retinol by holo-B >V (retinol-binding protein) to the cell cytosol (66). Retinol is then ultimately oxidized to retinoic acid and binds to a specific cellular retinoid-binding protein and is transported to the nucleus. Retinoic acid is then transferred to a nuclear retinoic acid receptor (RAR), which enhances the expression of a specific region of the genome. Transcription occurs and new proteins appear during the retinoic acid-induced differentiation of cells (56). [Pg.103]

Cellular screening systems can be developed with primary human cells cultured in biologically relevant contexts. The outputs of these systems are focused sets of biologically relevant parameters (gene transcription, protein... [Pg.184]

ECE isoforms are also involved in the degradation of A 3 peptide. A genetic variant of ECE-1 with an increased transcriptional activity is associated with a decreased risk for AD. Thus, the inhibition of ECE in the CNS may increase the risk for the development of Alzheimer s disease (AD). [Pg.475]

Originally described in the immune system, NFAT proteins comprise a family of transcriptional factors that play key roles in many cellular processes that control not only immune responses but also the development, regulation, and differentiation of many other tissues. Activation of NFAT proteins results in the expression of specific sets of genes that regulate multiple cell functions [1,2]. [Pg.846]

NFAT was first described in cells of the immune system, but these transcription factors are widely expressed and their function is crucial in the regulation, development, and differentiation of many nonimmune tissues. [Pg.848]

NFAT2 plays a key role in the development of the embryo s heart. In the precursor cells, there is a temporal and spatial specific expression of NFAT2, which directs the formation of the valves and the septum in the heart. In the adult heart, NFAT proteins also cooperate with transcription factors of the GATA and MEF2 families to regulate cardiac muscle hypertrophic responses. [Pg.849]

In addition to those described above, some of the newest compounds emerging in SERM development are ER 3-selective ligands and pathway-selective modulators that target the interaction of the ERs with the transcription factor NFkB. While such compounds are in the early stages of clinical evaluation, thus far they demonstrate great potential for use in the treatment of inflammatory disorders such as arthritis, inflammatory bowel disease, and like other SERMs, cancer [4]. [Pg.1116]

Since the SUMO pathway affects multiple pathways ranging from transcription, DNA repair, and intracellular trafficking over cell signaling and cell cycle control to basic metabolism, it is not suiprising that links to diseases and viral assaults are emerging. However, the field is not yet at a stage sufficiently developed for pharmacological intervention. Below we will describe selected examples for links of the SUMO pathway to diseases and viral functions. [Pg.1166]

Gill G (2005) Something about SUMO inhibits transcription. Curr Opin Genet Develop, 5 536-541... [Pg.1167]


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See also in sourсe #XX -- [ Pg.67 , Pg.68 , Pg.69 , Pg.70 ]




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