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Postnatal repression of the alpha-fetoprotein gene is enhancer independent.
Finally, rescue of adult viability was noted for homozygous males of several excision lines, in both enhancer-trap strains.
We have now started to unravel the basis of the specificity of this multitude of enhancers for their respective promoters.
The presence of further, as yet unidentified, modular enhancers must therefore be invoked.
This work demonstrates that it is possible to selectively improve cognitive performance in chronic, stable, high-functioning patients using targeted cognitive enhancers.
The need for enhancers in gene expression first appears during mouse development with formation of the zygotic nucleus.
During oogenesis and preimplantation development, promoter and enhancer utilization is altered dynamically.
In embryos at the late 2-cell stage, promoter activity is repressed and an enhancer is necessary for transcription.
Such agents bind non-covalently in the minor groove with affinities and specificities comparable or better to those of many cellular enhancer binding proteins.
Common to most gene therapy expression systems are the viral promoter and enhancer elements.
We found that the transposon in these two enhancer-trap lines drastically altered the amplitude of pheromone discrimination.
However, during development, this enhancer is progressively silenced, as transgene expression directed by the chicken enhancer becomes confined to outflow tract myocardium.
The corollary may also be true, that enhancers require the context of modulator elements, such as those identified here, more commonly than generally recognized.
Based on these analyses, potential regulatory regions have been assessed for enhancer, insulator and silencer activities in vitro.
Multiple nuclear factors interact with immunoglobulin enhancer sequence.
