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Titlebook: Gene Therapeutics; Methods and Applicat Jon A. Wolff Book 1994 Birkh?user Boston 1994 DNA.Promoter.Translation.gene expression.gene therapy

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發(fā)表于 2025-3-21 17:12:06 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Gene Therapeutics
副標題Methods and Applicat
編輯Jon A. Wolff
視頻videohttp://file.papertrans.cn/382/381962/381962.mp4
圖書封面Titlebook: Gene Therapeutics; Methods and Applicat Jon A. Wolff Book 1994 Birkh?user Boston 1994 DNA.Promoter.Translation.gene expression.gene therapy
描述During the first half century of genetics, coinciding with the first half of this cen- tury, geneticists dreamt of the repair of genetic disease by altering or replacing defective genes. H. J. Muller wrote of the great advantages of mutations, "nanoneedles" in his apt term, for delicately probing physiological and chemical processes. In the same spirit, genes could be used to provide treatments of needle point delicacy. Yet, during this period no realistic possibility appeared; it remained but a dream. The situation changed abruptly at the half century. Microbial genetics and its offshoot, cell culture genetics, provided the route. Pneumococcus transformation showed that exogenous DNA could become a permanent part of the genome; yet attempts to reproduce this in animals produced a few tantalizing hints of success, but mostly failures. Transduction, using a virus as mediator, offered a better op- portunity. The fITSt reproducible in vivo gene therapy in a whole animal came in 1981. This was in Drosophila, with a transposable element as carrier. Flies were "cured" of a mutant eye color by incorporation of the normal allele, and the effect was transmissible, foreshadowing not only som
出版日期Book 1994
關(guān)鍵詞DNA; Promoter; Translation; gene expression; gene therapy; genes; transcription
版次1
doihttps://doi.org/10.1007/978-1-4684-6822-9
isbn_softcover978-1-4684-6824-3
isbn_ebook978-1-4684-6822-9
copyrightBirkh?user Boston 1994
The information of publication is updating

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Producing Mouse Genetic Models for Human Diseasesluable to the basic research support of fields as wide-ranging as immunology, reproduction, oncology, nutrition, infectious diseases, transplantation, cardiology, and anesthesiology (Report of the Council on Scientific Affairs, 1989). Due to recent advances in the techniques required for somatic gen
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Post-Transcriptional Considerations of Gene Expression: Translation, MRNA Stability, and Poly(A) Proich the mRNA is synthesized, but also upon the rates at which the mRNA is processed, trans-ported and translated along with the rates at which the mRNA and protein are degraded. Therefore, each of these post-transcriptional processes is linked to “gene expression,” and it is important to know how ea
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Promoters, Enhancers, and Inducible Elements for Gene Therapyll in gestation. The midwives to the birth of this area are those molecular biologists who are actively involved in the study of the control of gene expression. In particular, the tremendous surge of the last several years in understanding of the promoter elements and the protein factors involved in
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In Vivo Gene Therapy via Receptor-Mediated DNA Deliverys in recombinant DNA methodologies have fostered molecular studies in such fields as regulation of gene expression, human genetics and disease states, and gene transfer techniques. The confluence of these fields has led to the emergence of gene therapy as a reality, albeit limited at present to a sm
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Calcium Phosphate-Mediated DNA Transfectione transcriptional and translational activities of exogenous DNA but also the regulation of gene expression by other genetic elements. Furthermore, the approach to somatic gene therapy is entirely based on introducing genes either to correct a prior genetic defect or to augment the genetic repertoire
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Cellular Internalization of Oligodeoxynucleotidesngs have been in contrast to the prevailing view that cells are impermeable to negatively charged large molecules. With this in mind, several groups have attempted to modify oligos in order to circumvent the problem of negative charge. Thus, methylphosphonates are ionically neutral, and poly-L-lysin
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