期刊
CELLULAR AND MOLECULAR LIFE SCIENCES
卷 64, 期 1, 页码 3-16出版社
SPRINGER BASEL AG
DOI: 10.1007/s00018-006-6296-z
关键词
lactose repressor; allostery; genetic regulation; transcription regulation; inducer; operator
资金
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR017708] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM008280, R01GM022441] Funding Source: NIH RePORTER
- NCRR NIH HHS [P20 RR 17708] Funding Source: Medline
- NIGMS NIH HHS [GM22441, T32 GM008280, GM08280] Funding Source: Medline
In 1961, Jacob and Monod proposed the operon model for gene regulation based on metabolism of lactose in Escherichia coli [1]. This proposal was followed by an explication of allosteric behavior by Monod and colleagues [2]. The operon model rationally depicted how genetic mechanisms can control metabolic events in response to environmental stimuli via coordinated transcription of a set of genes with related function (e.g. metabolism of lactose). The allosteric response found in the lactose repressor and many other proteins has been extended to a variety of cellular signaling pathways in all organisms. These two models have shaped our view of modern molecular biology and captivated the attention of a surprisingly broad range of scientists. More recently, the lactose repressor monomer was used as a model system for experimental and theoretical explorations of protein folding mechanisms. Thus, the lac system continues to advance our molecular understanding of genetic control and the relationship between sequence, structure and function.
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