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Minneapolis, MN, United States

The University of Minnesota, Twin Cities is a public research university located in Minneapolis and St. Paul, Minnesota, United States. The Minneapolis and St. Paul campuses are approximately 5 miles apart, and the Saint Paul campus is actually in neighboring Falcon Heights. It is the oldest and largest campus within the University of Minnesota system and has the sixth-largest main campus student body in the United States, with 51,853 students in 2012–2013. The university is organized into 19 colleges and schools, and it has sister campuses in Crookston, Duluth, Morris, and Rochester.Minnesota's athletic teams are known collectively as the Minnesota Golden Gophers and compete in the NCAA's Division I as members of the Big Ten Conference. Wikipedia.

Dunny G.M.,University of Minnesota
Annual Review of Genetics | Year: 2013

In Enterococcus faecalis, lateral transfer of conjugative plasmids that encode antibiotic resistance and virulence determinants can be induced by peptide sex pheromones. The tetracycline-resistance plasmid pCF10 represents a paradigm for illustrating important conserved features of a large family of pheromone-responsive enterococcal plasmids. The pheromone is released into the growth medium by plasmid-free recipient cells and sensed by plasmid-containing donors. The activity of the pheromone is antagonized by a plasmid-encoded inhibitor peptide that prevents conjugation in the absence of an inducing signal and is also required to return the system to the ground state following an induction cycle. The pheromone response involves multiple transcriptional and posttranscriptional mechanisms as well as bi-stable biological switch behavior. Multiple layers of regulation are essential for proper function, and evolution of this tight control system may have been favored by reduction of the fitness cost of plasmid maintenance to the host cell. © 2013 by Annual Reviews. All rights reserved. Source

Springer N.M.,University of Minnesota
Trends in Genetics | Year: 2013

There is considerable excitement about the potential for epigenetic information to contribute to heritable variation in many species. Our understanding of the molecular mechanisms of epigenetic inheritance is rapidly growing, and it is now possible to profile the epigenome at high resolution. Epigenetic information plays a role in developmental gene regulation, response to the environment, and in natural variation of gene expression levels. Because of these central roles, there is the potential for epigenetics to play a role in crop improvement strategies including the selection for favorable epigenetic states, creation of novel epialleles, and regulation of transgene expression. In this review we consider the potential, and the limitations, of epigenetic variation in crop improvement. © 2012 Elsevier Ltd. Source

Yee D.,University of Minnesota
Journal of the National Cancer Institute | Year: 2012

The success of targeted therapies for cancer is undisputed; strong preclinical evidence has resulted in the approval of several new agents for cancer treatment. The type I insulin-like growth factor receptor (IGF1R) appeared to be one of these promising new targets. Substantial population and preclinical data have all pointed toward this pathway as an important regulator of tumor cell biology. Although early results from clinical trials that targeted the IGF1R showed some evidence of response, larger randomized phase III trials have not shown clear clinical benefit of targeting this pathway in combination with conventional strategies. These disappointing results have resulted in the discontinuation of several anti-IGF1R programs. However, the conduct of these trials has brought to the forefront several important factors that need to be considered in the conduct of future clinical trials. The need to develop biomarkers, a clearer understanding of insulin receptor function, and defining rational combination regimens all require further consideration. In this commentary, the current state of IGF1R inhibitors in cancer therapy is reviewed. © 2012 The Author. Source

Tilman D.,University of California at Santa Barbara | Clark M.,University of Minnesota
Nature | Year: 2014

Diets link environmental and human health. Rising incomes and urbanization are driving a global dietary transition in which traditional diets are replaced by diets higher in refined sugars, refined fats, oils and meats. By 2050 these dietary trends, if unchecked, would be a major contributor to an estimated 80 per cent increase in global agricultural greenhouse gas emissions from food production and to global land clearing. Moreover, these dietary shifts are greatly increasing the incidence of type II diabetes, coronary heart disease and other chronic non-communicable diseases that lower global life expectancies. Alternative diets that offer substantial health benefits could, if widely adopted, reduce global agricultural greenhouse gas emissions, reduce land clearing and resultant species extinctions, and help prevent such diet-related chronic non-communicable diseases. The implementation of dietary solutions to the tightly linked diet-environment-health trilemma is a global challenge, and opportunity, of great environmental and public health importance. Source

Neufeld T.P.,University of Minnesota
Current Opinion in Cell Biology | Year: 2010

Induction of autophagy in response to starvation is a highly conserved ability of eukaryotic cells, indicating a crucial and ancient role of this process in adapting to nutrient conditions. The target of rapamycin (TOR) pathway is major conduit for such signals, and in most cell types TOR activity is necessary and sufficient to suppress autophagy under favorable growth conditions. Recent studies have begun to reveal how TOR activity is regulated in response to nutritional cues, and are shedding new light on the mechanisms by which TOR controls the autophagic machinery. In addition, a variety of signals, stressors and pharmacological agents that induce autophagy independent of nutrient conditions have been identified. In some cases these signals appear to have been spliced into the core TOR pathway, whereas others are able to bypass the control mechanisms regulated by TOR. Increasing evidence is pointing to an important role for both positive and negative feedback loops in controlling this pathway, leading to an emerging view that TOR signaling not only regulates autophagy but is also highly sensitive to cellular rates of autophagy and other TOR-dependent processes. © 2009 Elsevier Ltd. Source

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