Institution
Michigan State University
Education•East Lansing, Michigan, United States•
About: Michigan State University is a education organization based out in East Lansing, Michigan, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 60109 authors who have published 137074 publications receiving 5633022 citations. The organization is also known as: MSU & Michigan State.
Topics: Population, Poison control, Gene, Galaxy, Large Hadron Collider
Papers published on a yearly basis
Papers
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Michigan State University1, J. Craig Venter Institute2, National Institutes of Health3, Wellcome Trust Sanger Institute4, Plymouth Marine Laboratory5, University of Maryland, Baltimore6, University of Cambridge7, University of York8, United States Department of Energy9, Ghent University10, Pennsylvania State University11, Argonne National Laboratory12, University of California, San Diego13, Jacobs University Bremen14, University of Colorado Boulder15, National Science Foundation16, Edinburgh Napier University17, Boston Children's Hospital18, University of Georgia19, University of California, Berkeley20, Newcastle University21, Lawrence Berkeley National Laboratory22, University of California, Irvine23, University of Oxford24, Howard University25, Abertay University26, University of Manchester27, Technical University of Denmark28, University of Wyoming29, University of Pennsylvania30, University of New Mexico31
TL;DR: Here, the minimum information about a genome sequence (MIGS) specification is introduced with the intent of promoting participation in its development and discussing the resources that will be required to develop improved mechanisms of metadata capture and exchange.
Abstract: With the quantity of genomic data increasing at an exponential rate, it is imperative that these data be captured electronically, in a standard format. Standardization activities must proceed within the auspices of open-access and international working bodies. To tackle the issues surrounding the development of better descriptions of genomic investigations, we have formed the Genomic Standards Consortium (GSC). Here, we introduce the minimum information about a genome sequence (MIGS) specification with the intent of promoting participation in its development and discussing the resources that will be required to develop improved mechanisms of metadata capture and exchange. As part of its wider goals, the GSC also supports improving the 'transparency' of the information contained in existing genomic databases.
1,097 citations
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TL;DR: TNFα has been shown to play a pivotal role in orchestrating the cytokine cascade in many inflammatory diseases and because of this role as a "master-regulator" of inflammatory cytokine production, it has been proposed as a therapeutic target for a number of diseases.
Abstract: Tumor necrosis factor-α (TNFα) was cloned over 2 decades ago and its identification in part led to the discovery of a super family of tumor necrosis factors (TNFs) and their receptors. TNFα signals through two transmembrane receptors, TNFR1 and TNFR2, and regulates a number of critical cell functions including cell proliferation, survival, differentiation, and apoptosis. Macrophages are the major producers of TNFα and interestingly are also highly responsive to TNFα. Aberrant TNFα production and TNF receptor signaling have been associated with the pathogenesis of several diseases, including rheumatoid arthritis, Crohn's disease, atherosclerosis, psoriasis, sepsis, diabetes, and obesity. TNFα has been shown to play a pivotal role in orchestrating the cytokine cascade in many inflammatory diseases and because of this role as a "master-regulator" of inflammatory cytokine production, it has been proposed as a therapeutic target for a number of diseases. Indeed anti-TNFα drugs are now licensed for treating certain inflammatory diseases including rheumatoid arthritis and inflammatory bowel disease. In this review we discuss the discovery of TNFα and its actions especially in regulating macrophage biology. Given its importance in several human diseases, we also briefly discuss the role of anti-TNFα therapeutics in the treatment of inflammatory diseases.
1,094 citations
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TL;DR: A highly sensitive stain for visualizing proteins in polyacrylamide gels that will be especially useful for analysis of patterns of proteins from tissue where attainment of the high specific activity of isotope labeling which is necessary to detect minor protein components is expensive, technically difficult or prohibited.
1,091 citations
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TL;DR: It is proposed that cold-induced expression of CRT/DRE-containing COR genes involves a low temperature-stimulated signalling cascade in which CBF gene induction is an early event and theCBF gene family is not subject to autoregulation.
Abstract: Cold-induced expression of the Arabidopsis COR (cold-regulated) genes is mediated by a DNA regulatory element termed the CRT (C-repeat)/DRE (dehydration-responsive element). Recently, we identified a transcriptional activator, CBF1, that binds to the CRT/DRE and demonstrated that its overexpression in transgenic Arabidopsis plants at non-acclimating temperatures induces COR gene expression and increases plant freezing tolerance. Here we report that CBF1 belongs to a small family of closely related proteins which includes CBF2 and CBF3. DNA sequencing of an 8.7 kb region of the Arabidopsis genome along with genetic mapping experiments indicated that the three CBF genes are organized in direct repeat on chromosome 4 at 72.8 cM, closely linked to molecular markers PG11 and m600. Like CBF1, both CBF2 and CBF3 activated expression of reporter genes in yeast that contained the CRT/DRE as an upstream activator sequence. The transcript levels for all three CBF genes increased within 15 min of transferring plants to low temperature, followed by accumulation of COR gene transcripts at about 2 h. CBF transcripts also accumulated rapidly in response to mechanical agitation. The promoter regions of the CBF genes do not contain the CRT sequence, CCGAC, and overexpression of CBF1 did not have a detectable effect on CBF3 transcript levels, suggesting that the CBF gene family is not subject to autoregulation. We propose that cold-induced expression of CRT/DRE-containing COR genes involves a low temperature-stimulated signalling cascade in which CBF gene induction is an early event.
1,090 citations
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TL;DR: The authors revisited the effects of spending on student performance using data from the state of Michigan and found that spending has nontrivial and statistically significant effects, although the diminishing effect is not especially pronounced.
1,090 citations
Authors
Showing all 60636 results
Name | H-index | Papers | Citations |
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David Miller | 203 | 2573 | 204840 |
Anil K. Jain | 183 | 1016 | 192151 |
D. M. Strom | 176 | 3167 | 194314 |
Feng Zhang | 172 | 1278 | 181865 |
Derek R. Lovley | 168 | 582 | 95315 |
Donald G. Truhlar | 165 | 1518 | 157965 |
Donald E. Ingber | 164 | 610 | 100682 |
J. E. Brau | 162 | 1949 | 157675 |
Murray F. Brennan | 161 | 925 | 97087 |
Peter B. Reich | 159 | 790 | 110377 |
Wei Li | 158 | 1855 | 124748 |
Timothy C. Beers | 156 | 934 | 102581 |
Claude Bouchard | 153 | 1076 | 115307 |
Mercouri G. Kanatzidis | 152 | 1854 | 113022 |
James J. Collins | 151 | 669 | 89476 |