Institution
Rockefeller University
Education•New York, New York, United States•
About: Rockefeller University is a education organization based out in New York, New York, United States. It is known for research contribution in the topics: Population & Gene. The organization has 15867 authors who have published 32938 publications receiving 2940261 citations. The organization is also known as: Rockefeller University & Rockefeller Institute.
Topics: Population, Gene, Virus, Antigen, Receptor
Papers published on a yearly basis
Papers
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TL;DR: The increase in infectivity caused by proteolytic cleavage of the HA polypeptide provides a biochemical explanation for the previously observed enhancement of plaquing efficiency of influenza viruses by the inclusion of pancreation or trypsin in the agar overlay.
593 citations
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TL;DR: How well-established risk factors for CVD can originate from inflammation in other tissues is discussed, and possible mechanistic links between skin inflammation and increased risks of obesity or metabolic alterations and CVD are considered.
593 citations
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TL;DR: The predicted attenuation ofβ-amyloid content in the brain during CR can be reproduced in mouse neurons in vitro by manipulating cellular SIRT1 expression/activity through mechanisms involving the regulation of the serine/threonine Rho kinase ROCK1.
592 citations
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University of Kentucky1, Yonsei University2, University of Colorado Boulder3, University of Florida4, University of Pennsylvania5, Sungkyunkwan University6, Meharry Medical College7, University of Southern California8, Clark Atlanta University9, Australian National University10, University of Sydney11, Rockefeller University12, New York University13, Veterans Health Administration14, University of Utah15, Johns Hopkins University16, Laval University17
TL;DR: Findings reveal a miRNA-independent cell survival function for DICER1 involving retrotransposon transcript degradation, show that Alu RNA can directly cause human pathology, and identify new targets for a major cause of blindness.
Abstract: Geographic atrophy (GA), an untreatable advanced form of age-related macular degeneration, results from retinal pigmented epithelium (RPE) cell degeneration. Here we show that the microRNA (miRNA)-processing enzyme DICER1 is reduced in the RPE of humans with GA, and that conditional ablation of Dicer1, but not seven other miRNA-processing enzymes, induces RPE degeneration in mice. DICER1 knockdown induces accumulation of Alu RNA in human RPE cells and Alu-like B1 and B2 RNAs in mouse RPE. Alu RNA is increased in the RPE of humans with GA, and this pathogenic RNA induces human RPE cytotoxicity and RPE degeneration in mice. Antisense oligonucleotides targeting Alu/B1/B2 RNAs prevent DICER1 depletion-induced RPE degeneration despite global miRNA downregulation. DICER1 degrades Alu RNA, and this digested Alu RNA cannot induce RPE degeneration in mice. These findings reveal a miRNA-independent cell survival function for DICER1 involving retrotransposon transcript degradation, show that Alu RNA can directly cause human pathology, and identify new targets for a major cause of blindness.
590 citations
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TL;DR: The data suggest that the brain is a direct target for the weight-reducing and neuroendocrine effects of leptin and that the liver abnormalities of db/db mice are secondary to defective leptin signaling in the brain.
Abstract: Animals with mutations in the leptin receptor (ObR) exhibit an obese phenotype that is indistinguishable from that of leptin deficient ob/ob mice. ObR is expressed in many tissues, including brain, and the relative importance of leptin's effects on central versus peripheral sites has not been resolved. To address this, we generated mice with neuron-specific (ObR(SynI)KO) and hepatocyte-specific (ObR(Alb)KO) disruption of ObR. Among the ObR(SynI)KO mice, the extent of obesity was negatively correlated with the level of ObR in hypothalamus and those animals with the lowest levels of ObR exhibited an obese phenotype. The obese mice with low levels of hypothalamic ObR also show elevated plasma levels of leptin, glucose, insulin, and corticosterone. The hypothalamic levels of agouti-related protein and neuropeptide Y RNA are increased in these mice. These data indicate that leptin has direct effects on neurons and that a significant proportion, or perhaps the majority, of its weight-reducing effects are the result of its actions on brain. To explore possible direct effects of leptin on a peripheral tissue, we also characterized ObR(Alb)KO mice. These mice weigh the same as controls and have no alterations in body composition. Moreover, while db/db mice and ObR(SynI)KO mice have enlarged fatty livers, ObR(Alb)KO mice do not. In summary, these data suggest that the brain is a direct target for the weight-reducing and neuroendocrine effects of leptin and that the liver abnormalities of db/db mice are secondary to defective leptin signaling in the brain.
590 citations
Authors
Showing all 15925 results
Name | H-index | Papers | Citations |
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Bruce S. McEwen | 215 | 1163 | 200638 |
David Baltimore | 203 | 876 | 162955 |
Ronald M. Evans | 199 | 708 | 166722 |
Lewis C. Cantley | 196 | 748 | 169037 |
Ronald Klein | 194 | 1305 | 149140 |
Scott M. Grundy | 187 | 841 | 231821 |
Jie Zhang | 178 | 4857 | 221720 |
Andrea Bocci | 172 | 2402 | 176461 |
Ralph M. Steinman | 171 | 453 | 121518 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Zena Werb | 168 | 473 | 122629 |
Nahum Sonenberg | 167 | 647 | 104053 |
Michel C. Nussenzweig | 165 | 516 | 87665 |
Harvey F. Lodish | 165 | 782 | 101124 |
Dennis R. Burton | 164 | 683 | 90959 |