Institution
McGill University
Education•Montreal, Quebec, Canada•
About: McGill University is a education organization based out in Montreal, Quebec, Canada. It is known for research contribution in the topics: Population & Context (language use). The organization has 72688 authors who have published 162565 publications receiving 6966523 citations. The organization is also known as: Royal institution of advanced learning & University of McGill College.
Topics: Population, Context (language use), Poison control, Health care, Cancer
Papers published on a yearly basis
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TL;DR: It is shown that "naked" QDs induce damage to the plasma membrane, mitochondrion, and nucleus, leading to cell death, suggesting the critical role of several subcellular compartments in QD-induced cytotoxicity and point toward multiple molecular targets in nonclassical apoptosis.
694 citations
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University of Toulouse1, California Institute of Technology2, Massachusetts Institute of Technology3, Columbia University4, University of California, Berkeley5, Technical University of Denmark6, Lawrence Livermore National Laboratory7, University of Cambridge8, Goddard Space Flight Center9, McGill University10, Texas Tech University11, University of Michigan12
TL;DR: In this article, the authors reported broadband X-ray observations of the nuclear region of the galaxy M82 that reveal pulsations with an average period of 1.37 seconds and a 2.5-day sinusoidal modulation.
Abstract: The majority of ultraluminous X-ray sources are point sources that are spatially offset from the nuclei of nearby galaxies and whose X-ray luminosities exceed the theoretical maximum for spherical infall (the Eddington limit) onto stellar-mass black holes. Their X-ray luminosities in the 0.5–10 kiloelectronvolt energy band range from 10^(39) to 10^(41) ergs per second. Because higher masses imply less extreme ratios of the luminosity to the isotropic Eddington limit, theoretical models have focused on black hole rather than neutron star systems. The most challenging sources to explain are those at the luminous end of the range (more than 1040 ergs per second), which require black hole masses of 50–100 times the solar value or significant departures from the standard thin disk accretion that powers bright Galactic X-ray binaries, or both. Here we report broadband X-ray observations of the nuclear region of the galaxy M82 that reveal pulsations with an average period of 1.37 seconds and a 2.5-day sinusoidal modulation. The pulsations result from the rotation of a magnetized neutron star, and the modulation arises from its binary orbit. The pulsed flux alone corresponds to an X-ray luminosity in the 3–30 kiloelectronvolt range of 4.9 × 10^(39) ergs per second. The pulsating source is spatially coincident with a variable source that can reach an X-ray luminosity in the 0.3–10 kiloelectronvolt range of 1.8 × 10^(40) ergs per second. This association implies a luminosity of about 100 times the Eddington limit for a 1.4-solar-mass object, or more than ten times brighter than any known accreting pulsar. This implies that neutron stars may not be rare in the ultraluminous X-ray population, and it challenges physical models for the accretion of matter onto magnetized compact objects.
693 citations
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TL;DR: Endoscopic screening of FAP probands and relatives is advocated as early as the ages of 10–12 yr, with the objective of reducing the occurrence of colorectal cancer.
693 citations
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TL;DR: The data suggest that a reduction in frataxin results in oxidative damage, given the shared clinical features between Friedreich ataxia, vitamin E deficiency and some mitochondriopathies.
Abstract: Friedreich ataxia is a progressive neurodegenerative disorder caused by loss of function mutations in the frataxin gene. In order to unravel frataxin function we developed monoclonal antibodies raised against different regions of the protein. These antibodies detect a processed 18 kDa protein in various human and mouse tissues and cell lines that is severely reduced in Friedreich ataxia patients. By immunocytofluorescence and immunocytoelectron microscopy we show that frataxin is located in mitochondria, associated with the mitochondrial membranes and crests. Analysis of cellular localization of various truncated forms of frataxin expressed in cultured cells and evidence of removal of an N-terminal epitope during protein maturation demonstrated that the mitochondrial targetting sequence is encoded by the first 20 amino acids. Given the shared clinical features between Friedreich ataxia, vitamin E deficiency and some mitochondriopathies, our data suggest that a reduction in frataxin results in oxidative damage.
693 citations
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TL;DR: Light is shed on the mechanisms of eIF-4F assembly and on the translational regulation by insulin and growth factors and a 12-amino-acid sequence conserved between mammals and Saccharomyces cerevisiae that is critical for the interaction with eif-4E is identified.
Abstract: Eukaryotic translation initiation factor 4E (eIF-4E), which possesses cap-binding activity, functions in the recruitment of mRNA to polysomes as part of a three-subunit complex, eIF-4F (cap-binding complex). eIF-4E is the least abundant of all translation initiation factors and a target of growth regulatory pathways. Recently, two human cDNAs encoding novel eIF-4E-binding proteins (4E-BPs) which function as repressors of cap-dependent translation have been cloned. Their interaction with eIF-4E is negatively regulated by phosphorylation in response to cell treatment with insulin or growth factors. The present study aimed to characterize the molecular interactions between eIF-4E and the other subunits of eIF-4F and to similarly characterize the molecular interactions between eIF-4E and the 4E-BPs. A 49-amino-acid region of eIF-4 gamma, located in the N-terminal side of the site of cleavage by Picornaviridae protease 2A, was found to be sufficient for interacting with eIF-4E. Analysis of deletion mutants in this region led to the identification of a 12-amino-acid sequence conserved between mammals and Saccharomyces cerevisiae that is critical for the interaction with eIF-4E. A similar motif is found in the amino acid sequence of the 4E-BPs, and point mutations in this motif abolish the interaction with eIF-4E. These results shed light on the mechanisms of eIF-4F assembly and on the translational regulation by insulin and growth factors.
692 citations
Authors
Showing all 73373 results
Name | H-index | Papers | Citations |
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Karl J. Friston | 217 | 1267 | 217169 |
Yi Chen | 217 | 4342 | 293080 |
Yoshua Bengio | 202 | 1033 | 420313 |
Irving L. Weissman | 201 | 1141 | 172504 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Lewis C. Cantley | 196 | 748 | 169037 |
Martin White | 196 | 2038 | 232387 |
Michael Marmot | 193 | 1147 | 170338 |
Michael A. Strauss | 185 | 1688 | 208506 |
Alan C. Evans | 183 | 866 | 134642 |
Douglas R. Green | 182 | 661 | 145944 |
David A. Weitz | 178 | 1038 | 114182 |
David L. Kaplan | 177 | 1944 | 146082 |
Hyun-Chul Kim | 176 | 4076 | 183227 |
Feng Zhang | 172 | 1278 | 181865 |