Institution
Tel Aviv University
Education•Tel Aviv, Israel•
About: Tel Aviv University is a education organization based out in Tel Aviv, Israel. It is known for research contribution in the topics: Population & Medicine. The organization has 47791 authors who have published 115959 publications receiving 3904391 citations. The organization is also known as: TAU & Universiṭat Tel-Aviv.
Topics: Population, Medicine, Poison control, Context (language use), Cancer
Papers published on a yearly basis
Papers
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TL;DR: This new version of ConSurf includes an empirical Bayesian method for scoring conservation, which is more accurate than the maximum-likelihood method that was used in the earlier release and includes a measure of confidence for the inferred amino acid conservation scores.
Abstract: Key amino acid positions that are important for maintaining the 3D structure of a protein and/or its function(s), e.g. catalytic activity, binding to ligand, DNA or other proteins, are often under strong evolutionary constraints. Thus, the biological importance of a residue often correlates with its level of evolutionary conservation within the protein family. ConSurf (http://consurf.tau.ac.il/) is a web-based tool that automatically calculates evolutionary conservation scores and maps them on protein structures via a user-friendly interface. Structurally and functionally important regions in the protein typically appear as patches of evolutionarily conserved residues that are spatially close to each other. We present here version 3.0 of ConSurf. This new version includes an empirical Bayesian method for scoring conservation, which is more accurate than the maximum-likelihood method that was used in the earlier release. Various additional steps in the calculation can now be controlled by a number of advanced options, thus further improving the accuracy of the calculation. Moreover, ConSurf version 3.0 also includes a measure of confidence for the inferred amino acid conservation scores.
1,309 citations
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18 May 2014TL;DR: This paper formulate and construct decentralized anonymous payment schemes (DAP schemes) and builds Zero cash, a practical instantiation of the DAP scheme construction that is orders of magnitude more efficient than the less-anonymous Zero coin and competitive with plain Bit coin.
Abstract: Bit coin is the first digital currency to see widespread adoption. While payments are conducted between pseudonyms, Bit coin cannot offer strong privacy guarantees: payment transactions are recorded in a public decentralized ledger, from which much information can be deduced. Zero coin (Miers et al., IEEE SaP 2013) tackles some of these privacy issues by unlinking transactions from the payment's origin. Yet, it still reveals payments' destinations and amounts, and is limited in functionality. In this paper, we construct a full-fledged ledger-based digital currency with strong privacy guarantees. Our results leverage recent advances in zero-knowledge Succinct Non-interactive Arguments of Knowledge (zk-SNARKs). First, we formulate and construct decentralized anonymous payment schemes (DAP schemes). A DAP scheme enables users to directly pay each other privately: the corresponding transaction hides the payment's origin, destination, and transferred amount. We provide formal definitions and proofs of the construction's security. Second, we build Zero cash, a practical instantiation of our DAP scheme construction. In Zero cash, transactions are less than 1 kB and take under 6 ms to verify - orders of magnitude more efficient than the less-anonymous Zero coin and competitive with plain Bit coin.
1,305 citations
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Wellcome Trust Sanger Institute1, Université de Montréal2, University of Edinburgh3, University of Kiel4, Karolinska Institutet5, Cedars-Sinai Medical Center6, University of Cambridge7, University of Pennsylvania8, Casa Sollievo della Sofferenza9, University of Pittsburgh10, Université libre de Bruxelles11, University of Otago12, Johns Hopkins University13, Ludwig Maximilian University of Munich14, Charité15, Lille University of Science and Technology16, Cincinnati Children's Hospital Medical Center17, Ghent University18, Torbay Hospital19, University of Groningen20, Mater Health Services21, University of Liège22, University of Washington23, University of Utah24, QIMR Berghofer Medical Research Institute25, University of Paris26, University of Western Australia27, Tel Aviv University28, University of Dundee29, Harvard University30, University of Manchester31, Utrecht University32, University of Florence33, King's College London34, Yale University35, Royal Hospital for Sick Children36, Katholieke Universiteit Leuven37, Guy's and St Thomas' NHS Foundation Trust38, University of Barcelona39, University of Chicago40, University of Bern41, Agency for Science, Technology and Research42, University of California, San Francisco43, University of Toronto44, University of Oslo45, Leiden University46, University of Amsterdam47, Aarhus University48, National and Kapodistrian University of Athens49, Lithuanian University of Health Sciences50, Newcastle University51, Emory University52, Örebro University53, French Institute of Health and Medical Research54, Center for Applied Genomics55
TL;DR: A meta-analysis of six ulcerative colitis genome-wide association study datasets found many candidate genes that provide potentially important insights into disease pathogenesis, including IL1R2, IL8RA-IL8RB, IL7R, IL12B, DAP, PRDM1, JAK2, IRF5, GNA12 and LSP1.
Abstract: Genome-wide association studies and candidate gene studies in ulcerative colitis have identified 18 susceptibility loci. We conducted a meta-analysis of six ulcerative colitis genome-wide association study datasets, comprising 6,687 cases and 19,718 controls, and followed up the top association signals in 9,628 cases and 12,917 controls. We identified 29 additional risk loci (P < 5 × 10(-8)), increasing the number of ulcerative colitis-associated loci to 47. After annotating associated regions using GRAIL, expression quantitative trait loci data and correlations with non-synonymous SNPs, we identified many candidate genes that provide potentially important insights into disease pathogenesis, including IL1R2, IL8RA-IL8RB, IL7R, IL12B, DAP, PRDM1, JAK2, IRF5, GNA12 and LSP1. The total number of confirmed inflammatory bowel disease risk loci is now 99, including a minimum of 28 shared association signals between Crohn's disease and ulcerative colitis.
1,291 citations
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TL;DR: The findings show that HIV-specific CD4+ T cells are preferentially infected by HIV in vivo, which provides a potential mechanism to explain the loss of HIV- specific CD4- T-cell responses, and consequently theloss of immunological control of HIV replication.
Abstract: HIV infection is associated with the progressive loss of CD4(+) T cells through their destruction or decreased production. A central, yet unresolved issue of HIV disease is the mechanism for this loss, and in particular whether HIV-specific CD4(+) T cells are preferentially affected. Here we show that HIV-specific memory CD4(+) T cells in infected individuals contain more HIV viral DNA than other memory CD4(+) T cells, at all stages of HIV disease. Additionally, following viral rebound during interruption of antiretroviral therapy, the frequency of HIV viral DNA in the HIV-specific pool of memory CD4(+) T cells increases to a greater extent than in memory CD4(+) T cells of other specificities. These findings show that HIV-specific CD4(+) T cells are preferentially infected by HIV in vivo. This provides a potential mechanism to explain the loss of HIV-specific CD4(+) T-cell responses, and consequently the loss of immunological control of HIV replication. Furthermore, the phenomenon of HIV specifically infecting the very cells that respond to it adds a cautionary note to the practice of structured therapy interruption.
1,283 citations
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TL;DR: Evidence suggests that ATM-mediated phosphorylation has a role in the response to other types of genotoxic stress and it has become apparent that ATM is active in other cell signalling pathways involved in maintaining cellular homeostasis.
Abstract: The protein kinase ataxia-telangiectasia mutated (ATM) is best known for its role as an apical activator of the DNA damage response in the face of DNA double-strand breaks (DSBs). Following induction of DSBs, ATM mobilizes one of the most extensive signalling networks that responds to specific stimuli and modifies directly or indirectly a broad range of targets. Although most ATM research has focused on this function, evidence suggests that ATM-mediated phosphorylation has a role in the response to other types of genotoxic stress. Moreover, it has become apparent that ATM is active in other cell signalling pathways involved in maintaining cellular homeostasis.
1,281 citations
Authors
Showing all 48197 results
Name | H-index | Papers | Citations |
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Jing Wang | 184 | 4046 | 202769 |
Aviv Regev | 163 | 640 | 133857 |
Itamar Willner | 143 | 927 | 76316 |
M. Morii | 134 | 1664 | 102074 |
Halina Abramowicz | 134 | 1192 | 89294 |
Joost J. Oppenheim | 130 | 454 | 59601 |
Gideon Bella | 129 | 1301 | 87905 |
Avishay Gal-Yam | 129 | 795 | 56382 |
Erez Etzion | 129 | 1216 | 85577 |
Allen Mincer | 129 | 1040 | 80059 |
Abner Soffer | 129 | 1028 | 82149 |
Gideon Koren | 129 | 1994 | 81718 |
Alex Zunger | 128 | 826 | 78798 |
Odette Benary | 128 | 844 | 74238 |
Gideon Alexander | 128 | 1201 | 81555 |