Institution
University of Siena
Education•Siena, Italy•
About: University of Siena is a education organization based out in Siena, Italy. It is known for research contribution in the topics: Population & Cancer. The organization has 12179 authors who have published 33334 publications receiving 1008287 citations. The organization is also known as: Università degli studi di Siena & Universita degli studi di Siena.
Papers published on a yearly basis
Papers
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F. Kyle Satterstrom1, F. Kyle Satterstrom2, Jack A. Kosmicki, Jiebiao Wang3 +198 more•Institutions (53)
TL;DR: The largest exome sequencing study of autism spectrum disorder (ASD) to date, using an enhanced analytical framework to integrate de novo and case-control rare variation, identifies 102 risk genes at a false discovery rate of 0.1 or less, consistent with multiple paths to an excitatory-inhibitory imbalance underlying ASD.
1,169 citations
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Daniel J. Klionsky1, Amal Kamal Abdel-Aziz2, Sara Abdelfatah3, Mahmoud Abdellatif4 +2980 more•Institutions (777)
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
Abstract: In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
1,129 citations
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TL;DR: It has been shown that Rb protein (pRb) is responsible for a major G1 checkpoint, blocking S-phase entry and cell growth.
Abstract: The Rb protein is a tumor suppressor, which plays a pivotal role in the negative control of the cell cycle and in tumor progression. It has been shown that Rb protein (pRb) is responsible for a major G1 checkpoint, blocking S-phase entry and cell growth. The retinoblastoma family includes three members, Rb/p105, p107 and Rb2/p130, collectively referred to as 'pocket proteins'. The pRb protein represses gene transcription, required for transition from G1 to S phase, by directly binding to the transactivation domain of E2F and by binding to the promoter of these genes as a complex with E2F. pRb represses transcription also by remodeling chromatin structure through interaction with proteins such as hBRM, BRG1, HDAC1 and SUV39H1, which are involved in nucleosome remodeling, histone acetylation/deacetylation and methylation, respectively. Loss of pRb functions may induce cell cycle deregulation and so lead to a malignant phenotype. Gene inactivation of pRB through chromosomal mutations is one of the principal reasons for retinoblastoma tumor development. Functional inactivation of pRb by viral oncoprotein binding is also shown in many neoplasias such as cervical cancer, mesothelioma and AIDS-related Burkitt's lymphoma.
1,072 citations
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TL;DR: It is likely, but requiring further confirmation, that adult exposure to BPA affects the brain, the female reproductive system, and the immune system and that developmental effects occur in theFemale reproductive system.
1,065 citations
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Paris 12 Val de Marne University1, University of Göttingen2, University Hospital of Lausanne3, French Institute of Health and Medical Research4, University of Milan5, University of Otago6, University of Regensburg7, University of Marburg8, Ruhr University Bochum9, Ludwig Maximilian University of Munich10, University of Siena11, University of Texas at Dallas12, University of Tübingen13
TL;DR: It remains to be clarified whether the probable or possible therapeutic effects of tDCS are clinically meaningful and how to optimally perform tDCS in a therapeutic setting.
1,062 citations
Authors
Showing all 12352 results
Name | H-index | Papers | Citations |
---|---|---|---|
Johan Auwerx | 158 | 653 | 95779 |
I. V. Gorelov | 139 | 1916 | 103133 |
Roberto Tenchini | 133 | 1390 | 94541 |
Francesco Fabozzi | 133 | 1561 | 93364 |
M. Davier | 132 | 1449 | 107642 |
Roberto Dell'Orso | 132 | 1412 | 92792 |
Rino Rappuoli | 132 | 816 | 64660 |
Teimuraz Lomtadze | 129 | 893 | 80314 |
Manas Maity | 129 | 1309 | 87465 |
Dezso Horvath | 128 | 1283 | 88111 |
Paolo Azzurri | 126 | 1058 | 81651 |
Vincenzo Di Marzo | 126 | 659 | 60240 |
Igor Katkov | 125 | 972 | 71845 |
Ying Lu | 123 | 708 | 62645 |
Thomas Schwarz | 123 | 701 | 54560 |