Institution
University of Trento
Education•Trento, Italy•
About: University of Trento is a education organization based out in Trento, Italy. It is known for research contribution in the topics: Population & Context (language use). The organization has 10527 authors who have published 30978 publications receiving 896614 citations. The organization is also known as: Universitá degli Studi di Trento & Universita degli Studi di Trento.
Papers published on a yearly basis
Papers
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TL;DR: The properties of tyre waste and their potential reuse, the enhancement of end-of-life tires and the various types of recovery, such as the reconstruction of tyres and the material recovery are considered.
212 citations
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TL;DR: The capability-based view of the firm is based on the assumption that firms know how to do things as discussed by the authors, and it is used to deal with issues like horizontal and vertical boundaries of a firm, innovation and corporate performance.
Abstract: The capability-based view of the firm is based on the assumption that firms know how to do things. Assuming the existence of a thing called `organizational knowledge', in the first part of the paper we identify its main building blocks and we provide a description of its inner structure. This results in an analysis of the relationships among key concepts like organizational routines, organizational competencies and skills. In the second part, we consider some empirical implications of the adoption of a capability-based view of the firm in dealing with issues like horizontal and vertical boundaries of the firm, innovation and corporate performance. Some implications for strategic management are also discussed.
212 citations
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TL;DR: The construction of artificial, non-living cellular mimics that are engineered to activate or repress already existing natural sensory pathways of living cells through chemical communication are described.
Abstract: Previous efforts to control cellular behaviour have largely relied upon various forms of genetic engineering. Once the genetic content of a living cell is modified, the behaviour of that cell typically changes as well. However, other methods of cellular control are possible. All cells sense and respond to their environment. Therefore, artificial, non-living cellular mimics could be engineered to activate or repress already existing natural sensory pathways of living cells through chemical communication. Here we describe the construction of such a system. The artificial cells expand the senses of Escherichia coli by translating a chemical message that E. coli cannot sense on its own to a molecule that activates a natural cellular response. This methodology could open new opportunities in engineering cellular behaviour without exploiting genetically modified organisms.
211 citations
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S. Chatrchyan1, Vardan Khachatryan1, Albert M. Sirunyan1, Armen Tumasyan1 +3880 more•Institutions (142)
TL;DR: In this paper, an inclusive search for supersymmetric processes that produce final states with jets and missing transverse energy is performed in pp collisions at a centre-of-mass energy of 8 TeV.
Abstract: An inclusive search for supersymmetric processes that produce final states with jets and missing transverse energy is performed in pp collisions at a centre-of-mass energy of 8 TeV. The data sample corresponds to an integrated luminosity of 11.7 fb−1 collected by the CMS experiment at the LHC. In this search, a dimensionless kinematic variable, α T, is used to discriminate between events with genuine and misreconstructed missing transverse energy. The search is based on an examination of the number of reconstructed jets per event, the scalar sum of transverse energies of these jets, and the number of these jets identified as originating from bottom quarks. No significant excess of events over the standard model expectation is found. Exclusion limits are set in the parameter space of simplified models, with a special emphasis on both compressed-spectrum scenarios and direct or gluino-induced production of third-generation squarks. For the case of gluino-mediated squark production, gluino masses up to 950–1125 GeV are excluded depending on the assumed model. For the direct pair-production of squarks, masses up to 450 GeV are excluded for a single light first- or second-generation squark, increasing to 600 GeV for bottom squarks.
211 citations
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TL;DR: It is reported that PC-associated SPOP mutants cannot interact with SRC-3 protein or promote its ubiquitination and degradation, suggesting that wild-type SPOP plays a critical tumor suppressor role in PC cells, promoting the turnover of SRC -3 protein and suppressing androgen receptor transcriptional activity.
Abstract: The p160 steroid receptor coactivators (SRCs) SRC-1, SRC-2 [nuclear receptor coactivator (NCOA)2], and SRC-3 [amplified in breast cancer 1 (AIB1)/NCOA3] are key pleiotropic "master regulators" of transcription factor activity necessary for cancer cell proliferation, survival, metabolism, and metastasis. SRC overexpression and overactivation occur in numerous human cancers and are associated with poor clinical outcomes and resistance to therapy. In prostate cancer (PC), the p160 SRCs play critical roles in androgen receptor transcriptional activity, cell proliferation, and resistance to androgen deprivation therapy. We recently demonstrated that the E3 ubiquitin ligase adaptor speckle-type poxvirus and zinc finger (POZ) domain protein (SPOP) interacts directly with SRC-3 and promotes its cullin 3-dependent ubiquitination and proteolysis in breast cancer, thus functioning as a potential tumor suppressor. Interestingly, somatic heterozygous missense mutations in the SPOP substrate-binding cleft recently were identified in up to 15% of human PCs (making SPOP the gene most commonly affected by nonsynonymous point mutations in PC), but their contribution to PC pathophysiology remains unknown. We now report that PC-associated SPOP mutants cannot interact with SRC-3 protein or promote its ubiquitination and degradation. Our data suggest that wild-type SPOP plays a critical tumor suppressor role in PC cells, promoting the turnover of SRC-3 protein and suppressing androgen receptor transcriptional activity. This tumor suppressor effect is abrogated by the PC-associated SPOP mutations. These studies provide a possible explanation for the role of SPOP mutations in PC, and highlight the potential of SRC-3 as a therapeutic target in PC.
211 citations
Authors
Showing all 10758 results
Name | H-index | Papers | Citations |
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Yi Chen | 217 | 4342 | 293080 |
Jie Zhang | 178 | 4857 | 221720 |
Richard B. Lipton | 176 | 2110 | 140776 |
Jasvinder A. Singh | 176 | 2382 | 223370 |
J. N. Butler | 172 | 2525 | 175561 |
Andrea Bocci | 172 | 2402 | 176461 |
P. Chang | 170 | 2154 | 151783 |
Bradley Cox | 169 | 2150 | 156200 |
Marc Weber | 167 | 2716 | 153502 |
Guenakh Mitselmakher | 165 | 1951 | 164435 |
Brian L Winer | 162 | 1832 | 128850 |
J. S. Lange | 160 | 2083 | 145919 |
Ralph A. DeFronzo | 160 | 759 | 132993 |
Darien Wood | 160 | 2174 | 136596 |
Robert Stone | 160 | 1756 | 167901 |