@misc{9811, abstract = {This document contains additional supporting evidence presented as supplemental tables. (XLSX 50Â kb)}, author = {Zapata, Luis and Pich, Oriol and Serrano, Luis and Kondrashov, Fyodor and Ossowski, Stephan and Schaefer, Martin}, publisher = {Springer Nature}, title = {{Additional file 1: Of negative selection in tumor genome evolution acts on essential cellular functions and the immunopeptidome}}, doi = {10.6084/m9.figshare.6401390.v1}, year = {2018}, } @article{20, abstract = {Background: Norepinephrine (NE) signaling has a key role in white adipose tissue (WAT) functions, including lipolysis, free fatty acid liberation and, under certain conditions, conversion of white into brite (brown-in-white) adipocytes. However, acute effects of NE stimulation have not been described at the transcriptional network level. Results: We used RNA-seq to uncover a broad transcriptional response. The inference of protein-protein and protein-DNA interaction networks allowed us to identify a set of immediate-early genes (IEGs) with high betweenness, validating our approach and suggesting a hierarchical control of transcriptional regulation. In addition, we identified a transcriptional regulatory network with IEGs as master regulators, including HSF1 and NFIL3 as novel NE-induced IEG candidates. Moreover, a functional enrichment analysis and gene clustering into functional modules suggest a crosstalk between metabolic, signaling, and immune responses. Conclusions: Altogether, our network biology approach explores for the first time the immediate-early systems level response of human adipocytes to acute sympathetic activation, thereby providing a first network basis of early cell fate programs and crosstalks between metabolic and transcriptional networks required for proper WAT function.}, author = {Higareda Almaraz, Juan and Karbiener, Michael and Giroud, Maude and Pauler, Florian and Gerhalter, Teresa and Herzig, Stephan and Scheideler, Marcel}, issn = {1471-2164}, journal = {BMC Genomics}, number = {1}, publisher = {BioMed Central}, title = {{Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes}}, doi = {10.1186/s12864-018-5173-0}, volume = {19}, year = {2018}, } @article{107, abstract = {We introduce the notion of “non-malleable codes” which relaxes the notion of error correction and error detection. Informally, a code is non-malleable if the message contained in a modified codeword is either the original message, or a completely unrelated value. In contrast to error correction and error detection, non-malleability can be achieved for very rich classes of modifications. We construct an efficient code that is non-malleable with respect to modifications that affect each bit of the codeword arbitrarily (i.e., leave it untouched, flip it, or set it to either 0 or 1), but independently of the value of the other bits of the codeword. Using the probabilistic method, we also show a very strong and general statement: there exists a non-malleable code for every “small enough” family F of functions via which codewords can be modified. Although this probabilistic method argument does not directly yield efficient constructions, it gives us efficient non-malleable codes in the random-oracle model for very general classes of tampering functions—e.g., functions where every bit in the tampered codeword can depend arbitrarily on any 99% of the bits in the original codeword. As an application of non-malleable codes, we show that they provide an elegant algorithmic solution to the task of protecting functionalities implemented in hardware (e.g., signature cards) against “tampering attacks.” In such attacks, the secret state of a physical system is tampered, in the hopes that future interaction with the modified system will reveal some secret information. This problem was previously studied in the work of Gennaro et al. in 2004 under the name “algorithmic tamper proof security” (ATP). We show that non-malleable codes can be used to achieve important improvements over the prior work. In particular, we show that any functionality can be made secure against a large class of tampering attacks, simply by encoding the secret state with a non-malleable code while it is stored in memory.}, author = {Dziembowski, Stefan and Pietrzak, Krzysztof Z and Wichs, Daniel}, journal = {Journal of the ACM}, number = {4}, publisher = {ACM}, title = {{Non-malleable codes}}, doi = {10.1145/3178432}, volume = {65}, year = {2018}, } @article{5676, abstract = {In epithelial tissues, cells tightly connect to each other through cell–cell junctions, but they also present the remarkable capacity of reorganizing themselves without compromising tissue integrity. Upon injury, simple epithelia efficiently resolve small lesions through the action of actin cytoskeleton contractile structures at the wound edge and cellular rearrangements. However, the underlying mechanisms and how they cooperate are still poorly understood. In this study, we combine live imaging and theoretical modeling to reveal a novel and indispensable role for occluding junctions (OJs) in this process. We demonstrate that OJ loss of function leads to defects in wound-closure dynamics: instead of contracting, wounds dramatically increase their area. OJ mutants exhibit phenotypes in cell shape, cellular rearrangements, and mechanical properties as well as in actin cytoskeleton dynamics at the wound edge. We propose that OJs are essential for wound closure by impacting on epithelial mechanics at the tissue level, which in turn is crucial for correct regulation of the cellular events occurring at the wound edge.}, author = {Carvalho, Lara and Patricio, Pedro and Ponte, Susana and Heisenberg, Carl-Philipp J and Almeida, Luis and Nunes, André S. and Araújo, Nuno A.M. and Jacinto, Antonio}, issn = {00219525}, journal = {Journal of Cell Biology}, number = {12}, pages = {4267--4283}, publisher = {Rockefeller University Press}, title = {{Occluding junctions as novel regulators of tissue mechanics during wound repair}}, doi = {10.1083/jcb.201804048}, volume = {217}, year = {2018}, } @misc{9807, abstract = {Table S1. Genes with highest betweenness. Table S2. Local and Master regulators up-regulated. Table S3. Local and Master regulators down-regulated (XLSX 23 kb).}, author = {Higareda Almaraz, Juan and Karbiener, Michael and Giroud, Maude and Pauler, Florian and Gerhalter, Teresa and Herzig, Stephan and Scheideler, Marcel}, publisher = {Springer Nature}, title = {{Additional file 1: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes}}, doi = {10.6084/m9.figshare.7295339.v1}, year = {2018}, }