@article{20080, abstract = {Introduction: Acid-growth theory has been postulated in the 70s to explain the rapid elongation of plant cells in response to the hormone auxin. More recently, it has been demonstrated that activation of the proton ATPs pump (H+-ATPs) promoting acidification of the apoplast is the principal mechanism by which auxin and other hormones such as brassinosteroids (BR) induce cell elongation. Despite these advances, the impact of this acidification on the mechanical properties of the cell wall remained largely unexplored. Methods: Here, we use elongation assays of Arabidopsis thaliana hypocotyls and Atomic Force Microscopy (AFM) to correlate hormone-induced tissue elongation and local changes in cell wall mechanical properties. Furthermore, employing transgenic lines over-expressing Pectin Methyl Esterase (PME), along with calcium chelators, we investigate the effect of pectin modification in hormone-driven cell elongation. Results: We demonstrate that acidification of apoplast is necessary and sufficient to induce cell elongation through promoting cell wall softening. Moreover, we show that enhanced PME activity can induce both cell wall softening or stiffening in extracellular calcium dependent-manner and that tight control of PME activity is required for proper hypocotyl elongation. Discussion: Our results confirm a dual role of PME in plant cell elongation. However, further investigation is needed to assess the status of pectin following short- or long-term PME treatments in order to determine if pectin methyl-esterification might promote its degradation as well as the role of PME inhibitors upon PME induction.}, author = {Gallemi, Marçal and Montesinos López, Juan C and Zarevski, Nikola and Pribyl, Jan and Skládal, Petr and Hannezo, Edouard B and Benková, Eva}, issn = {1664-462X}, journal = {Frontiers in Plant Science}, publisher = {Frontiers Media}, title = {{Dual role of pectin methyl esterase activity in the regulation of plant cell wall biophysical properties}}, doi = {10.3389/fpls.2025.1612366}, volume = {16}, year = {2025}, } @article{20081, abstract = {Information measures can be constructed from Rényi divergences much like mutual information from Kullback-Leibler divergence. One such information measure is known as Sibson α-mutual information and has received renewed attention recently in several contexts: concentration of measure under dependence, statistical learning, hypothesis testing, and estimation theory. In this paper, we survey and extend the state of the art. In particular, we introduce variational representations for Sibson α-mutual information and employ them in each described context to derive novel results. Namely, we produce generalized Transportation-Cost inequalities and Fano-type inequalities. We also present an overview of known applications, spanning from learning theory and Bayesian risk to universal prediction.}, author = {Esposito, Amedeo Roberto and Gastpar, Michael and Issa, Ibrahim}, issn = {1557-9654}, journal = {IEEE Transactions on Information Theory}, publisher = {IEEE}, title = {{Sibson α-mutual information and its variational representations}}, doi = {10.1109/TIT.2025.3587340}, year = {2025}, } @article{20082, abstract = {Efficient immune responses rely on the capacity of leukocytes to traverse diverse and complex tissues. To meet such changing environmental conditions, leukocytes usually adopt an ameboid configuration, using their forward-positioned nucleus as a probe to identify and follow the path of least resistance among pre-existing pores. We show that, in dense environments where even the largest pores preclude free passage, leukocytes position their nucleus behind the centrosome and organelles. The local compression imposed on the cell body by its surroundings triggers assembly of a central F-actin pool, located between cell front and nucleus. Central actin pushes outward to transiently dilate a path for organelles and nucleus. Pools of central and front actin are tightly coupled and experimental depletion of the central pool enhances actin accumulation and protrusion formation at the cell front. Although this shifted balance speeds up cells in permissive environments, migration in restrictive environments is impaired, as the unleashed leading edge dissociates from the trapped cell body. Our findings establish an actin regulatory loop that balances path dilation with advancement of the leading edge to maintain cellular coherence.}, author = {Dos Reis Rodrigues, Patricia and Avellaneda Sarrió, Mario and Canigova, Nikola and Gärtner, Florian R and Vaahtomeri, Kari and Riedl, Michael and De Vries, Ingrid and Merrin, Jack and Hauschild, Robert and Fukui, Yoshinori and Juanes Garcia, Alba and Sixt, Michael K}, issn = {1529-2916}, journal = {Nature Immunology}, pages = {1258–1266}, publisher = {Springer Nature}, title = {{Migrating immune cells globally coordinate protrusive forces}}, doi = {10.1038/s41590-025-02211-w}, volume = {26}, year = {2025}, } @article{20098, abstract = {Climate change is causing wildfires to become more frequent and intense. While predicting burned areas using bioclimatic and anthropogenic factors is an active research area, few studies have examined what drives the economic damages of wildfires. Our study aims to fill this gap by analyzing key factors influencing global economic wildfire damages and projecting future damages under three shared socioeconomic pathways (SSPs). We apply regression analyses to identify significant predictors of economic wildfire damages at country levels and use the fitted model to project future damages under SSP126, SSP245, and SSP370. Results show that the human vulnerability index (HVI), reflecting socioeconomic conditions, is the strongest predictor of historical wildfire damages, followed by water vapor pressure deficit during the fire season and population density around forested areas. We found high population density to be associated with lower damages. These findings contrast with studies of burned areas, where climate factors are more dominant. Our model projects that by 2070, average global economic wildfire damages will be three times higher under SSP370 than SSP126. Our model also shows that following SSP126 not only reduces wildfire damages but also lessens the inequalities in damage distribution across countries. This pathway’s dual focus on equitable socioeconomic progress and climate action potentially enhances a country’s resilience that helps mitigate wildfire damages. Our analyses also indicate that strong socioeconomic development can offset wildfire damages associated with climate hazards, although this is less certain under SSP370. SSP126’s integrated approach improves both socioeconomic conditions and limits global warming, providing substantial benefits to less developed countries while still reducing damages in developed nations, despite their already low HVI scores. Our work complements existing research on burned areas and underscores the importance of sustainable development and international collaboration in reducing the economic damages of wildfires.}, author = {Hwong, Yi-Ling and Byers, Edward and Werning, Michaela and Quilcaille, Yann}, issn = {2752-5295}, journal = {Environmental Research: Climate}, number = {3}, publisher = {IOP Publishing}, title = {{Sustainable development key to limiting climate change-driven wildfire damages}}, doi = {10.1088/2752-5295/adec11}, volume = {4}, year = {2025}, } @article{20099, abstract = {The hippocampus, critical for learning and memory, is dogmatically described as a trisynaptic circuit where dentate gyrus granule cells (GCs), CA3 pyramidal neurons (PNs), and CA1 PNs are serially connected. However, CA3 also forms an autoassociative network, and its PNs have diverse morphologies, intrinsic properties, and GC input levels. How PN subtypes compose this recurrent network is unknown. To determine the synaptic arrangement of identified CA3 PNs, we combine multicellular patch-clamp recording and post hoc morphological analysis in mouse hippocampal slices. PNs can be divided into distinct “superficial” and “deep” subclasses, the latter including previously reported “athorny” cells. Subclasses have distinct input-output transformations and asymmetric connectivity, which is more abundant from superficial to deep PNs, splitting CA3 locally into two parallel recurrent networks. Coincident spontaneous inhibition occurs frequently within but not between subclasses, implying subclass-specific inhibitory innervation. Our results suggest two separately controlled sublayers for parallel information processing in hippocampal CA3.}, author = {Watson, Jake and Vargas Barroso, Victor M and Jonas, Peter M}, issn = {2211-1247}, journal = {Cell Reports}, number = {8}, publisher = {Elsevier}, title = {{Cell-specific wiring routes information flow through hippocampal CA3}}, doi = {10.1016/j.celrep.2025.116080}, volume = {44}, year = {2025}, } @article{20100, abstract = {A key step in protein structure prediction involves the detection of co-evolving pairs of residues, a signal for spatial proximity. This information is gleaned from multiple sequence alignment and underscores Alphafold’s structure prediction for almost every known protein. A simple means to create proteins beyond those found in nature, is by unnaturally fusing together two known proteins or protein parts. Here we demonstrate that structured peptides are predicted with significantly reduced accuracy when added to the terminal ends of scaffold proteins. Appending the multiple sequence alignment for the individual peptide tags to that of the scaffold protein often restores prediction accuracy. This work suggests that this windowed multiple sequence alignment approach can be a useful tool for predicting the structure of fused, chimeric proteins.}, author = {Vedula, Sanketh and Bronstein, Alexander and Marx, Ailie}, issn = {2001-0370}, journal = {Computational and Structural Biotechnology Journal}, pages = {3292--3298}, publisher = {Elsevier}, title = {{Improving prediction accuracy in chimeric proteins with windowed multiple sequence alignment}}, doi = {10.1016/j.csbj.2025.07.039}, volume = {27}, year = {2025}, } @article{20101, abstract = {Evading imminent threat from predators is critical for animal survival. Effective defensive strategies can vary, even between closely related species. However, the neural basis of such species-specific behaviours remains poorly understood1,2,3,4. Here we find that two sister species of deer mice (genus Peromyscus)5 show different responses to the same looming stimulus: Peromyscus maniculatus, which occupies densely vegetated habitats, predominantly escapes, whereas the open field specialist, Peromyscus polionotus, briefly freezes. This difference arises from species-specific escape thresholds, is largely context-independent, and can be triggered by both visual and auditory threat stimuli. Using immunohistochemistry and electrophysiological recordings, we find that although visual threat activates the superior colliculus in both species, the role of the dorsal periaqueductal grey (dPAG) in driving behaviour differs. Whereas dPAG activity scales with running speed in P. maniculatus, neural activity in the dPAG of P. polionotus correlates poorly with movement, including during visually triggered escape. Moreover, optogenetic activation of dPAG neurons elicits acceleration in P. maniculatus but not in P. polionotus, and their chemogenetic inhibition during a looming stimulus delays escape onset in P. maniculatus to match that of P. polionotus. Together, we trace species-specific escape thresholds to a central circuit node, downstream of peripheral sensory neurons, localizing an ecologically relevant behavioural difference to a specific region of the mammalian brain.}, author = {Baier, Felix and Reinhard, Katja and Nuttin, Bram and Sans-Dublanc, Arnau and Liu, Chen and Tong, Victoria and Murmann, Julie Stefanie and Wierda, Keimpe and Farrow, Karl and Hoekstra, Hopi E.}, issn = {1476-4687}, journal = {Nature}, pages = {439--447}, publisher = {Springer Nature}, title = {{The neural basis of species-specific defensive behaviour in Peromyscus mice}}, doi = {10.1038/s41586-025-09241-2}, volume = {645}, year = {2025}, } @article{20102, abstract = {Speciation is rarely observable directly. A way forward is to compare pairs of ecotypes that evolved in parallel in similar contexts but have reached different degrees of reproductive isolation. Such comparisons are possible in the marine snail Littorina saxatilis by contrasting barriers to gene flow between parallel ecotypes in Spain and Sweden. In both countries, divergent ecotypes have evolved to withstand either crab predation or wave action. Here, we explore transects spanning contact zones between the Crab and the Wave ecotypes using low-coverage whole-genome sequencing, morphological and behavioural traits. Despite parallel phenotypic divergence, distinct patterns of differentiation between the ecotypes emerged: a continuous cline in Sweden indicating a weak barrier to gene flow, but two highly genetically and phenotypically divergent, and partly spatially overlapping clusters in Spain suggesting a much stronger barrier to gene flow. The absence of Spanish early-generation hybrids supported strong isolation, but a low level of gene flow is evident from molecular data. In both countries, highly differentiated loci were located in both shared and country-specific chromosomal inversions but were also present in collinear regions. Despite being considered the same species and showing similar levels of phenotypic divergence, the Spanish ecotypes are much closer to full reproductive isolation than the Swedish ones. Barriers to gene flow of very different strengths between ecotypes within the same species might be explained by dissimilarities in the spatial arrangement of habitats, the selection gradients or the ages of the systems.}, author = {Raffini, Francesca and De Jode, Aurélien and Johannesson, Kerstin and Faria, Rui and Zagrodzka, Zuzanna B. and Westram, Anja M and Galindo, Juan and Rolán-Alvarez, Emilio and Butlin, Roger K.}, issn = {1365-294X}, journal = {Molecular Ecology}, number = {21}, publisher = {Wiley}, title = {{Phenotypic divergence and genomic architecture between parallel ecotypes at two different points on the speciation continuum in a marine snail}}, doi = {10.1111/mec.70025}, volume = {34}, year = {2025}, } @misc{20103, abstract = {Official implementation, windowed MSAs, and the predictions as reported in the manuscript titled "Improving Prediction Accuracy in Chimeric Proteins with Windowed Multiple Sequence Alignment". (2025-06-27)}, author = {Vedula, Sanketh and Bronstein, Alexander and Marx, Ailie}, publisher = {Harvard Dataverse}, title = {{Replication Data for: "Improving Prediction Accuracy in Chimeric Proteins with Windowed Multiple Sequence Alignment"}}, doi = {10.7910/DVN/DYEBVM}, year = {2025}, } @misc{20107, abstract = {This repository contains the data and scripts required to reproduce the results of the manuscript "Sustainable Development Key to Limiting Climate Change-Driven Wildfire Damages" submitted to the Environmental Research Climate Journal (ERCL). }, author = {Hwong, Yi-Ling and Byers, Edward and Werning, Michaela and Quilcaille, Yann}, publisher = {Zenodo}, title = {{Data - Sustainable Development Key to Limiting Climate Change-Driven Wildfire Damages}}, doi = {10.5281/ZENODO.13988679}, year = {2025}, } @article{20116, abstract = {Auxin regulates various aspects of plant growth and development by modulating the transcription of target genes through the degradation of auxin/indole-3-acetic acid (Aux/IAA) repressors via the 26S proteasome. Proteasome regulator 1 (PTRE1), a positive regulator of proteasome activity, has been implicated in auxin-mediated proteasome suppression; however, the mechanism by which auxin modulates PTRE1 function remains unclear. Here, we demonstrate that auxin promotes the interaction between germin-like protein 1 (GLP1) and PTRE1, facilitating PTRE1 retention at the plasma membrane. The relocation of PTRE1 results in reduced nuclear 26S proteasome activity, and thus the attenuated Aux/IAA degradation and altered Aux/IAA homeostasis, ultimately resulting in suppressed auxin-mediated transcriptional regulation. Our findings uncover a previously uncharacterized regulatory axis in auxin signaling that controls Aux/IAA protein stability, functioning alongside the TIR1- and TRANSMEMBRANE KINASE 1 (TMK1)-mediated pathways, and highlight the coordination of auxin signaling from the cell surface to the nucleus via auxin-induced PTRE1 relocation, which fine-tunes Aux/IAA protein homeostasis and auxin responses.}, author = {Xu, Faqing and Yu, Yongqiang and Guan, Bin and Xu, Tongda and Xu, Zhihong and Xue, Hongwei}, issn = {2211-1247}, journal = {Cell Reports}, number = {8}, publisher = {Elsevier}, title = {{Germin-like protein 1 interacts with proteasome regulator 1 to regulate auxin signaling by controlling Aux/IAA homeostasis}}, doi = {10.1016/j.celrep.2025.116056}, volume = {44}, year = {2025}, } @phdthesis{20117, author = {Wang, Yiqun}, issn = {2663-337X}, pages = {108}, publisher = {Institute of Science and Technology Austria}, title = {{The role of dynamin related protein 2A in cytokinin regulated plant growth and development}}, doi = {10.15479/AT-ISTA-20117}, year = {2025}, } @phdthesis{20138, abstract = {The evolution shapes the world around us. Not only in biology, where the fittest individuals spread their genes but also in physics and social dynamics, the evolutionary forces determine the development of a state of matter or public opinions. Many models describe these dynamics. This thesis examines the role of the structure in the models of selection. The population structure is represented as a graph or a network, and each vertex is occupied by one individual. Every individual has a type and fitness that represents the reproductive potential and depends on the type, occupied vertex, and the arrangement of the neighbors. The evolution is modeled in discrete steps; in one step, one individual is replaced by a neighbor selected randomly with the influence of fitness. The role of the networks is widely examined in the literature. The structures that promote the spread of the desired type compared to the structureless case are called amplifiers. The existence of amplifiers in various settings is an intensively studied topic, and in some settings, the amplifiers have been identified. Moreover, there are other important questions about the number of steps until one type spreads over the whole network (fixation time), the computational complexity, and the questions about the robustness of these processes. This thesis explores the role of structure in evolution from many perspectives. First, it introduces different models and various choices that can be made in the models of evolution. It highlights the role of the structure in the real world and how this is reflected in these models. Then, it describes the previous results and open problems. Second, the thesis describes an amplifier for two variants of the Moran process: one with a constant birth rate and the other with a constant death rate. This is an important contribution to the robustness of the amplification. Third, the thesis determines the complexity of spatial games. These are processes where the fitness comes from a game, and the strength of selection is high. It shows that determining the fate of cooperation in these games is a PSPACE-complete problem. Fourth, the thesis describes the amplifier of cooperation for spatial games. This is the first amplifier in this setting. Fifth, the thesis examines the coexistence in the Moran process with environmental heterogeneity. In this setting, the fitness depends not only on the type of the individual but also on the occupied vertex. The chapter determines the relationship between the interactions of vertices of different types and the coexistence time. Sixth, the thesis examines the social balance on networks and proposes a stochastic dynamic partially aware of the state of the graph, which reaches a balanced position quickly. Finally, the thesis presents conclusions and outlines the directions for future work. }, author = {Svoboda, Jakub}, issn = {2663-337X}, pages = {167}, publisher = {Institute of Science and Technology Austria}, title = {{Structural properties of games on graphs}}, doi = {10.15479/AT-ISTA-20138}, year = {2025}, } @article{20143, abstract = {Bacteria and archaea deploy diverse antiviral defense systems, many of which remain mechanistically uncharacterized. Here, we characterize Kiwa, a widespread two-component system composed of the transmembrane sensor KwaA and the DNA-binding effector KwaB. Cryogenic electron microscopy (cryo-EM) analysis reveals that KwaA and KwaB assemble into a large, membrane-associated supercomplex. Upon phage binding, KwaA senses infection at the membrane, leading to KwaB binding of ejected phage DNA and inhibition of replication and late transcription, without inducing host cell death. Although KwaB can bind DNA independently, its antiviral activity requires association with KwaA, suggesting spatial or conformational regulation. We show that the phage-encoded DNA-mimic protein Gam directly binds and inhibits KwaB but that co-expression with the Gam-targeted RecBCD system restores protection by Kiwa. Our findings support a model in which Kiwa coordinates membrane-associated detection of phage infection with downstream DNA binding by its effector, forming a spatially coordinated antiviral mechanism.}, author = {Zhang, Zhiying and Todeschini, Thomas C. and Wu, Yi and Kogay, Roman and Naji, Ameena and Cardenas Rodriguez, Joaquin and Mondi, Rupavidhya and Kaganovich, Daniel and Taylor, David W. and Bravo, Jack Peter Kelly and Teplova, Marianna and Amen, Triana and Koonin, Eugene and Patel, Dinshaw J. and Nobrega, Franklin L.}, issn = {1097-4172}, journal = {Cell}, number = {21}, pages = {5862--5877.e23}, publisher = {Elsevier}, title = {{Kiwa is a membrane-embedded defense supercomplex activated at phage attachment sites}}, doi = {10.1016/j.cell.2025.07.002}, volume = {188}, year = {2025}, } @techreport{20146, abstract = {This criteria catalogue and the accompanying assessment questions were developed by a working group of KEMÖ (Kooperation E-Medien Österreich, the Austrian Academic Library Consortium). They are intended to support research institutions and organisations in the evaluation of Open Science Infrastructures. The 20 criteria outlined in the catalogue provide a structured basis for making informed decisions regarding the financial support of these infrastructures. The assessment questions are intended to be completed by Open Science Infrastructures and can be shared with them accordingly.}, author = {Gredler, Paul and Kaier, Christian and Danowski, Patrick and Zoyer, Michael and Rieck, Katharina and Ferus, Andreas and Rosenberger, Elisabeth and Löffler, Alexander and Hofer, Lisa and Still, Laura}, publisher = {Zenodo}, title = {{Catalogue of criteria for assessing the funding eligibility of Open Science infrastructures}}, doi = {10.5281/zenodo.15269364}, year = {2025}, } @phdthesis{20147, abstract = {Quantitative properties offer a framework for specifying and verifying system behaviors beyond the traditional boolean perspective. For example, while a boolean property may specify whether a server eventually grants every request it receives, a quantitative one may map each server execution to its average response time. This quantitative view is relatively well-studied in the context of static verification. However, although such properties often appear in practice as performance or robustness measures in a dynamic verification context, a general theoretical framework for their analysis and classification from a monitoring perspective is still missing. In this thesis, we aim to develop such a framework that takes resource-precision tradeoffs of monitors as a central consideration. We present the first theory of monitorability for quantitative properties where monitors can be naturally approximate and compared regarding their precision and resource use. In particular, we show that additional monitor resources such as registers or states lead to strictly better approximations for some properties. To enable such analyses in a machine-model independent way, we describe an abstract notion of monitors that can be instantiated with concrete models of monitors. Within this framework, we study how abstract monitors behave and identify classes of properties amenable to approximate monitoring with resource-precision considerations. We then extend the boolean safety-liveness dichotomy and safety-progress hierarchy to the quantitative setting with a monitoring perspective. In particular, we prove that every property is the pointwise minimum of a safety property and a liveness property, and properties that are both safe and co-safe can be approximately monitored arbitrarily precisely using only finitely many states. We also study the classes of quantitative properties definable by finite-state quantitative automata and provide algorithms for deciding their safety or liveness as well as their safety-liveness decompositions. Finally, we present the first general-purpose tool for automating the analysis, verification, and monitoring of quantitative automata. -------------------------------------------------------------------------------------------------------------------------------------------------------------- In reference to IEEE copyrighted material which is used with permission in this thesis, the IEEE does not endorse any of ISTA's products or services. Internal or personal use of this material is permitted. If interested in reprinting/republishing IEEE copyrighted material for advertising or promotional purposes or for creating new collective works for resale or redistribution, please go to http://www.ieee.org/publications_standards/publications/rights/rights_link.html to learn how to obtain a License from RightsLink. }, author = {Sarac, Naci E}, issn = {2663-337X}, pages = {149}, publisher = {Institute of Science and Technology Austria}, title = {{A monitoring-oriented theory and classification of quantitative specifications}}, doi = {10.15479/AT-ISTA-20147}, year = {2025}, } @phdthesis{20149, abstract = {Immune responses depend on the coordinated and efficient migration of leukocytes. These cells, which are embedded and tightly confined within tissues, must navigate and traverse diverse and complex three-dimensional environments. Leukocytes adapt their locomotory behavior to the mechanical, geometrical, and biochemical characteristics of their surroundings. In low-density environments, where the pore size of the interstitial matrix allows free passage, these cells position the nucleus directly behind the lamellipodium, the protrusive actin structure that forms the leading front of the cell. In this configuration, they use the nucleus as a gauge to identify the path of least resistance. Here, we show that in high-density environments, where the pore size precludes free passage of the cell body, leukocytes reposition the microtubule-organizing center (MTOC) and associated organelles in front of the nucleus. In this configuration, they use actin structures protruding orthogonally to the direction of migration in order to open a path for the cell body. We identify two distinct actin populations that serve this purpose at different subcellular localizations. At the leading edge, local indentation of the plasma membrane leads to recruitment of the Wiskott-Aldrich syndrome protein (WASp), which, via Arp2/3, results in the formation of individual actin foci. At the cell body, actin polymerization is triggered by DOCK8, a Cdc42 exchange factor, resulting in the formation of a central actin pool. We demonstrate that the central and peripheral actin pools are functionally communicating and that depletion of the central actin pool leads to increased actin accumulation at the cell front, resulting in excessive extension of the leading edge.}, author = {Dos Reis Rodrigues, Patricia}, issn = {2663-337X}, pages = {114}, publisher = {Institute of Science and Technology Austria}, title = {{Coordination of protrusive forces in immune cell migration }}, doi = {10.15479/AT-ISTA-20149}, year = {2025}, } @article{20154, abstract = {In long-lived mammals, including humans, brain cell homeostasis is critical for maintaining brain function throughout life. Most neurons are generated during development and must maintain their cellular identity and plasticity to preserve brain function. Although extensive studies indicate the importance of recycling and regenerating cellular molecules to maintain cellular homeostasis, recent evidence has shown that some proteins and RNAs do not turn over for months and even years. We propose that these long-lived cellular molecules may be the basis for maintaining brain function in the long term, but also a potential convergent target of brain aging. We highlight key discoveries and challenges, and propose potential directions to unravel the mystery of brain cell longevity.}, author = {Hetzer, Martin W and Toda, Tomohisa}, issn = {1878-108X}, journal = {Trends in Neurosciences}, number = {9}, pages = {645--654}, publisher = {Elsevier}, title = {{Long-lived cellular molecules in the brain}}, doi = {10.1016/j.tins.2025.07.004}, volume = {48}, year = {2025}, } @article{20155, abstract = {We study time averages for the norm of solutions to kinetic Fokker–Planck equations associated with general Hamiltonians. We provide fully explicit and constructive decay estimates for systems subject to a confining potential, allowing fat-tail, subexponential and (super-)exponential local equilibria, which also include the classic Maxwellian case. The key step in our estimates is a modified Poincaré inequality, obtained via a Lions–Poincaré inequality and an averaging lemma.}, author = {Brigati, Giovanni and Stoltz, Gabriel}, issn = {1095-7154}, journal = {SIAM Journal on Mathematical Analysis}, number = {4}, pages = {3587--3622}, publisher = {Society for Industrial and Applied Mathematics}, title = {{How to construct explicit decay rates for kinetic Fokker–Planck equations?}}, doi = {10.1137/24M1700351}, volume = {57}, year = {2025}, } @phdthesis{20167, author = {Schön, Hanna}, isbn = {978-3-99078-061-9}, issn = {2663-337X}, pages = {171}, publisher = {Institute of Science and Technology Austria}, title = {{The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs encoding GPCRs}}, doi = {10.15479/AT-ISTA-20167}, year = {2025}, }