@unpublished{21291, abstract = {The complexity and specificity of movement in vertebrates is driven by a rich diversity of spinal motor and interneuron cell types. During development, eleven spinal cord progenitor domains generate an equivalent number of cardinal neuron types. How progenitor domains, individual progenitors, and post-mitotic diversity relate is still unknown. We performed high-resolution, single-progenitor cell lineage tracing in the embryonic mouse spinal cord using mosaic analysis with double markers (MADM). Our quantitative study of lineage progression revealed that spinal cord progenitors undergo highly variable numbers of proliferative, neurogenic, and gliogenic cell divisions. The nascent clonally-related neurons migrate radially over large distances, span the dorsoventral axis, and even cross the midline, demonstrating striking bilaterality. Molecular and morphometric analysis indicate high levels of progenitor multipotency, with an individual progenitor capable of producing several molecularly and morphologically distinct neuron types, as well as astrocytes. These findings redefine spinal cord development as a process in which lineage variability — rather than rigid progenitor identity — drives the generation of cellular diversity.}, author = {Gobeil, Sophie A and Da Silveira Neto, Francisco and Silvestrelli, Giulia and Smits, Matthijs Geert and Streicher, Carmen and Cheung, Giselle T and Hippenmeyer, Simon and Sweeney, Lora Beatrice Jaeger}, booktitle = {bioRxiv}, title = {{Lineage origin of spinal cord cell type diversity}}, doi = {10.64898/2026.02.12.705305}, year = {2026}, } @article{21746, abstract = {As vertebrates transitioned from water to land, locomotion shifted from undulatory swimming to limb-based movement. How spinal circuits and their cell types evolved to support this transition remains unclear. We leverage frog metamorphosis, which recapitulates this transition within a single organism, to define how spinal circuits generate aquatic versus terrestrial motor patterns. At swim stages, spinal architecture is uniform, with a transcriptionally and anatomically homogeneous motor and interneurons. As limbs develop and their movement complexifies, spinal circuits expand in neuron number and subtype diversity. This expansion is most pronounced for V1 inhibitory neurons, which increase ∼70-fold and diversify into transcriptionally distinct subtypes. Disrupting transcription factors defining emerging motor and V1 populations reveals molecular segregation between swim and limb circuits, highlighting the role of subtype diversity in motor coordination. A multifold increase in inhibitory neuron diversity thus underlies the tail-to-limb locomotor transition, providing a framework for spinal circuit adaptation during vertebrate evolution.}, author = {Vijatovic, David and Toma, Florina Alexandra and Ignatyev, Y and Harrington, Zoe P and Sommer, Christoph M and Hauschild, Robert and Smits, Matthijs Geert and Dalla Vecchia, Marco and Trevisan, Alexandra J. and Chapman, Phillip and Julseth, Mara and Brenner-Morton, Susan and Gabitto, Mariano I. and Dasen, Jeremy S. and Bikoff, Jay B. and Sweeney, Lora Beatrice Jaeger}, issn = {2211-1247}, journal = {Cell Reports}, number = {4}, publisher = {Elsevier}, title = {{Multifold increase in spinal inhibitory cell types with emergence of limb movement}}, doi = {10.1016/j.celrep.2026.117227}, volume = {45}, year = {2026}, } @unpublished{21920, abstract = {Vertebrates display remarkable diversity of sensorimotor behaviors, each adapted to distinct ecological and survival demands. This diversity raises fundamental questions about the evolutionary origin of motor control: do conserved spinal circuits underlie these behaviors, and how have they diverged across species. Recent studies detail spinal cell-type architecture in mammals but comparable, high-resolution atlases of the non-mammalian spinal cord are lacking. Here, we compare spinal cord cell types between fish, frogs, mice and humans, spanning ∼450 million years of evolution. Across species, we define highly conserved programs of cell type specification that segregate spinal neurons into nearly identical cardinal classes during development. This contrasts with adult stages, when spinal cell-type composition selectively diverges for excitatory neuron subpopulations. Using spatial transcriptomics, we localize this species divergence to the superficial, dorsal spinal cord, where variant neuropeptide expression defines mammalian-specific cell types. The most dorsal spinal cord thus emerges as a recently evolved hub for sensory integration in mammals, a neospinal cord analogous to the neocortex.}, author = {Ignatyev, Yuri and Papadopoulos, Stavros and Soretić, Mateja and Yeung, Jake and Lin, Tzi-Yang and Tanaka, Elly M and Peshkin, Leonid and Levine, Ariel J and Gabitto, Mariano I and Sweeney, Lora Beatrice Jaeger}, booktitle = {bioRxiv}, title = {{Innovations in spinal cord cell type heterogeneity across vertebrate evolution}}, doi = {10.1101/2025.10.09.680955}, year = {2025}, } @article{15016, abstract = {Amphibians, by virtue of their phylogenetic position, provide invaluable insights on nervous system evolution, development, and remodeling. The genetic toolkit for amphibians, however, remains limited. Recombinant adeno-associated viral vectors (AAVs) are a powerful alternative to transgenesis for labeling and manipulating neurons. Although successful in mammals, AAVs have never been shown to transduce amphibian cells efficiently. We screened AAVs in three amphibian species—the frogs Xenopus laevis and Pelophylax bedriagae and the salamander Pleurodeles waltl—and identified at least two AAV serotypes per species that transduce neurons. In developing amphibians, AAVs labeled groups of neurons generated at the same time during development. In the mature brain, AAVrg retrogradely traced long-range projections. Our study introduces AAVs as a tool for amphibian research, establishes a generalizable workflow for AAV screening in new species, and expands opportunities for cross-species comparisons of nervous system development, function, and evolution.}, author = {Jaeger, Eliza C.B. and Vijatovic, David and Deryckere, Astrid and Zorin, Nikol and Nguyen, Akemi L. and Ivanian, Georgiy and Woych, Jamie and Arnold, Rebecca C and Ortega Gurrola, Alonso and Shvartsman, Arik and Barbieri, Francesca and Toma, Florina-Alexandra and Gorbsky, Gary J. and Horb, Marko E. and Cline, Hollis T. and Shay, Timothy F. and Kelley, Darcy B. and Yamaguchi, Ayako and Shein-Idelson, Mark and Tosches, Maria Antonietta and Sweeney, Lora Beatrice Jaeger}, issn = {1878-1551}, journal = {Developmental Cell}, number = {5}, pages = {794--812.e6}, publisher = {Elsevier}, title = {{Adeno-associated viral tools to trace neural development and connectivity across amphibians}}, doi = {10.1016/j.devcel.2024.10.025}, volume = {60}, year = {2025}, } @article{19366, abstract = {Staphylococcus aureus (S. aureus) is one of the most common causative agents of mammary gland infection and mastitis, but the specific role of S. aureus-derived extracellular vesicles (SaEVs) in mastitis has been poorly studied to date. Here, we aimed to investigate the response of bovine monocyte-derived macrophages (boMdM) to SaEVs of the genotype B (GTB) mastitis-related strain M5512B. Specifically, we evaluated the effects on the actin cytoskeleton, gene expression, and the SaEV proteomic cargo. Furthermore, we assessed to what extent the cellular and molecular response of boMdM to SaEVs differed from peripheral mononuclear blood cells (PBMCs) used for in vitro derivation of the former. We observed that SaEVs induced morphological changes in boMdM, leading to a pro-inflammatory and pyroptosis-related increased gene expression. Additionally, our study revealed that boMdM and PBMCs exhibited stimulus-specific differing responses. The proteomic analysis of SaEVs identified clusters of proteins related to virulence and antibiotic resistance, supporting the theory that S. aureus might use EVs to evade host defences and colonize the mammary gland. Our results bring new insights into how SaEVs might impact the host during an S. aureus infection, which can be useful for future S. aureus vaccine development.}, author = {Saenz-De-Juano, Mara D. and Silvestrelli, Giulia and Buri, Samuel and Zinsli, Léa V. and Schmelcher, Mathias and Ulbrich, Susanne E.}, issn = {2045-2322}, journal = {Scientific Reports}, pages = {6059}, publisher = {Springer Nature}, title = {{Mastitis-related Staphylococcus aureus-derived extracellular vesicles induce a pro-inflammatory response in bovine monocyte-derived macrophages}}, doi = {10.1038/s41598-025-90466-6}, volume = {15}, year = {2025}, } @phdthesis{20735, abstract = {Left–right alternation is a defining feature of spinal locomotor circuits, yet the level of neuronal detail required to generate and maintain this pattern remains unclear. This thesis investigates how models spanning multiple levels of abstraction—from biophysically detailed Hodgkin–Huxley (HH) neurons to adaptive integrate–and–fire (I&F) formulations and synfire-chain modules—can account for the generation of fictive swimming in the spinal cord of the Xenopus laevis tadpole. The guiding hypothesis is that a small set of neuronal mechanisms is sufficient to reproduce the essential features of rhythmic alternation, and that moving between modeling scales helps distinguish core principles from biological detail. A minimal bilateral HH network comprising only four canonical neuron classes—excitatory descending interneurons (dINs), inhibitory commissural interneurons (cINs), ipsilateral inhibitory interneurons (aINs) and motoneurons—served as a biophysical proof of concept. Tuned to reproduce experimentally observed firing modes, the model demonstrated that rebound-prone dIN excitability, contralateral inhibition and modest electrical coupling are sufficient to generate stable alternating activity, even in very small networks. These results motivated the transition to simpler models capable of efficient analysis and scaling. Adaptive exponential I&F (AdEx) neurons were calibrated to physiological recordings using simulation-based inference, yielding tonic and phasic/rebound templates that preserved the key dynamical signatures of the HH model. Phase-plane analysis clarified the mechanisms underlying single-spike responses and rebound firing in dINs. At network level, the I&F models robustly reproduced left–right alternation, while highlighting constraints on synaptic kinetics and adaptation needed to avoid multi-spike responses. Finally, a synfire-chain framework provided a complementary, timing-centric perspective, demonstrating how precise spike synchrony, synaptic delays and minimal inhibitory coupling can generate alternating left–right sequences in a feedforward setting. Together, these approaches converge on a common conclusion: rebound-prone ipsilateral excitation combined with precisely timed contralateral inhibition constitutes a sufficient substrate for alternating spinal rhythms. By integrating bottom-up and top-down modeling strategies, this thesis provides a unified, extensible framework for studying spinal pattern generation. The results show that essential locomotor dynamics can be captured across multiple abstraction levels, offering both mechanistic insight and practical tools for future data-driven investigations of spinal circuit development, robustness and modulation.}, author = {Wilson, Alexia C}, issn = {2791-4585}, pages = {110}, publisher = {Institute of Science and Technology Austria}, title = {{Modelling the spinal cord of a tadpole: Exploring different ways to model the spinal cord in the Xenopus frog}}, doi = {10.15479/AT-ISTA-20735}, year = {2025}, } @article{15335, abstract = {Stable matching of neurotransmitters with their receptors is fundamental to synapse function and reliable communication in neural circuits. Presynaptic neurotransmitters regulate the stabilization of postsynaptic transmitter receptors. Whether postsynaptic receptors regulate stabilization of presynaptic transmitters has received less attention. Here, we show that blockade of endogenous postsynaptic acetylcholine receptors (AChR) at the neuromuscular junction destabilizes the cholinergic phenotype in motor neurons and stabilizes an earlier, developmentally transient glutamatergic phenotype. Further, expression of exogenous postsynaptic gamma-aminobutyric acid type A receptors (GABAA receptors) in muscle cells stabilizes an earlier, developmentally transient GABAergic motor neuron phenotype. Both AChR and GABAA receptors are linked to presynaptic neurons through transsynaptic bridges. Knockdown of specific components of these transsynaptic bridges prevents stabilization of the cholinergic or GABAergic phenotypes. Bidirectional communication can enforce a match between transmitter and receptor and ensure the fidelity of synaptic transmission. Our findings suggest a potential role of dysfunctional transmitter receptors in neurological disorders that involve the loss of the presynaptic transmitter.}, author = {Godavarthi, Swetha K. and Hiramoto, Masaki and Ignatyev, Yuri and Levin, Jacqueline B. and Li, Hui Quan and Pratelli, Marta and Borchardt, Jennifer and Czajkowski, Cynthia and Borodinsky, Laura N. and Sweeney, Lora Beatrice Jaeger and Cline, Hollis T. and Spitzer, Nicholas C.}, issn = {1091-6490}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, number = {15}, publisher = {National Academy of Sciences}, title = {{Postsynaptic receptors regulate presynaptic transmitter stability through transsynaptic bridges}}, doi = {10.1073/pnas.2318041121}, volume = {121}, year = {2024}, } @unpublished{19520, abstract = {Vertebrates exhibit a wide range of motor behaviors, ranging from swimming to complex limb-based movements. Here we take advantage of frog metamorphosis, which captures a swim-to-limb-based movement transformation during the development of a single organism, to explore changes in the underlying spinal circuits. We find that the tadpole spinal cord contains small and largely homogeneous populations of motor neurons (MNs) and V1 interneurons (V1s) at early escape swimming stages. These neuronal populations only modestly increase in number and subtype heterogeneity with the emergence of free swimming. In contrast, during frog metamorphosis and the emergence of limb movement, there is a dramatic expansion of MN and V1 interneuron number and transcriptional heterogeneity, culminating in cohorts of neurons that exhibit striking molecular similarity to mammalian motor circuits. CRISPR/Cas9-mediated gene disruption of the limb MN and V1 determinants FoxP1 and Engrailed-1, respectively, results in severe but selective deficits in tail and limb function. Our work thus demonstrates that neural diversity scales exponentially with increasing behavioral complexity and illustrates striking evolutionary conservation in the molecular organization and function of motor circuits across species.}, author = {Vijatovic, David and Toma, Florina Alexandra and Harrington, Zoe P and Sommer, Christoph M and Hauschild, Robert and Trevisan, Alexandra J. and Chapman, Phillip and Julseth, Mara and Brenner-Morton, Susan and Gabitto, Mariano I. and Dasen, Jeremy S. and Bikoff, Jay B. and Sweeney, Lora Beatrice Jaeger}, booktitle = {bioRxiv}, title = {{Spinal neuron diversity scales exponentially with swim-to-limb transformation during frog metamorphosis}}, doi = {10.1101/2024.09.20.614050}, year = {2024}, } @article{18305, abstract = {Motor circuits represent the main output of the central nervous system and produce dynamic behaviors ranging from relatively simple rhythmic activities like swimming in fish and breathing in mammals to highly sophisticated dexterous movements in humans. Despite decades of research, the development and function of motor circuits remain poorly understood. Breakthroughs in the field recently provided new tools and tractable model systems that set the stage to discover the molecular mechanisms and circuit logic underlying motor control. Here, we describe recent advances from both vertebrate (mouse, frog) and invertebrate (nematode, fruit fly) systems on cellular and molecular mechanisms that enable motor circuits to develop and function and highlight conserved and divergent mechanisms necessary for motor circuit development.}, author = {Kratsios, Paschalis and Zampieri, Niccolò and Carrillo, Robert and Mizumoto, Kota and Sweeney, Lora Beatrice Jaeger and Philippidou, Polyxeni}, issn = {1529-2401}, journal = {The Journal of Neuroscience}, number = {40}, publisher = {Society for Neuroscience}, title = {{Molecular and cellular mechanisms of motor circuit development}}, doi = {10.1523/JNEUROSCI.1238-24.2024}, volume = {44}, year = {2024}, } @article{13097, abstract = {Vertebrate movement is orchestrated by spinal inter- and motor neurons that, together with sensory and cognitive input, produce dynamic motor behaviors. These behaviors vary from the simple undulatory swimming of fish and larval aquatic species to the highly coordinated running, reaching and grasping of mice, humans and other mammals. This variation raises the fundamental question of how spinal circuits have changed in register with motor behavior. In simple, undulatory fish, exemplified by the lamprey, two broad classes of interneurons shape motor neuron output: ipsilateral-projecting excitatory neurons, and commissural-projecting inhibitory neurons. An additional class of ipsilateral inhibitory neurons is required to generate escape swim behavior in larval zebrafish and tadpoles. In limbed vertebrates, a more complex spinal neuron composition is observed. In this review, we provide evidence that movement elaboration correlates with an increase and specialization of these three basic interneuron types into molecularly, anatomically, and functionally distinct subpopulations. We summarize recent work linking neuron types to movement-pattern generation across fish, amphibians, reptiles, birds and mammals.}, author = {Wilson, Alexia C and Sweeney, Lora Beatrice Jaeger}, issn = {1662-5110}, journal = {Frontiers in Neural Circuits}, publisher = {Frontiers}, title = {{Spinal cords: Symphonies of interneurons across species}}, doi = {10.3389/fncir.2023.1146449}, volume = {17}, year = {2023}, } @article{10918, abstract = {Cellular metabolism must adapt to changing demands to enable homeostasis. During immune responses or cancer metastasis, cells leading migration into challenging environments require an energy boost, but what controls this capacity is unclear. Here, we study a previously uncharacterized nuclear protein, Atossa (encoded by CG9005), which supports macrophage invasion into the germband of Drosophila by controlling cellular metabolism. First, nuclear Atossa increases mRNA levels of Porthos, a DEAD-box protein, and of two metabolic enzymes, lysine-α-ketoglutarate reductase (LKR/SDH) and NADPH glyoxylate reductase (GR/HPR), thus enhancing mitochondrial bioenergetics. Then Porthos supports ribosome assembly and thereby raises the translational efficiency of a subset of mRNAs, including those affecting mitochondrial functions, the electron transport chain, and metabolism. Mitochondrial respiration measurements, metabolomics, and live imaging indicate that Atossa and Porthos power up OxPhos and energy production to promote the forging of a path into tissues by leading macrophages. Since many crucial physiological responses require increases in mitochondrial energy output, this previously undescribed genetic program may modulate a wide range of cellular behaviors.}, author = {Emtenani, Shamsi and Martin, Elliot T and György, Attila and Bicher, Julia and Genger, Jakob-Wendelin and Köcher, Thomas and Akhmanova, Maria and Pereira Guarda, Mariana and Roblek, Marko and Bergthaler, Andreas and Hurd, Thomas R and Rangan, Prashanth and Siekhaus, Daria E}, issn = {1460-2075}, journal = {The Embo Journal}, publisher = {Embo Press}, title = {{Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos axis in Drosophila}}, doi = {10.15252/embj.2021109049}, volume = {41}, year = {2022}, } @article{9363, abstract = {Optogenetics has been harnessed to shed new mechanistic light on current and future therapeutic strategies. This has been to date achieved by the regulation of ion flow and electrical signals in neuronal cells and neural circuits that are known to be affected by disease. In contrast, the optogenetic delivery of trophic biochemical signals, which support cell survival and are implicated in degenerative disorders, has never been demonstrated in an animal model of disease. Here, we reengineered the human and Drosophila melanogaster REarranged during Transfection (hRET and dRET) receptors to be activated by light, creating one-component optogenetic tools termed Opto-hRET and Opto-dRET. Upon blue light stimulation, these receptors robustly induced the MAPK/ERK proliferative signaling pathway in cultured cells. In PINK1B9 flies that exhibit loss of PTEN-induced putative kinase 1 (PINK1), a kinase associated with familial Parkinson’s disease (PD), light activation of Opto-dRET suppressed mitochondrial defects, tissue degeneration and behavioral deficits. In human cells with PINK1 loss-of-function, mitochondrial fragmentation was rescued using Opto-dRET via the PI3K/NF-кB pathway. Our results demonstrate that a light-activated receptor can ameliorate disease hallmarks in a genetic model of PD. The optogenetic delivery of trophic signals is cell type-specific and reversible and thus has the potential to inspire novel strategies towards a spatio-temporal regulation of tissue repair.}, author = {Inglés Prieto, Álvaro and Furthmann, Nikolas and Crossman, Samuel H. and Tichy, Alexandra Madelaine and Hoyer, Nina and Petersen, Meike and Zheden, Vanessa and Bicher, Julia and Gschaider-Reichhart, Eva and György, Attila and Siekhaus, Daria E and Soba, Peter and Winklhofer, Konstanze F. and Janovjak, Harald L}, issn = {1553-7404}, journal = {PLoS genetics}, number = {4}, pages = {e1009479}, publisher = {Public Library of Science}, title = {{Optogenetic delivery of trophic signals in a genetic model of Parkinson's disease}}, doi = {10.1371/journal.pgen.1009479}, volume = {17}, year = {2021}, } @article{9603, abstract = {Mosaic analysis with double markers (MADM) offers one approach to visualize and concomitantly manipulate genetically defined cells in mice with single-cell resolution. MADM applications include the analysis of lineage, single-cell morphology and physiology, genomic imprinting phenotypes, and dissection of cell-autonomous gene functions in vivo in health and disease. Yet, MADM can only be applied to <25% of all mouse genes on select chromosomes to date. To overcome this limitation, we generate transgenic mice with knocked-in MADM cassettes near the centromeres of all 19 autosomes and validate their use across organs. With this resource, >96% of the entire mouse genome can now be subjected to single-cell genetic mosaic analysis. Beyond a proof of principle, we apply our MADM library to systematically trace sister chromatid segregation in distinct mitotic cell lineages. We find striking chromosome-specific biases in segregation patterns, reflecting a putative mechanism for the asymmetric segregation of genetic determinants in somatic stem cell division.}, author = {Contreras, Ximena and Amberg, Nicole and Davaatseren, Amarbayasgalan and Hansen, Andi H and Sonntag, Johanna and Andersen, Lill and Bernthaler, Tina and Streicher, Carmen and Heger, Anna-Magdalena and Johnson, Randy L. and Schwarz, Lindsay A. and Luo, Liqun and Rülicke, Thomas and Hippenmeyer, Simon}, issn = {2211-1247}, journal = {Cell Reports}, number = {12}, publisher = {Cell Press}, title = {{A genome-wide library of MADM mice for single-cell genetic mosaic analysis}}, doi = {10.1016/j.celrep.2021.109274}, volume = {35}, year = {2021}, } @article{8914, abstract = {Amyotrophic lateral sclerosis (ALS) leads to a loss of specific motor neuron populations in the spinal cord and cortex. Emerging evidence suggests that interneurons may also be affected, but a detailed characterization of interneuron loss and its potential impacts on motor neuron loss and disease progression is lacking. To examine this issue, the fate of V1 inhibitory neurons during ALS was assessed in the ventral spinal cord using the SODG93A mouse model. The V1 population makes up ∼30% of all ventral inhibitory neurons, ∼50% of direct inhibitory synaptic contacts onto motor neuron cell bodies, and is thought to play a key role in modulating motor output, in part through recurrent and reciprocal inhibitory circuits. We find that approximately half of V1 inhibitory neurons are lost in SODG93A mice at late disease stages, but that this loss is delayed relative to the loss of motor neurons and V2a excitatory neurons. We further identify V1 subpopulations based on transcription factor expression that are differentially susceptible to degeneration in SODG93A mice. At an early disease stage, we show that V1 synaptic contacts with motor neuron cell bodies increase, suggesting an upregulation of inhibition before V1 neurons are lost in substantial numbers. These data support a model in which progressive changes in V1 synaptic contacts early in disease, and in select V1 subpopulations at later stages, represent a compensatory upregulation and then deleterious breakdown of specific interneuron circuits within the spinal cord.}, author = {Salamatina, Alina and Yang, Jerry H and Brenner-Morton, Susan and Bikoff, Jay B and Fang, Linjing and Kintner, Christopher R and Jessell, Thomas M and Sweeney, Lora Beatrice Jaeger}, issn = {0306-4522}, journal = {Neuroscience}, pages = {81--95}, publisher = {Elsevier}, title = {{Differential loss of spinal interneurons in a mouse model of ALS}}, doi = {10.1016/j.neuroscience.2020.08.011}, volume = {450}, year = {2020}, } @article{19544, abstract = {Medicinal bioinorganic chemistry is a thriving field of drug research for cancer treatment. Transition metal complexes coordinated to essential biological scaffolds represent a highly promising class of compounds for design of novel target-specific therapeutics. We report here the biological evaluation of a novel Isatin-Schiff base derivative and its Cu(II) complex in several tumor cell lines by assessing their effects on cellular metabolism, real-time cell proliferation and induction of apoptosis. Further, the impact of compounds on the p53 protein and expression of its target genes, including MDM2, p21/CDKN1A, and PUMA was evaluated. Results obtained in this study provide further evidence in support of our prior data suggesting the p53-mediated mechanism of action for Isatin-Schiff base derivatives and their complexes and also shed light on potential use of these compounds for stimulation of apoptosis in breast cancer cells via activation of the pro-apoptotic PUMA gene.}, author = {Bulatov, Emil and Sayarova, Regina and Mingaleeva, Rimma and Miftakhova, Regina and Gomzikova, Marina and Ignatev, Iurii and Petukhov, Alexey and Davidovich, Pavel and Rizvanov, Albert and Barlev, Nickolai A.}, issn = {2058-7716}, journal = {Cell Death Discovery}, publisher = {Springer Nature}, title = {{Isatin-Schiff base-copper (II) complex induces cell death in p53-positive tumors}}, doi = {10.1038/s41420-018-0120-z}, volume = {4}, year = {2018}, }