Claudia Colussi

Scopus Publications

Oxidative Stress and the Central Nervous System
Marcello D’Ascenzo, Claudia Colussi
Antioxidants, 2025
Reactive oxygen and nitrogen species (ROS; RNS) are natural bioproducts of cellular metabolism, particularly produced within the mitochondria during energy production [...]
SUMOylation balance: a key determinant in synapse physiology
Alessia Bertozzi, Walter Toscanelli, Giuditta Castellitto, Claudio Grassi, Claudia Colussi
Frontiers in Physiology, 2025
Neuronal communication relies on the precise regulation of synaptic compartments, where protein activity, localization, and turnover are tightly controlled. Among the mechanisms ensuring this regulation, post-translational modifications (PTMs) play a central role. SUMOylation, the covalent attachment of Small Ubiquitin-like Modifier (SUMO) proteins to target substrates, has emerged as a dynamic key PTM in the nervous system, modulating synaptic structure and function. Target SUMOylation occurs through an enzymatic cascade and requires the presence of a consensus sequence. Reversible addition of SUMO monomers or chains may contribute to distinct functional outcomes changing the conformation of the protein thus favoring/inhibiting molecular interaction among proteins or stabilizing the protein inhibiting degradation or influencing subcellular localization. All these SUMO dependent effects are crucial in the regulation of the tiny and highly specialized synaptic compartments to achieve spatiotemporal control for proper neurotransmission and synaptic plasticity in response to environmental stimuli. Dysregulation of this system has been implicated in various neurological disorders, including Alzheimer’s disease, where imbalances in SUMO1 versus SUMO2/3 levels contribute to synaptic dysfunction. As such, comprehension of SUMO related mechanisms may give important insights into both physiological regulation of synapses and potential therapeutic approaches for neurodegenerative diseases. Thus, in this review we will first introduce the enzymatic cascade of SUMOylation and its impact on protein function, then we will focus on its role within the synaptic compartment. Finally, we will discuss the therapeutic potential of modulating SUMOylation in Alzheimer’s disease as example of neurodegenerative disorders.
Glycine-induced activation of GPR158 increases the intrinsic excitability of medium spiny neurons in the nucleus accumbens
Giuseppe Aceto, Luca Nardella, Simona Nanni, Valeria Pecci, Alessia Bertozzi, et al.
Cellular and Molecular Life Sciences, 2024
It has been recently established that GPR158, a class C orphan G protein-coupled receptor, serves as a metabotropic glycine receptor. GPR158 is highly expressed in the nucleus accumbens (NAc), a major input structure of the basal ganglia that integrates information from cortical and subcortical structures to mediate goal-directed behaviors. However, whether glycine modulates neuronal activity in the NAc through GPR158 activation has not been investigated yet. Using whole-cell patch-clamp recordings, we found that glycine-dependent activation of GPR158 increased the firing rate of NAc medium spiny neurons (MSNs) while it failed to significantly affect the excitability of cholinergic interneurons (CIN). In MSNs GPR158 activation reduced the latency to fire, increased the action potential half-width, and reduced action potential afterhyperpolarization, effects that are all consistent with negative modulation of potassium M-currents, that in the central nervous system are mainly carried out by Kv7/KCNQ-channels. Indeed, we found that the GPR158-induced increase in MSN excitability was associated with decreased M-current amplitude, and selective pharmacological inhibition of the M-current mimicked and occluded the effects of GPR158 activation. In addition, when the protein kinase A (PKA) or extracellular signal-regulated kinase (ERK) signaling was pharmacologically blocked, modulation of MSN excitability by GPR158 activation was suppressed. Moreover, GPR158 activation increased the phosphorylation of ERK and Kv7.2 serine residues. Collectively, our findings suggest that GPR158/PKA/ERK signaling controls MSN excitability via Kv7.2 modulation. Glycine-dependent activation of GPR158 may significantly affect MSN firing in vivo, thus potentially mediating specific aspects of goal-induced behaviors.
Structural and functional alterations of neurons derived from sporadic Alzheimer’s disease hiPSCs are associated with downregulation of the LIMK1-cofilin axis
Raimondo Sollazzo, Domenica Donatella Li Puma, Giuseppe Aceto, Fabiola Paciello, Claudia Colussi, et al.
Alzheimer S Research and Therapy, 2024
Nucleoporin 153 deficiency in adult neural stem cells defines a pathological protein-network signature and defective neurogenesis in a mouse model of AD
Claudia Colussi, Alessia Bertozzi, Lucia Leone, Marco Rinaudo, Raimondo Sollazzo, et al.
Stem Cell Research and Therapy, 2024
Background Reduction of adult hippocampal neurogenesis is an early critical event in Alzheimer’s disease (AD), contributing to progressive memory loss and cognitive decline. Reduced levels of the nucleoporin 153 (Nup153), a key epigenetic regulator of NSC stemness, characterize the neural stem cells isolated from a mouse model of AD (3×Tg) (AD-NSCs) and determine their altered plasticity and gene expression. Methods Nup153-regulated mechanisms contributing to NSC function were investigated: (1) in cultured NSCs isolated from AD and wild type (WT) mice by proteomics; (2) in vivo by lentiviral-mediated delivery of Nup153 or GFP in the hippocampus of AD and control mice analyzing neurogenesis and cognitive function; (3) in human iPSC-derived brain organoids obtained from AD patients and control subjects as a model of neurodevelopment. Results Proteomic approach identified Nup153 interactors in WT- and AD-NSCs potentially implicated in neurogenesis regulation. Gene ontology (GO) analysis showed that Nup153-bound proteins in WT-NSCs were involved in RNA metabolism, nuclear import and epigenetic mechanisms. Nup153-bound proteins in AD-NSCs were involved in pathways of neurodegeneration, mitochondrial dysfunction, proteasomal processing and RNA degradation. Furthermore, recovery of Nup153 levels in AD-NSCs reduced the levels of oxidative stress markers and recovered proteasomal activity. Lentiviral-mediated delivery of Nup153 in the hippocampal niche of AD mice increased the proliferation of early progenitors, marked by BrdU/DCX and BrdU/PSANCAM positivity and, later, the integration of differentiating neurons in the cell granule layer (BrdU/NeuN+ cells) compared with GFP-injected AD mice. Consistently, Nup153-injected AD mice showed an improvement of cognitive performance in comparison to AD-GFP mice at 1 month after virus delivery assessed by Morris Water Maze. To validate the role of Nup153 in neurogenesis we took advantage of brain organoids derived from AD-iPSCs characterized by fewer neuroepithelial progenitor loops and reduced differentiation areas. The upregulation of Nup153 in AD organoids recovered the formation of neural-like tubes and differentiation. Conclusions Our data suggest that the positive effect of Nup153 on neurogenesis is based on a complex regulatory network orchestrated by Nup153 and that this protein is a valuable disease target.
Interleukin 1β triggers synaptic and memory deficits in Herpes simplex virus type-1-infected mice by downregulating the expression of synaptic plasticity-related genes via the epigenetic MeCP2/HDAC4 complex
Domenica Donatella Li Puma, Claudia Colussi, Bruno Bandiera, Giulia Puliatti, Marco Rinaudo, et al.
Cellular and Molecular Life Sciences, 2023
Extensive research provides evidence that neuroinflammation underlies numerous brain disorders. However, the molecular mechanisms by which inflammatory mediators determine synaptic and cognitive dysfunction occurring in neurodegenerative diseases (e.g., Alzheimer’s disease) are far from being fully understood. Here we investigated the role of interleukin 1β (IL-1β), and the molecular cascade downstream the activation of its receptor, to the synaptic dysfunction occurring in the mouse model of multiple Herpes simplex virus type-1 (HSV-1) reactivations within the brain. These mice are characterized by neuroinflammation and memory deficits associated with a progressive accumulation of neurodegenerative hallmarks (e.g., amyloid-β protein and tau hyperphosphorylation). Here we show that mice undergone two HSV-1 reactivations in the brain exhibited increased levels of IL-1β along with significant alterations of: (1) cognitive performances; (2) hippocampal long-term potentiation; (3) expression synaptic-related genes and pre- and post-synaptic proteins; (4) dendritic spine density and morphology. These effects correlated with activation of the epigenetic repressor MeCP2 that, in association with HDAC4, affected the expression of synaptic plasticity-related genes. Specifically, in response to HSV-1 infection, HDAC4 accumulated in the nucleus and promoted MeCP2 SUMOylation that is a post-translational modification critically affecting the repressive activity of MeCP2. The blockade of IL-1 receptors by the specific antagonist Anakinra prevented the MeCP2 increase and the consequent downregulation of gene expression along with rescuing structural and functional indices of neurodegeneration. Collectively, our findings provide novel mechanistic evidence on the role played by HSV-1-activated IL-1β signaling pathways in synaptic deficits leading to cognitive impairment.
Cytoplasmic HDAC4 recovers synaptic function in the 3×Tg mouse model of Alzheimer's disease
Claudia Colussi, Giuseppe Aceto, Cristian Ripoli, Alessia Bertozzi, Domenica Donatella Li Puma, et al.
Neuropathology and Applied Neurobiology, 2023
Early dysfunction in Alzheimer's disease (AD) is characterised by alterations of synapse structure and function leading to dysmorphic neurites, decreased spine density, impaired synaptic plasticity and cognitive deficits. The class II member HDAC4, which recently emerged as a crucial factor in shaping synaptic plasticity and memory, was found to be altered in AD. We investigated how the modulation of HDAC4 may contribute to counteracting AD pathogenesis.
Near-infrared controlled release of mesenchymal stem cells secretome from bioprinted graphenebased microbeads for nerve regeneration
Giordano Perini, Valentina Palmieri, Marcello D’Ascenzo, Claudia Colussi, Claudio Grassi, et al.
International Journal of Bioprinting, 2023
&nbsp;Nerve damage is a prevalent and debilitating condition with limited treatment options. Recent years have seen an increased incidence of neural damage due to factors such as aging populations and traumatic brain injuries. Addressing the urgent need for effective therapies, this study explores the controlled delivery of mesenchymal stem cells (MSCs) secretome, a complex mixture of bioactive factors, which is currently being investigated for its potential in nerve regeneration. The secretome offers significant advantages over stem cells themselves, as it can be more easily characterized and controlled, enabling precise regulation of therapeutic interventions. However, the challenge lies in delivering the secretome specifically to the target anatomical region. To overcome this limitation, we propose a novel approach utilizing near-infrared (NIR) radiation-responsive bioprinted alginate-graphene oxide (AGO) microbeads. Graphene oxide (GO) is a highly biocompatible material with unique properties, including NIR responsiveness, enabling controlled release of therapeutic agents upon NIR exposure. We hypothesized that AGO microbeads could encapsulate MSCs secretome and release it in a controlled manner using NIR radiation. To investigate our hypothesis, controlled damage was induced to hippocampal neurons, and MSCs secretome was encapsulated within AGO microbeads. Subsequently, NIR radiation was applied to trigger the release of the secretome. We compared the efficacy of MSCs secretome with that of astrocytes, which also possess nerve growth and proliferation-promoting capabilities. Our findings demonstrated that the controlled release of MSCs secretome from AGO microbeads through non-invasive NIR radiation significantly promoted the proliferation and regeneration of neurons following nerve injury. AGO microbeads offer multiple advantages over conventional delivery methods, including precise control over the timing, location, and dosage of therapeutic agents. Furthermore, the potential for reduced immunogenicity and tumorigenicity enhances the safety profile of the therapy. Consequently, this study presents a promising avenue for the development of MSC-based therapies for nerve regeneration, with implications for the treatment of various neuropathies and injuries. &nbsp;
Acute restraint stress impairs histamine type 2 receptor ability to increase the excitability of medium spiny neurons in the nucleus accumbens
Giuseppe Aceto, Luca Nardella, Giacomo Lazzarino, Barbara Tavazzi, Alessia Bertozzi, et al.
Neurobiology of Disease, 2022
Activation of histamine type 2 receptors enhances intrinsic excitability of medium spiny neurons in the nucleus accumbens
Giuseppe Aceto, Luca Nardella, Simona Nanni, Valeria Pecci, Alessia Bertozzi, et al.
Journal of Physiology, 2022
Histaminergic neurons are exclusively located in the hypothalamic tuberomammillary nucleus, from where they project to many brain areas including the nucleus accumbens (NAc), a brain area that integrates diverse monoaminergic inputs to coordinate motivated behaviours. While the NAc expresses various histamine receptor subtypes, the mechanisms by which histamine modulates NAc activity are still poorly understood. Using whole‐cell patch‐clamp recordings, we found that pharmacological activation of histamine 2 (H2) receptors elevates the excitability of NAc medium spiny neurons (MSNs), while activation of H1 receptors failed to significantly affect MSN excitability. The evoked firing of MSNs increased after seconds of local H2 agonist administration and remained elevated for minutes. H2 receptor (H2R) activation accelerated subthreshold depolarization in response to current injection, reduced the latency to fire, diminished action potential afterhyperpolarization and increased the action potential half‐width. The increased excitability was protein kinase A‐dependent and associated with decreased A‐type K+ currents. In addition, selective pharmacological inhibition of the Kv4.2 channel, the main molecular determinant of A‐type K+ currents in MSNs, mimicked and occluded the increased excitability induced by H2R activation. Our results indicate that histaminergic transmission in the NAc increases MSN intrinsic excitability through H2R‐dependent modulation of Kv4.2 channels. Activation of H2R will significantly alter spike firing in MSNs in vivo, and this effect could be an important mechanism by which these receptors mediate certain aspects of goal‐induced behaviours.
Epigenetic regulation of neural stem cells: The emerging role of nucleoporins
Claudia Colussi, Claudio Grassi
Stem Cells, 2021
Connexin hemichannel activation by s-nitrosoglutathione synergizes strongly with photodynamic therapy potentiating anti-tumor bystander killing
Chiara Nardin, Chiara Peres, Sabrina Putti, Tiziana Orsini, Claudia Colussi, et al.
Cancers, 2021
Enhancing Plasticity Mechanisms in the Mouse Motor Cortex by Anodal Transcranial Direct-Current Stimulation: The Contribution of Nitric Oxide Signaling
Saviana Antonella Barbati, Sara Cocco, Valentina Longo, Matteo Spinelli, Katia Gironi, et al.
Cerebral Cortex, 2020
Chronic mild stress alters synaptic plasticity in the nucleus accumbens through GSK3β-dependent modulation of Kv4.2 channels
Giuseppe Aceto, Claudia Colussi, Lucia Leone, Salvatore Fusco, Marco Rinaudo, et al.
Proceedings of the National Academy of Sciences of the United States of America, 2020
Erratum: GSK3β Modulates Timing-Dependent Long-Term Depression Through Direct Phosphorylation of Kv4.2 Channels (Cerebral Cortex (bhy042) DOI: 10.1093/cercor/bhy042)
Giuseppe Aceto, Agnese Re, Andrea Mattera, Lucia Leone, Claudia Colussi, et al.
Cerebral Cortex, 2019
Altered Nup153 Expression Impairs the Function of Cultured Hippocampal Neural Stem Cells Isolated from a Mouse Model of Alzheimer’s Disease
Lucia Leone, Claudia Colussi, Katia Gironi, Valentina Longo, Salvatore Fusco, et al.
Molecular Neurobiology, 2019
GSK3β modulates timing-dependent long-term depression through direct phosphorylation of Kv4.2 channels
Giuseppe Aceto, Agnese Re, Andrea Mattera, Lucia Leone, Claudia Colussi, et al.
Cerebral Cortex, 2019
Olfactory memory is enhanced in mice exposed to extremely low-frequency electromagnetic fields via Wnt/β-catenin dependent modulation of subventricular zone neurogenesis
Alessia Mastrodonato, Saviana Antonella Barbati, Lucia Leone, Claudia Colussi, Katia Gironi, et al.
Scientific Reports, 2018
Sildenafil normalizes MALAT1 level in diabetic cardiomyopathy
Lorenza Bacci, Saviana A. Barbati, Claudia Colussi, Aurora Aiello, Andrea M. Isidori, et al.
Endocrine, 2018
Nucleoporin 153 regulates estrogen-dependent nuclear translocation of endothelial nitric oxide synthase and estrogen receptor beta in prostate cancer
Agnese Re, Claudia Colussi, Simona Nanni, Aurora Aiello, Lorenza Bacci, et al.
Oncotarget, 2018
Olfactory receptors in semen and in the male tract: From proteome to proteins
Domenico Milardi, Claudia Colussi, Giuseppe Grande, Federica Vincenzoni, Francesco Pierconti, et al.
Frontiers in Endocrinology, 2018
Transcription factor CREM mediates high glucose response in cardiomyocytes and in a male mouse model of prolonged hyperglycemia
Saviana A. Barbati, Claudia Colussi, Lorenza Bacci, Aurora Aiello, Agnese Re, et al.
Endocrinology, 2017
The nuclear pore protein Nup153 associates with chromatin and regulates cardiac gene expression in dystrophic mdx hearts
Simona Nanni, Agnese Re, Cristian Ripoli, Aoife Gowran, Patrizia Nigro, et al.
Cardiovascular Research, 2016
Anacardic acid and thyroid hormone enhance cardiomyocytes production from undifferentiated mouse ES cells along functionally distinct pathways
Agnese Re, Simona Nanni, Aurora Aiello, Serena Granata, Claudia Colussi, et al.
Endocrine, 2016
Anodal transcranial direct current stimulation boosts synaptic plasticity and memory in mice via epigenetic regulation of Bdnf expression
Maria Vittoria Podda, Sara Cocco, Alessia Mastrodonato, Salvatore Fusco, Lucia Leone, et al.
Scientific Reports, 2016
Acetylation mediates Cx43 reduction caused by electrical stimulation
Viviana Meraviglia, Valerio Azzimato, Claudia Colussi, Maria Cristina Florio, Anna Binda, et al.
Journal of Molecular and Cellular Cardiology, 2015
Adventitial vessel growth and progenitor cells activation in an ex vivo culture system mimicking human saphenous vein wall strain after coronary artery bypass grafting
Francesca Prandi, Marco Piola, Monica Soncini, Claudia Colussi, Yuri D’Alessandra, et al.
Plos One, 2015
The histone acetylase activator pentadecylidenemalonate 1b rescues proliferation and differentiation in the human cardiac mesenchymal cells of type 2 diabetic patients
Matteo Vecellio, Francesco Spallotta, Simona Nanni, Claudia Colussi, Chiara Cencioni, et al.
Diabetes, 2014
Detrimental effect of class-selective histone deacetylase inhibitors during tissue regeneration following hindlimb ischemia
Francesco Spallotta, Silvia Tardivo, Simona Nanni, Jessica D. Rosati, Stefania Straino, et al.
Journal of Biological Chemistry, 2013
Estrogen-Dependent Dynamic Profile of eNOS-DNA Associations in Prostate Cancer
Simona Nanni, Aurora Aiello, Agnese Re, Alessandro Guffanti, Valentina Benvenuti, et al.
Plos One, 2013
A nitric oxide-dependent cross-talk between class i and III histone deacetylases accelerates skin repair
Francesco Spallotta, Chiara Cencioni, Stefania Straino, Simona Nanni, Jessica Rosati, et al.
Journal of Biological Chemistry, 2013
P300/CBP associated factor regulates nitroglycerin-dependent arterial relaxation by nε-lysine acetylation of contractile proteins
Claudia Colussi, Alessandro Scopece, Serena Vitale, Francesco Spallotta, Stefania Mattiussi, et al.
Arteriosclerosis Thrombosis and Vascular Biology, 2012
Silencing of GSTP1, a prostate cancer prognostic gene, by the estrogen receptor-β and endothelial nitric oxide synthase complex
A. Re, A. Aiello, S. Nanni, A. Grasselli, V. Benvenuti, et al.
Molecular Endocrinology, 2011
NO points to epigenetics in vascular development
B. Illi, C. Colussi, J. Rosati, F. Spallotta, S. Nanni, et al.
Cardiovascular Research, 2011
Smad-interacting protein-1 and microRNA 200 family define a nitric oxide-dependent molecular circuitry involved in embryonic stem cell mesendoderm differentiation
Jessica Rosati, Francesco Spallotta, Simona Nanni, Annalisa Grasselli, Annalisa Antonini, et al.
Arteriosclerosis Thrombosis and Vascular Biology, 2011
Nε-lysine acetylation determines dissociation from GAP junctions and lateralization of connexin 43 in normal and dystrophic heart
Claudia Colussi, Jessica Rosati, Stefania Straino, Francesco Spallotta, Roberta Berni, et al.
Proceedings of the National Academy of Sciences of the United States of America, 2011
Histone deacetylase inhibitors: Keeping momentum for neuromuscular and cardiovascular diseases treatment
Claudia Colussi, Barbara Illi, Jessica Rosati, Francesco Spallotta, Antonella Farsetti, et al.
Pharmacological Research, 2010
The histone deacetylase inhibitor suberoylanilide hydroxamic acid reduces cardiac arrhythmias in dystrophic mice
Claudia Colussi, Roberta Berni, Jessica Rosati, Stefania Straino, Serena Vitale, et al.
Cardiovascular Research, 2010
Proteomic profile of differentially expressed plasma proteins from dystrophic mice and following suberoylanilide hydroxamic acid treatment
C. Colussi, C. Banfi, M. Brioschi, E. Tremoli, S. Straino, et al.
Proteomics Clinical Applications, 2010
Common micro-RNA signature in skeletal muscle damage and regeneration induced by Duchenne muscular dystrophy and acute ischemia
Simona Greco, Marco De Simone, Claudia Colussi, Germana Zaccagnini, Pasquale Fasanaro, et al.
FASEB Journal, 2009
NO sparks off chromatin: Tales of a multifaceted epigenetic regulator
Barbara Illi, Claudia Colussi, Annalisa Grasselli, Antonella Farsetti, Maurizio C. Capogrossi, et al.
Pharmacology and Therapeutics, 2009
Nitric oxide deficiency determines global chromatin changes in Duchenne muscular dystrophy
Claudia Colussi, Aymone Gurtner, Jessica Rosati, Barbara Illi, Gianluca Ragone, et al.
FASEB Journal, 2009
Endothelial NOS, estrogen receptor β, and HIFs cooperate in the activation of a prognostic transcriptional pattern in aggressive human prostate cancer
Simona Nanni, Valentina Benvenuti, Annalisa Grasselli, Carmen Priolo, Aurora Aiello, et al.
Journal of Clinical Investigation, 2009
Erratum: HDAC2 blockade by nitric oxide and histone deacetylase inhibitors reveals a common target in Duchenne muscular dystrophy treatment (Proceedings of the National Academy of Sciences of the United States of America (2008) 105 (19183-19187) DOI: 10.1073/pnas.0805514105))
Proceedings of the National Academy of Sciences of the United States of America, 2009
HDAC2 blockade by nitric oxide and histone deacetylase inhibitors reveals a common target in Duchenne muscular dystrophy treatment
Claudia Colussi, Chiara Mozzetta, Aymone Gurtner, Barbara Illi, Jessica Rosati, et al.
Proceedings of the National Academy of Sciences of the United States of America, 2008
AAV-dependent targeting of myostatin function: Follistatin strikes back at muscular dystrophy
C Colussi, C Gaetano, M C Capogrossi
Gene Therapy, 2008
Estrogen receptor-α and endothelial nitric oxide synthase nuclear complex regulates transcription of human telomerase
Annalisa Grasselli, Simona Nanni, Claudia Colussi, Aurora Aiello, Valentina Benvenuti, et al.
Circulation Research, 2008
NF-Y dependent epigenetic modifications discriminate between proliferating and postmitotic tissue
Aymone Gurtner, Paola Fuschi, Fiorenza Magi, Claudia Colussi, Carlo Gaetano, et al.
Plos One, 2008
Nitric oxide modulates chromatin folding in human endothelial cells via protein phosphatase 2A activation and class II histone deacetylases nuclear shuttling
Barbara Illi, Claudio Dello Russo, Claudia Colussi, Jessica Rosati, Michele Pallaoro, et al.
Circulation Research, 2008
PEDF, PPAR-γ, p53: Deadly circuits arise when worlds collide
C GAETANO, C COLUSSI, M CAPOGROSSI
Cardiovascular Research, 2007
Functional and morphological recovery of dystrophic muscles in mice treated with deacetylase inhibitors
G C Minetti, C Colussi, R Adami, C Serra, C Mozzetta, et al.
Nature Medicine, 2006
Senescence and death of primitive cells and myocytes lead to premature cardiac aging and heart failure
Cristina Chimenti, Jan Kajstura, Daniele Torella, Konrad Urbanek, Hubert Heleniak, et al.
Circulation Research, 2003
The Mammalian Mismatch Repair pathway removes DNA 8-oxodGMP incorporated from the oxidized dNTP pool
Claudia Colussi, Eleonora Parlanti, Paolo Degan, Gabriele Aquilina, Deborah Barnes, et al.
Current Biology, 2002
1,2-Dimethylhydrazine-induced colon carcinoma and lymphoma in msh2-/- mice
C. Colussi, S. Fiumicino, A. Giuliani, S. Rosini, P. Musiani, et al.
Journal of the National Cancer Institute, 2001
Hypersensitivity to camptothecin in MSH2 deficient cells is correlated with a role for MSH2 protein in recombinational repair
Pietro Pichierri, Annapaola Franchitto, Rita Piergentili, Claudia Colussi, Fabrizio Palitti
Carcinogenesis, 2001
Sensitivity to DNA cross-linking chemotherapeutic agents in mismatch repair-defective cells in vitro and in xenografts
Silvia Fiumicino, Simone Martinelli, Claudia Colussi, Gabriele Aquilina, Carlo Leonetti, et al.
International Journal of Cancer, 2000
H2O2-induced block of glycolysis as an active ADP-ribosylation reaction protecting cells from apoptosis
C. Colussi, M.C. Albertini, S. Coppola, S. Rovidati, F. Galli, et al.
FASEB Journal, 2000
Magnetic fields increase cell survival by inhibiting apoptosis via modulation of Ca2+ influx
C. FANELLI, S. COPPOLA, R. BARONE, C. COLUSSI, G. GUALANDI, et al.
FASEB Journal, 1999
Rescue of cells from apoptosis by inhibition of active GSH extrusion
L. Ghibelli, C. Fanelli, G. Rotilio, E. Lafavia, S. Coppola, et al.
FASEB Journal, 1998
ADP-Ribosylations in oxidative stress-induced apoptosis
S. Coppola, C. Colussi, C. Albertini, S. Rovidati, F. Canestrari, et al.
Biochemical Society Transactions, 1996

Claudia Colussi

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