Francesca Brambilla
@wwe.cnr.it
Itb cnr
Scopus Publications
- Glioblastoma: Overview of Proteomic Investigations and Biobank Approaches for the Development of a Multidisciplinary Translational Network
Giusy Ciuffreda, Sara Casati, Francesca Brambilla, Mauro Campello, Valentina De Falco, Dario Di Silvestre, Antonio Frigeri, Marco Locatelli, Lorenzo Magrassi, Andrea Salmaggi, Marco Salvetti, Francesco Signorelli, Yvan Torrente, Giuseppe Emanuele Umana, Raffaello Viganò, Pietro Luigi Mauri
Cancers, 2025
Glioblastoma is a highly aggressive, infiltrative brain tumor of the central nervous system (CNS). Its extensive molecular and biochemical heterogenicity hinders the identification of reliable biomarkers and therapeutic targets, thereby making prognosis and existing therapy ineffective. In recent years, breakthroughs in the use of proteomics on a range of biological samples, such as plasma, cerebrospinal fluid (CSF), tissues, brain cells, and exosomes, represent a potential improvement to GBM investigations. Mass spectrometry-based approaches represent an important technique in the characterization of the tumoral proteome, for the identification of differentially expressed proteins, and for studying altered molecular pathways involved in tumor stages. Proteomics studies advance our knowledge about GBM pathogenesis, the discovery of reliable diagnostic and prognostic markers, and therapeutic approaches, also. In this context, for the effective application of proteomics on GBM, it is mandatory to develop a translational network by integrating hospitals, biobanks, and research institutions into a single network, to enable a collaborative approach across disciplines, thereby enabling rapid translation to clinical application of new proteomic insights. Today, high-quality biobanks play a key role in enabling collaborative, ethically compliant research, supporting the effective application of proteomics in glioblastoma studies and the translation of discoveries into clinical practice. This review explores current trends in proteomics and GBM research, highlighting how leveraging biobank infrastructure and fostering institutional cooperation can drive the development of targeted pilot projects to enhance the impact and effectiveness of glioblastoma research. - CSPG4.CAR-T Cells Modulate Extracellular Matrix Remodeling in DMD Cardiomyopathy
Maria Grazia Ceraolo, Marika Milan, Nicole Fratini, Raffaello Viganò, Salma Bousselmi, Andrea Soluri, Elisa Pesce, Pier Luigi Mauri, Giusy Ciuffreda, Elisa Landoni, Francesca Brambilla, Gianpietro Dotti, Dario Di Silvestre, Fabio Maiullari, Claudia Bearzi, Roberto Rizzi
International Journal of Molecular Sciences, 2025
Targeting fibrosis in Duchenne muscular dystrophy (DMD)-associated cardiomyopathy is a critical outstanding clinical issue, as cardiac failure remains a leading cause of death despite advances in supportive care. This study evaluates the therapeutic efficacy of CSPG4-targeted chimeric antigen receptor (CAR) T cells in reducing cardiac fibrosis and improving heart function in a preclinical model of the disease. DMD is a progressive genetic disorder characterized by degeneration of skeletal and cardiac muscle. Cardiomyopathy, driven by fibrosis and chronic inflammation, is a leading contributor to mortality in affected patients. Proteoglycans such as CSPG4, critical regulators of extracellular matrix dynamics, are markedly overexpressed in dystrophic hearts and promote pathological remodeling. Current treatments do not adequately target the fibrotic and inflammatory processes underlying cardiac dysfunction. CSPG4-specific CAR-T cells were engineered and administered to dystrophic mice. Therapeutic efficacy was assessed through histological, molecular, and echocardiographic analyses evaluating cardiac fibrosis, inflammation, innervation, and overall function. Treatment with CSPG4 CAR-T cells preserved myocardial integrity, improved cardiac performance, and reduced both fibrosis and inflammatory markers. The therapy also restored cardiac innervation, indicating a reversal of neural remodeling commonly seen in muscular dystrophy-related cardiomyopathy. CSPG4-targeted CAR-T therapy offers a novel, cell-based strategy to mitigate cardiac remodeling in dystrophic hearts. By addressing core fibrotic and inflammatory drivers of disease, this approach represents a significant advancement in the development of precision immune therapies for muscular dystrophies and cardiovascular conditions. - MicroRNA-142-3p shuttling in extracellular vesicles marks regulatory T cell dysfunction in multiple sclerosis
Giusy De Rosa, Claudia Russo, Silvia Garavelli, Dario Di Silvestre, Ilaria Spatocco, Giorgia Mele, Claudia La Rocca, Alessandra Colamatteo, Fortunata Carbone, Clorinda Fusco, Fabiana Passaro, Donatella Carpi, Elena Tagliabue, Francesco Prattichizzo, Francesca Brambilla, Pierluigi Mauri, Mirjam Hoxha, Valentina Bollati, Ilaria Giusti, Vincenza Dolo, Paola D’Antona, Paola Campomenosi, Valentina Mangolini, Annalisa Radeghieri, Paolo Bergese, Ivana Morabito, Alessandra Mandelli, Annamaria Finardi, Francesca Beretta, Edoardo Dalmato Schilke, Guido Cavaletti, Ettore Dolcetti, Fabio Buttari, Gianmarco Abbadessa, Simona Bonavita, Giacomo Lus, Elisabetta Signoriello, Roberta Lanzillo, Vincenzo Brescia Morra, Maria Mottola, Bruno Zuccarelli, Antonio Uccelli, Marco Salvetti, Diego Centonze, Roberto Furlan, Giuseppe Matarese, Claudio Procaccini, Paola de Candia
Science Translational Medicine, 2025
CD4 + CD25 hi FoxP3 + regulatory T cells (T reg cells) are key controllers of immune self-tolerance, and their suppressive function is impaired in people with relapsing-remitting multiple sclerosis (pwRR-MS). Because the mechanisms underlying this condition are still ill-defined, we investigated the role of T reg cell–derived extracellular vesicles (T reg -EVs) in T reg cell dysfunction observed in pwRR-MS. We found that T reg -EVs from healthy individuals inhibit CD4 + conventional T (T conv ) cells by shuttling miR-142-3p from the T reg cell to the T conv cell. There, miR-142-3p down-regulated mRNAs necessary for T conv cell growth and effector functions, such as the redox controller cystine carrier SLC7A11 . However, T reg cells from pwRR-MS released EVs containing reduced amounts of miR-142-3p, resulting in impaired suppressive function. Furthermore, T reg -EV miR-142-3p inversely correlated with the disability score and gadolinium-enhancing lesions in pwRR-MS. Together, our results elucidate a molecular mechanism involving miR-142-3p shuttled by T reg -EVs in the control of immune self-tolerance and unveil its pathogenetic implications in human autoimmunity. - Mimicking the Dystrophic Cardiac Extracellular Environment through DystroGel
Maila Chirivì, Fabio Maiullari, Marika Milan, Maria Grazia Ceraolo, Nicole Fratini, Alessandra Fasciani, Salma Bousselmi, Michael Stirm, Francesca Scalera, Francesca Gervaso, Michela Villa, Raffaello Viganò, Francesca Brambilla, Pierluigi Mauri, Elena De Falco, Dario Di Silvestre, Marco Costantini, Eckhard Wolf, Claudia Bearzi, Roberto Rizzi
Advanced Healthcare Materials, 2025
Advances in understanding the mechanisms behind genetic diseases like Duchenne muscular dystrophy (DMD) underscore the critical role of the extracellular matrix (ECM) composition in disease progression. Effective in vitro models must replicate the intercellular relationships and physicochemical properties of native ECM to fully capture disease‐specific characteristics. Although recent biomaterials support the in vitro biofabrication of pathophysiological environments, they often lack disease‐specific ECM features. In this study, DystroGel, a hydrogel derived from the cardiac ECM of a porcine DMD model, replicates the distinct molecular composition of dystrophic cardiac tissue for the first time. The findings indicate that the dystrophic ECM matrix exhibits a unique protein profile, impacting cellular processes critical to DMD pathology. This work demonstrates the importance of using a 3D substrate that recreates intercellular dynamics within a defined pathological environment, enhancing the ability to model genetic disorders and providing a valuable tool for advancing personalized therapeutic strategies. - Computational Tools and Methods for the Study of Systemic Amyloidosis at the Clinical and Molecular Level
Dario Di Silvestre, Francesca Brambilla, Giampaolo Merlini, Pierluigi Mauri
Methods in Molecular Biology, 2025 - Macrophages producing chondroitin sulfate proteoglycan-4 induce neuro-cardiac junction impairment in Duchenne muscular dystrophy
Marika Milan, Fabio Maiullari, Maila Chirivì, Maria Grazia Ceraolo, Rebecca Zigiotto, Andrea Soluri, Silvia Maiullari, Elisa Landoni, Dario Di Silvestre, Francesca Brambilla, Pierluigi Mauri, Veronica De Paolis, Nicole Fratini, Maria Cristina Crosti, Chiara Cordiglieri, Chiara Parisi, Antonella Calogero, Dror Seliktar, Yvan Torrente, Chiara Lanzuolo, Gianpietro Dotti, Mirco Toccafondi, Mauro Bombaci, Elena De Falco, Claudia Bearzi, Roberto Rizzi
Journal of Pathology, 2025
Duchenne muscular dystrophy (DMD) is caused by the absence of the full form of the dystrophin protein, which is essential for maintaining the structural integrity of muscle cells, including those in the heart and respiratory system. Despite progress in understanding the molecular mechanisms associated with DMD, myocardial insufficiency persists as the primary cause of mortality, and existing therapeutic strategies remain limited. This study investigates the hypothesis that a dysregulation of the biological communication between infiltrating macrophages (MPs) and neurocardiac junctions exists in dystrophic cardiac tissue. In a mouse model of DMD (mdx), this phenomenon is influenced by the over‐release of chondroitin sulfate proteoglycan‐4 (CSPG4), a key inhibitor of nerve sprouting and a modulator of the neural function, by MPs infiltrating the cardiac tissue and associated with dilated cardiomyopathy, a hallmark of DMD. Givinostat, the histone deacetylase inhibitor under current development as a clinical treatment for DMD, is effective at both restoring a physiological microenvironment at the neuro‐cardiac junction and cardiac function in mdx mice in addition to a reduction in cardiac fibrosis, MP‐mediated inflammation, and tissue CSPG4 content. This study provides novel insight into the pathophysiology of DMD in the heart, identifying potential new biological targets. © 2024 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Enhancing neovascularization post-myocardial infarction through injectable hydrogel functionalized with endothelial-derived EVs
Fabio Maiullari, Marika Milan, Maila Chirivì, Maria Grazia Ceraolo, Salma Bousselmi, Nicole Fratini, Matteo Galbiati, Orazio Fortunato, Marco Costantini, Francesca Brambilla, Pierluigi Mauri, Dario Di Silvestre, Antonella Calogero, Tommaso Sciarra, Roberto Rizzi, Claudia Bearzi
Biofabrication, 2024
Over the past three decades, cell therapy development has fallen short of expectations, with many cellular sources demonstrating a ‘Janus effect’ and raising safety concerns. Extracellular vesicles (EVs), supported by advanced technologies, present a promising avenue in regenerative medicine, offering benefits such as immune tolerance and avoidance of negative aspects associated with cell transplants. Our previous research showcased enhanced and organized subcutaneous vascularization using three-dimensional bioprinted patches containing HUVEC-derived EVs in immunodeficient animal models. In this context, stress conditions on the cells of origin further boosted the EVs’ neoangiogenic potential. Since neovascularization is the first regenerative target requiring restoration, the present study aims to complement our previous work by employing an injectable gelatin methacrylate (GelMA) hydrogel functionalized with HUVEC-derived EVs in a pathological condition of acute myocardial infarction. This bioactive hydrogel resulted in reduced fibrosis, improved contractility, and promoted angiogenesis, showing promise in countering tissue deterioration and addressing vascular deficits. Moreover, the molecular characterization of EVs through miRNome and proteomic analyses further supports their potential as bio-additives for hydrogel functionalization. This cell-free approach mitigates immune rejection and oncogenic risks, offering innovative therapeutic advantages. - Proteomic Analysis on Sequential Samples of Cystic Fluid Obtained from Human Brain Tumors
Lorenzo Magrassi, Francesca Brambilla, Raffaello Viganò, Dario Di Silvestre, Louise Benazzi, Giuseppe Bellantoni, Gian Marco Danesino, Sergio Comincini, Pierluigi Mauri
Cancers, 2023
Cystic formation in human primary brain tumors is a relatively rare event whose incidence varies widely according to the histotype of the tumor. Composition of the cystic fluid has mostly been characterized in samples collected at the time of tumor resection and no indications of the evolution of cystic content are available. We characterized the evolution of the proteome of cystic fluid using a bottom-up proteomic approach on sequential samples obtained from secretory meningioma (SM), cystic schwannoma (CS) and cystic high-grade glioma (CG). We identified 1008 different proteins; 74 of these proteins were found at least once in the cystic fluid of all tumors. The most abundant proteins common to all tumors studied derived from plasma, with the exception of prostaglandin D2 synthase, which is a marker of cerebrospinal fluid origin. Overall, the protein composition of cystic fluid obtained at different times from the same tumor remained stable. After the identification of differentially expressed proteins (DEPs) and the protein–protein interaction network analysis, we identified the presence of tumor-specific pathways that may help to characterize tumor–host interactions. Our results suggest that plasma proteins leaking from local blood–brain barrier disruption are important contributors to cyst fluid formation, but cerebrospinal fluid (CSF) and the tumor itself also contribute to the cystic fluid proteome and, in some cases, as with immunoglobulin G, shows tumor-specific variations that cannot be simply explained by differences in vessel permeability or blood contamination. - The Protein Network in Subcutaneous Fat Biopsies from Patients with AL Amyloidosis: More Than Diagnosis?
Dario Di Silvestre, Francesca Brambilla, Francesca Lavatelli, Maila Chirivì, Diana Canetti, Claudia Bearzi, Roberto Rizzi, Johan Bijzet, Bouke P. C. Hazenberg, Vittorio Bellotti, Julian D. Gillmore, Pierluigi Mauri
Cells, 2023
AL amyloidosis is caused by the misfolding of immunoglobulin light chains leading to an impaired function of tissues and organs in which they accumulate. Due to the paucity of -omics profiles from undissected samples, few studies have addressed amyloid-related damage system wide. To fill this gap, we evaluated proteome changes in the abdominal subcutaneous adipose tissue of patients affected by the AL isotypes κ and λ. Through our retrospective analysis based on graph theory, we have herein deduced new insights representing a step forward from the pioneering proteomic investigations previously published by our group. ECM/cytoskeleton, oxidative stress and proteostasis were confirmed as leading processes. In this scenario, some proteins, including glutathione peroxidase 1 (GPX1), tubulins and the TRiC complex, were classified as biologically and topologically relevant. These and other results overlap with those already reported for other amyloidoses, supporting the hypothesis that amyloidogenic proteins could induce similar mechanisms independently of the main fibril precursor and of the target tissues/organs. Of course, further studies based on larger patient cohorts and different tissues/organs will be essential, which would be a key point that would allow for a more robust selection of the main molecular players and a more accurate correlation with clinical aspects. - Thymic Epithelial Cell Alterations and Defective Thymopoiesis Lead to Central and Peripheral Tolerance Perturbation in MHCII Deficiency
Francesca Ferrua, Ileana Bortolomai, Elena Fontana, Dario Di Silvestre, Rosita Rigoni, Genni Enza Marcovecchio, Elena Draghici, Francesca Brambilla, Maria Carmina Castiello, Gloria Delfanti, Despina Moshous, Capucine Picard, Tom Taghon, Victoria Bordon, Ansgar S. Schulz, Catharina Schuetz, Silvia Giliani, Annarosa Soresina, Andrew R. Gennery, Sara Signa, Blachy J. Dávila Saldaña, Ottavia M. Delmonte, Luigi D. Notarangelo, Chaim M. Roifman, Pietro Luigi Poliani, Paolo Uva, Pier Luigi Mauri, Anna Villa, Marita Bosticardo
Frontiers in Immunology, 2021
Major Histocompatibility Complex (MHC) class II (MHCII) deficiency (MHCII-D), also known as Bare Lymphocyte Syndrome (BLS), is a rare combined immunodeficiency due to mutations in genes regulating expression of MHCII molecules. MHCII deficiency results in impaired cellular and humoral immune responses, leading to severe infections and autoimmunity. Abnormal cross-talk with developing T cells due to the absence of MHCII expression likely leads to defects in thymic epithelial cells (TEC). However, the contribution of TEC alterations to the pathogenesis of this primary immunodeficiency has not been well characterized to date, in particular in regard to immune dysregulation. To this aim, we have performed an in-depth cellular and molecular characterization of TEC in this disease. We observed an overall perturbation of thymic structure and function in both MHCII−/−mice and patients. Transcriptomic and proteomic profiling of murine TEC revealed several alterations. In particular, we demonstrated that impairment of lymphostromal cross-talk in the thymus of MHCII−/−mice affects mTEC maturation and promiscuous gene expression and causes defects of central tolerance. Furthermore, we observed peripheral tolerance impairment, likely due to defective Treg cell generation and/or function and B cell tolerance breakdown. Overall, our findings reveal disease-specific TEC defects resulting in perturbation of central tolerance and limiting the potential benefits of hematopoietic stem cell transplantation in MHCII deficiency. - Equine mesenchymal stem/stromal cells freeze-dried secretome (Lyosecretome) for the treatment of musculoskeletal diseases: Production process validation and batch release test for clinical use
Michela Mocchi, Stefano Grolli, Silvia Dotti, Dario Di Silvestre, Riccardo Villa, Priscilla Berni, Virna Conti, Giulia Passignani, Francesca Brambilla, Maurizio Del Bue, Laura Catenacci, Milena Sorrenti, Lorena Segale, Elia Bari, Pierluigi Mauri, Maria Luisa Torre, Sara Perteghella
Pharmaceuticals, 2021 - Plasma exosomes characterization reveals a perioperative protein signature in older patients undergoing different types of on-pump cardiac surgery
Alessandro Carrozzo, Valentina Casieri, Dario Di Silvestre, Francesca Brambilla, Emanuele De Nitto, Nicola Sardaro, Gaia Papini, Simona Storti, Giuseppina Settanni, Marco Solinas, Pierluigi Mauri, Domenico Paparella, Vincenzo Lionetti
Geroscience, 2021 - Clinical amyloid typing by proteomics: Performance evaluation and data sharing between two centres
Diana Canetti, Francesca Brambilla, Nigel B. Rendell, Paola Nocerino, Janet A. Gilbertson, Dario Di Silvestre, Andrea Bergamaschi, Francesca Lavatelli, Giampaolo Merlini, Julian D. Gillmore, Vittorio Bellotti, Pierluigi Mauri, Graham W. Taylor
Molecules, 2021 - Caloric Restriction Promotes Immunometabolic Reprogramming Leading to Protection from Tuberculosis
Carla Palma, Claudia La Rocca, Vincenzo Gigantino, Gabriella Aquino, Giovanni Piccaro, Dario Di Silvestre, Francesca Brambilla, Rossana Rossi, Fabrizia Bonacina, Maria Teresa Lepore, Matteo Audano, Nico Mitro, Gerardo Botti, Sara Bruzzaniti, Clorinda Fusco, Claudio Procaccini, Veronica De Rosa, Mario Galgani, Carlo Alviggi, Annibale Puca, Fabio Grassi, Tanja Rezzonico-Jost, Giuseppe Danilo Norata, Pierluigi Mauri, Mihai G. Netea, Paola de Candia, Giuseppe Matarese
Cell Metabolism, 2021 - A new pathway promotes adaptation of human glioblastoma cells to glucose starvation
Alberto Azzalin, Francesca Brambilla, Eloisa Arbustini, Katia Basello, Attilio Speciani, Pierluigi Mauri, Paola Bezzi, Lorenzo Magrassi
Cells, 2020 - Cryo-EM structure of cardiac amyloid fibrils from an immunoglobulin light chain AL amyloidosis patient
Paolo Swuec, Francesca Lavatelli, Masayoshi Tasaki, Cristina Paissoni, Paola Rognoni, Martina Maritan, Francesca Brambilla, Paolo Milani, Pierluigi Mauri, Carlo Camilloni, Giovanni Palladini, Giampaolo Merlini, Stefano Ricagno, Martino Bolognesi
Nature Communications, 2019 - Cardioprotection by cardiac progenitor cell-secreted exosomes: Role of pregnancy-associated plasma protein-A
Lucio Barile, Elisabetta Cervio, Vincenzo Lionetti, Giuseppina Milano, Alessandra Ciullo, Vanessa Biemmi, Sara Bolis, Claudia Altomare, Marco Matteucci, Dario Di Silvestre, Francesca Brambilla, Tudor Emanuel Fertig, Tiziano Torre, Stefanos Demertzis, Pierluigi Mauri, Tiziano Moccetti, Giuseppe Vassalli
Cardiovascular Research, 2018 - Proteomics-based network analysis characterizes biological processes and pathways activated by preconditioned mesenchymal stem cells in cardiac repair mechanisms
Dario Di Silvestre, Francesca Brambilla, Giovanni Scardoni, Pietro Brunetti, Sara Motta, Marco Matteucci, Carlo Laudanna, Fabio A. Recchia, Vincenzo Lionetti, Pierluigi Mauri
Biochimica Et Biophysica Acta General Subjects, 2017 - The Proteomic Landscape of Human Ex Vivo Regulatory and Conventional T Cells Reveals Specific Metabolic Requirements [Immunity 44, 406-421, (2016)]
Claudio Procaccini, Fortunata Carbone, Dario Di Silvestre, Francesca Brambilla, Veronica De Rosa, Mario Galgani, Deriggio Faicchia, Gianni Marone, Donatella Tramontano, Marco Corona, Carlo Alviggi, Antonio Porcellini, Antonio La Cava, Pierluigi Mauri, Giuseppe Matarese
Immunity, 2016 - The Proteomic Landscape of Human Ex Vivo Regulatory and Conventional T Cells Reveals Specific Metabolic Requirements
Claudio Procaccini, Fortunata Carbone, Dario Di Silvestre, Francesca Brambilla, Veronica De Rosa, Mario Galgani, Deriggio Faicchia, Gianni Marone, Donatella Tramontano, Marco Corona, Carlo Alviggi, Antonio Porcellini, Antonio La Cava, Pierluigi Mauri, Giuseppe Matarese
Immunity, 2016 - Bottom-Up Proteomics
Dario Di Silvestre, Francesca Brambilla, Giulio Agnetti, Pierluigi Mauri
Manual of Cardiovascular Proteomics, 2016 - Evaluation of Proteomic Data: From Profiling to Network Analysis by Way of Biomarker Discovery
Dario Di Silvestre, Francesca Brambilla, Sara Motta, Pierluigi Mauri
Biomarker Validation Technological Clinical and Commercial Aspects, 2015 - Regional mapping of myocardial hibernation phenotype in idiopathic end-stage dilated cardiomyopathy
Vincenzo Lionetti, Marco Matteucci, Marco Ribezzo, Dario Di Silvestre, Francesca Brambilla, Silvia Agostini, Pierluigi Mauri, Luigi Padeletti, Alessandro Pingitore, Luisa Delsedime, Mauro Rinaldi, Fabio A. Recchia, Angela Pucci
Journal of Cellular and Molecular Medicine, 2014 - Shotgun protein profile of human adipose tissue and its changes in relation to systemic amyloidoses
Francesca Brambilla, Francesca Lavatelli, Dario Di Silvestre, Veronica Valentini, Giovanni Palladini, Giampaolo Merlini, Pierluigi Mauri
Journal of Proteome Research, 2013 - Availability of MudPIT data for classification of biological samples
Dario Silvestre, Italo Zoppis, Francesca Brambilla, Valeria Bellettato, Giancarlo Mauri, Pierluigi Mauri
Journal of Clinical Bioinformatics, 2013 - Multidimensional protein identification technology for direct-tissue proteomics of heart
Dario Di Silvestre, Francesca Brambilla, Pier Luigi Mauri
Methods in Molecular Biology, 2013 - Clinical proteomics for diagnosis and typing of systemic amyloidoses
Francesca Brambilla, Francesca Lavatelli, Giampaolo Merlini, Pierluigi Mauri
Proteomics Clinical Applications, 2013 - Changes in tissue proteome associated with ATTR amyloidosis: Insights into pathogenesis
Francesca Brambilla, Francesca Lavatelli, Veronica Valentini, Dario Di Silvestre, Laura Obici, Pierluigi Mauri, Giampaolo Merlini
Amyloid, 2012 - HPLC-Chip-Multiple Reaction Monitoring (MRM) method for the label-free absolute quantification of γ-conglutin in lupin: Proteotypic peptides and standard addition method
Donatella Resta, Francesca Brambilla, Anna Arnoldi
Food Chemistry, 2012 - Reliable typing of systemic amyloidoses through proteomic analysis of subcutaneous adipose tissue
Francesca Brambilla, Francesca Lavatelli, Dario Di Silvestre, Veronica Valentini, Rossana Rossi, Giovanni Palladini, Laura Obici, Laura Verga, Pierluigi Mauri, Giampaolo Merlini
Blood, 2012 - A novel approach for the purification and proteomic analysis of pathogenic immunoglobulin free light chains from serum
Francesca Lavatelli, Francesca Brambilla, Veronica Valentini, Paola Rognoni, Simona Casarini, Dario Di Silvestre, Vittorio Perfetti, Giovanni Palladini, Gabriele Sarais, Pierluigi Mauri, Giampaolo Merlini
Biochimica Et Biophysica Acta Proteins and Proteomics, 2011 - The effects of various processing conditions on a protein isolate from Lupinus angustifolius
Elena Sirtori, Donatella Resta, Francesca Brambilla, Christian Zacherl, Anna Arnoldi
Food Chemistry, 2010 - A label-free internal standard method for the differential analysis of bioactive lupin proteins using nano HPLC-Chip coupled with Ion Trap mass spectrometry
Francesca Brambilla, Donatella Resta, Ilena Isak, Marco Zanotti, Anna Arnoldi
Proteomics, 2009 - Parameters for the evaluation of the thermal damage and nutraceutical potential of lupin-based ingredients and food products
Anna Arnoldi, Donatella Resta, Francesca Brambilla, Giovanna Boschin, Alessandra D'Agostina, Elena Sirtori, Francesca O'Kane
Molecular Nutrition and Food Research, 2007
