Balint Csoboz

• Munoz, Sara Orellana; Haberkorn, Chloé; Csoboz, Balint; Stelkens, Rike & Peris, David (2026). Mitochondrial inheritance as an important parameter for the rational design of synthetic yeast polyploids. BioRxiv. ISSN 0362-4331. doi: https:/www.biorxiv.org/content/10.64898/2026.09.22.753424v1. Fulltekst i vitenarkiv
• Csoboz, Balint; Gombos, Imre; Kóta, Zoltán; Dukic, Barbara; Klement, Éva & Varga-Zsíros, Vanda [Vis alle 10 forfattere av denne artikkelen] (2022). The Small Heat Shock Protein, HSPB1, Interacts with and Modulates the Physical Structure of Membranes. International Journal of Molecular Sciences. ISSN 1661-6596. 23(13). doi: 10.3390/ijms23137317. Fulltekst i vitenarkiv Vis sammendrag

  Small heat shock proteins (sHSPs) have been demonstrated to interact with lipids and modulate the physical state of membranes across species. Through these interactions, sHSPs contribute to the maintenance of membrane integrity. HSPB1 is a major sHSP in mammals, but its lipid interaction profile has so far been unexplored. In this study, we characterized the interaction between HSPB1 and phospholipids. HSPB1 not only associated with membranes via membrane-forming lipids, but also showed a strong affinity towards highly fluid membranes. It participated in the modulation of the physical properties of the interacting membranes by altering rotational and lateral lipid mobility. In addition, the in vivo expression of HSPB1 greatly affected the phase behavior of the plasma membrane under membrane fluidizing stress conditions. In light of our current findings, we propose a new function for HSPB1 as a membrane chaperone.

• Dukay, Brigitta; Walter, Fruzsina; Vigh, Judit; Barabasi, Beata; Hajdu, Petra & Balassa, Tamas [Vis alle 19 forfattere av denne artikkelen] (2021). Neuroinflammatory processes are augmented in mice overexpressing human heat-shock protein B1 following ethanol-induced brain injury. Journal of Neuroinflammation. 18. doi: 10.1186/s12974-020-02070-2. Fulltekst i vitenarkiv Vis sammendrag

  Background - Heat-shock protein B1 (HSPB1) is among the most well-known and versatile member of the evolutionarily conserved family of small heat-shock proteins. It has been implicated to serve a neuroprotective role against various neurological disorders via its modulatory activity on inflammation, yet its exact role in neuroinflammation is poorly understood. In order to shed light on the exact mechanism of inflammation modulation by HSPB1, we investigated the effect of HSPB1 on neuroinflammatory processes in an in vivo and in vitro model of acute brain injury.<p> <p>Methods - In this study, we used a transgenic mouse strain overexpressing the human HSPB1 protein. In the in vivo experiments, 7-day-old transgenic and wild-type mice were treated with ethanol. Apoptotic cells were detected using TUNEL assay. The mRNA and protein levels of cytokines and glial cell markers were examined using RT-PCR and immunohistochemistry in the brain. We also established primary neuronal, astrocyte, and microglial cultures which were subjected to cytokine and ethanol treatments. TNFα and hHSPB1 levels were measured from the supernates by ELISA, and intracellular hHSPB1 expression was analyzed using fluorescent immunohistochemistry.<p> <p>Results - Following ethanol treatment, the brains of hHSPB1-overexpressing mice showed a significantly higher mRNA level of pro-inflammatory cytokines (Tnf, Il1b), microglia (Cd68, Arg1), and astrocyte (Gfap) markers compared to wild-type brains. Microglial activation, and 1 week later, reactive astrogliosis was higher in certain brain areas of ethanol-treated transgenic mice compared to those of wild-types. Despite the remarkably high expression of pro-apoptotic Tnf, hHSPB1-overexpressing mice did not exhibit higher level of apoptosis. Our data suggest that intracellular hHSPB1, showing the highest level in primary astrocytes, was responsible for the inflammation-regulating effects. Microglia cells were the main source of TNFα in our model. Microglia isolated from hHSPB1-overexpressing mice showed a significantly higher release of TNFα compared to wild-type cells under inflammatory conditions.<p> <p>Conclusions</i> - Our work provides novel in vivo evidence that hHSPB1 overexpression has a regulating effect on acute neuroinflammation by intensifying the expression of pro-inflammatory cytokines and enhancing glial cell activation, but not increasing neuronal apoptosis. These results suggest that hHSPB1 may play a complex role in the modulation of the ethanol-induced neuroinflammatory response.

• Crul, Tim; Csoboz, Balint; Gombos, Imre; Marton, Annamaria; Peter, Maria & Balogh, Gabor [Vis alle 9 forfattere av denne artikkelen] (2020). Modulation of Plasma Membrane Composition and Microdomain Organization Impairs Heat Shock Protein Expression in B16-F10 Mouse Melanoma Cells. Cells. 9(4), s. 1–14. doi: 10.3390/cells9040951. Fulltekst i vitenarkiv Vis sammendrag

  The heat shock response (HSR) regulates induction of stress/heat shock proteins (HSPs) to preserve proteostasis during cellular stress. Earlier, our group established that the plasma membrane (PM) acts as a sensor and regulator of HSR through changes in its microdomain organization. PM microdomains such as lipid rafts, dynamic nanoscale assemblies enriched in cholesterol and sphingomyelin, and caveolae, cholesterol-rich PM invaginations, constitute clustering platforms for proteins functional in signaling cascades. Here, we aimed to compare the effect of cyclodextrin (MβCD)- and nystatin-induced cholesterol modulations on stress-activated expression of the representative HSPs, HSP70, and HSP25 in mouse B16-F10 melanoma cells. Depletion of cholesterol levels with MβCD impaired the heat-inducibility of both HSP70 and HSP25. Sequestration of cholesterol with nystatin impaired the heat-inducibility of HSP25 but not of HSP70. Imaging fluorescent correlation spectroscopy marked a modulated lateral diffusion constant of fluorescently labelled cholesterol in PM during cholesterol deprived conditions. Lipidomics analysis upon MβCD treatment revealed, next to cholesterol reductions, decreased lysophosphatidylcholine and phosphatidic acid levels. These data not only highlight the involvement of PM integrity in HSR but also suggest that altered dynamics of specific cholesterol pools could represent a mechanism to fine tune HSP expression.

• Csoboz, Balint; Rasheed, Kashif; Sveinbjørnsson, Baldur & Moens, Ugo (2020). Merkel cell polyomavirus and non-Merkel cell carcinomas: Guilty or circumstantial evidence? APMIS - Journal of Pathologiy, Microbiology and Immunology. ISSN 0903-4641. s. 1–17. doi: 10.1111/apm.13019. Fulltekst i vitenarkiv Vis sammendrag

  Merkel cell polyomavirus (MCPyV) is the major causative factor of the rare but aggressive cancer, Merkel cell carcinoma (MCC). Two characteristics of MCPyV‐positive MCCs are integration of the viral genome and expression of a truncated version of one of its oncogenic proteins, namely large T antigen. The strong association of MCPyV with MCC development has incited researchers to further investigate a possible role of this virus in other cancers. However, many of the examples displaying the presence of the virus in the various non‐MCC cancers are not able to clearly demonstrate a direct connection between cellular transformation and the presence of the virus. The prevalence of the virus is significantly lower in non‐MCC cancers compared to MCCs, with a lower level of viral load and sparse viral protein expression. Moreover, the state of the viral genome, and whether a truncated large T antigen is expressed, has rarely been investigated. Nonetheless, considering the strong oncogenic potential of MCPyV proteins in MCC, the plausible contribution of MCPyV to transformation and cancer growth in non‐MCC tumors cannot be ruled out. Furthermore, the absence of MCPyV in cancers does not exclude a hit‐and‐run mechanism, or the oncoproteins of MCPyV may potentiate the neoplastic process mediated by co‐infecting oncoviruses such as high‐risk human papillomaviruses and Epstein–Barr virus. The current review is focusing on the available data describing the presence of MCPyV in non‐MCC tumors, with an aim to provide a comprehensive overview of the corresponding literature and to discuss the potential contribution of MCPyV to non‐MCC cancer in light of this.

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• Munoz, Sara Orellana; Haberkorn, Chloé; Csoboz, Balint; Stelkens, Rike & Peris, David (2026). Mitochondrial–nuclear interactions shape hybrid physiology in Saccharomyces. Fulltekst i vitenarkiv
• Peris, David; Munoz, Sara Orellana; Csoboz, Balint; Sorribes-Daudén, Raquel; Vanacloig-Pedrós, Elena & Aguilar-Díaz, Alejandro [Vis alle 11 forfattere av denne artikkelen] (2025). FunGIALab: Connecting Fungal Diversity, Evolution, and Biotechnological Applications. Fulltekst i vitenarkiv
• Csoboz, Balint (2022). Identification of MCPyV related metabolomic markers for Merkel Cell Carcinoma. Fulltekst i vitenarkiv
• Opstad, Ida Sundvor; Csoboz, Balint & Zabirnyk, Arsenii (2022). Big business comes with big responsibilities - Taking the leap by the Danish way. Digitalt Life Norway Blog. Fulltekst i vitenarkiv
• Csoboz, Balint; Konstantinell, Aelita Gloria Virginia; Skalko-Basnet, Natasa; Weng-Onn, Lui; Sveinbjørnsson, Baldur & Moens, Ugo (2019). Exosomal microRNA Profiles of Polyomavirus–Positive and -Negative Merkel Cell Carcinomas. Fulltekst i vitenarkiv

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