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1.

001-es BibID:BIBFORM036955
Első szerző:Beyer Dániel (molekuláris biológus)
Cím:Microcystin-LR, a protein phosphatase inhibitor, induces alterations in mitotic chromatin and microtubule organization leading to the formation of micronuclei in Vicia faba / Beyer, D., Tandor, I., Konya, Z., Batori, R., Roszik, J., Vereb, G., Erdodi, F., Vasas, G., M-Hamvas, M., Jambrovics, K., Mathe, C.
Dátum:2012
ISSN:0305-7364
Megjegyzések:Background and Aims Microcystin-LR (MCY-LR) is a cyanobacterial toxin, a specific inhibitor of type 1 and 2A protein phosphatases (PP1 and PP2A) with significant impact on aquatic ecosystems. It has the potential to alter regulation of the plant cell cycle. The aim of this study was improved understanding of the mitotic alterations induced by cyanotoxin in Vicia faba, a model organism for plant cell biology studies. Methods Vicia faba seedlings were treated over the long and short term with MCY-LR purified in our laboratory. Short-term treatments were performed on root meristems synchronized with hydroxylurea. Sections of lateral root tips were labelled for chromatin, phosphorylated histone H3 and β-tubulin via histochemical and immunohistochemical methods. Mitotic activity and the occurrence of mitotic alterations were detected and analysed by fluorescence microscopy. The phosphorylation state of histone H3 was studied by Western blotting. Key Results Long-term MCY-LR exposure of lateral root tip meristems increased the percentage of either early or late mitosis in a concentration-dependent manner. We observed hypercondensed chromosomes and altered sister chromatid segregation (lagging chromosomes) leading to the formation of micronuclei, accompanied by the formation of disrupted, multipolar and monopolar spindles, disrupted phragmoplasts and the hyperphosphorylation of histone H3 at Ser10. Short-term MCY-LR treatment of synchronized cells showed that PP1 and PP2A inhibition delayed the onset of anaphase at 1 mikrog mL(-1) MCY-LR, accelerated cell cycle at 10 mikrog mL(-1) MCY-LR and induced the formation of lagging chromosomes. In this case mitotic microtubule alterations were not detected, but histone H3 was hyperphosphorylated. Conclusions MCY-LR delayed metaphase-anaphase transition. Consequently, it induced aberrant chromatid segregation and micronucleus formation that could be associated with both H3 hyperphosphorylation and altered microtubule organization. However, these two phenomena seemed to be independent. The toxin may be a useful tool in the study of plant cell cycle regulation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
microcystin-LR
protein phosphatase
mitosis
chromatin
microtubule
phospho-histone H3
micronucleus
Vicia faba
Molekuláris Medicina
Megjelenés:Annals Of Botany 110 : 4 (2012), p. 797-808. -
További szerzők:Tándor Ildikó Kónya Zoltán (1986-) (molekuláris biológus, biokémikus) Bátori Róbert Károly (1983-) (biológus, biotechnológus) Roszik János (1979-) (biofizikus) Vereb György (1965-) (biofizikus, orvos) Erdődi Ferenc (1953-) (biokémikus) Vasas Gábor (1975-) (biológus-vegyész) Mikóné Hamvas Márta (1963-) (biológus) Jambrovics Károly (1988-) (biológus, gyógyszer-biotechnológus) Máthé Csaba (1966-) (biológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Biomolekuláris interakciók jellemzőinek kvantitatív meghatározása
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
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2.

001-es BibID:BIBFORM007283
Első szerző:Beyer Dániel (molekuláris biológus)
Cím:Cylindrospermopsin induces alterations of root histology and microtubule organization in common reed (Phragmites australis) plantlets cultured in vitro / Beyer D., Surányi G., Vasas G., Roszik J., Erdődi F., M-Hamvas M., Bácsi I., Bátori R., Serfőző Z., Szigeti Zs., Vereb Gy., Demeter Z., Gonda S., Máthé C.
Dátum:2009
ISSN:0041-0101
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
cylindrospermopsin
microtubules
chromatin
cell swelling
necrosis
Phragmites australis
Megjelenés:Toxicon 54 : 4 (2009), p. 440-449. -
További szerzők:Surányi Gyula (1957-) (biológus) Vasas Gábor (1975-) (biológus-vegyész) Roszik János (1979-) (biofizikus) Erdődi Ferenc (1953-) (biokémikus) Mikóné Hamvas Márta (1963-) (biológus) Bácsi István (1977-) (biológus) Bátori Róbert Károly (1983-) (biológus, biotechnológus) Serfőző Zoltán Máthéné Szigeti Zsuzsa (1976-) (biológus-ökológus) Vereb György (1965-) (biofizikus, orvos) Demeter Zita (1985-) (biológia-kémia szakos tanár) Gonda Sándor (1984-) (gyógyszerész) Máthé Csaba (1966-) (biológus)
Internet cím:DOI
elektronikus változat
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3.

001-es BibID:BIBFORM057538
035-os BibID:(scopus)84910122146 (wos)000345023400059
Első szerző:Govers, Coen
Cím:TCRs genetically linked to CD28 and CD3[epszilon] do not mispair with endogenous TCR chains and mediate enhanced t cell persistence and anti-melanoma activity / Coen Govers, Zsolt Sebestyén, János Roszik, Mandy van Brakel, Cor Berrevoets, Árpád Szöőr, Konstantina Panoutsopoulou, Marieke Broertjes, Tan Van, György Vereb, János Szöllősi, Reno Debets
Dátum:2014
ISSN:0022-1767 1550-6606
Megjegyzések:Adoptive transfer of T cells that are gene engineered to express a defined TCR represents a feasible and promising therapy for patients with tumors. However, TCR gene therapy is hindered by the transient presence and effectiveness of transferred T cells, which are anticipated to be improved by adequate T cell costimulation. In this article, we report the identification and characterization of a novel two-chain TCR linked to CD28 and CD3[epszilon] (i.e., TCR:28[epszilon]). This modified TCR demonstrates enhanced binding of peptide-MHC and mediates enhanced T cell function following stimulation with peptide compared with wild-type TCR. Surface expression of TCR:28[epszilon] depends on the transmembrane domain of CD28, whereas T cell functions depend on the intracellular domains of both CD28 and CD3[epszilon], with IL-2 production showing dependency on CD28:LCK binding. TCR:28[epszilon], but not wild-type TCR, induces detectable immune synapses in primary human T cells, and such immune synapses show significantly enhanced accumulation of TCR transgenes and markers of early TCR signaling, such as phosphorylated LCK and ERK. Importantly, TCR:28[epszilon] does not show signs of off-target recognition, as evidenced by lack of TCR mispairing, as well as preserved specificity. Notably, when testing TCR:28[epszilon] in immune-competent mice, we observed a drastic increase in T cell survival, which was accompanied by regression of large melanomas with limited recurrence. Our data argue that TCR transgenes that contain CD28, and, thereby, may provide T cell costimulation in an immune-suppressive environment, represent candidate receptors to treat patients with tumors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
TCR
T Cell
Megjelenés:Journal Of Immunology. - 193 : 10 (2014), p. 5315-5326. -
További szerzők:Sebestyén Zsolt Roszik János (1979-) (biofizikus) van Brakel, Mandy Berrevoets, Cor Szöőr Árpád (1984-) (orvos) Panoutsopoulou, Konstantina Broertjes, Marieke Van, Tan Vereb György (1965-) (biofizikus, orvos) Szöllősi János (1953-) (biofizikus) Debets, Reno
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
TÁMOP-4.2.2/B-10/1/2010-0024
TÁMOP
TÁMOP-4.2.2/A-11/1/KONV-20120025
TÁMOP
OTKA-NK101337
OTKA
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4.

001-es BibID:BIBFORM009423
Első szerző:Máthéné Szigeti Zsuzsa (biológus-ökológus)
Cím:Cytoskeletal and developmental alterations in Ceratophyllum demersum induced by microcystin-LR, a cyanobacterial toxin / Zsuzsa M. Szigeti, Katalin Jámbrik, János Roszik, Márta M-Hamvas, Ildikó Tándor, Dániel Beyer, Gábor Vasas, György Vereb, Gyula Surányi, Csaba Máthé
Dátum:2010
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Aquatic Botany. - 92 : 3 (2010), p. 179-184. -
További szerzők:Jámbrik Katalin Roszik János (1979-) (biofizikus) Mikóné Hamvas Márta (1963-) (biológus) Tándor Ildikó Beyer Dániel (1982-) (molekuláris biológus) Vasas Gábor (1975-) (biológus-vegyész) Vereb György (1965-) (biofizikus, orvos) Surányi Gyula (1957-) (biológus) Máthé Csaba (1966-) (biológus)
Internet cím:elektronikus változat
DOI
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5.

001-es BibID:BIBFORM073668
Első szerző:Roszik János (biofizikus)
Cím:Validating pharmacological disruption of protein-protein interactions by acceptor photobleaching FRET imaging / Janos Roszik, Gábor Tóth, János Szöllősi, György Vereb
Dátum:2013
Megjegyzések:Proteins are the major targets of drug discovery and many of the new drugs are designed to exert theireffect by disrupting protein-protein interactions. Validation of the inhibition of molecular interactions isgenerally done by biochemical methods, however, these are often not feasible when the interaction is notstable enough. Fluorescence resonance energy transfer (FRET) is an excellent tool for determining directmolecular interactions between two molecules in the cell membrane or inside cells in their natural state.Although originally established as a ? ow cytometric approach, FRET has been adapted for microscopy,allowing for analysis of sub-cellular co-localization at the single cell level. In this chapter, we provide theoreticalintroductionto the phenomenon of FRET,and a protocol- including labeling techniques, measurement,and evaluation of microscopyimages - of the simplest microscopicFRET approach,acceptorphotobleachingFRET.This technique is generally usable for studying proteininteractions and requiresonlya standardconfocal laser scanning microscope.Todemonstrate the value of image based FRET fortestingpharmacologicaldisruptionof protein-proteininteractions, we show how inhibition of the heterodimerizationof ErbB2 and ErbB1 by the humanized monoclonal antibody pertuzumab can be validated using this technique.
ISBN:978 162 703 310 7
Tárgyszavak:Orvostudományok Elméleti orvostudományok könyvfejezet
Förster resonance energy transfer
Image cytometry
Protein interactions
Pertuzumab
ErbB2
ErbB1
Molekuláris Medicina
Megjelenés:Target Identification and Validation in Drug Discovery / eds. Jürgen Moll, Riccardo Colombo. - p. 165-78. -
További szerzők:Tóth Gábor (1989-) (általános orvos) Szöllősi János (1953-) (biofizikus) Vereb György (1965-) (biofizikus, orvos)
Pályázati támogatás:K75752
OTKA
NK101337
OTKA
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Receptor tirozin kinázok mint terápiás célpontok: működésük szabályozásának, és a közöttük fellépő molekuláris kölcsönhatások vizsgálata
4.2.2/A-11/1/KONV-2012-0025
TÁMOP
Baross Gabor programme REG-EA-09-1-2009-0010
Egyéb
ETT 362-01/2009
Egyéb
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6.

001-es BibID:BIBFORM020768
Első szerző:Roszik János (biofizikus)
Cím:T-cell synapse formation depends on antigen recognition but not CD3 interaction : studies with TCR : zeta, a candidate transgene for TCR gene therapy / Roszik J., Sebestyén Z., Govers C., Guri Y., Szöor A., Pályi-Krekk Z., Vereb G., Nagy P., Szöllosi J., Debets R.
Dátum:2011
Megjegyzések:T-cell receptors (TCRs) can be genetically modified to improve gene-engineered T-cell responses, a strategy considered critical for the success of clinical TCR gene therapy to treat cancers. TCR:zeta, which is a heterodimer of TCRalpha and beta chains each coupled to complete human CD3zeta, overcomes issues of mis-pairing with endogenous TCR chains, shows high surface expression and mediates antigen-specific T-cell functions in vitro. In the current study, we further characterized TCR:zeta in gene-engineered T cells and assessed whether this receptor is able to interact with surface molecules and drive correct synapse formation in Jurkat T cells. The results showed that TCR:zeta mediates the formation of synaptic areas with antigen-positive target cells, interacts closely with CD8alpha and MHC class I (MHCI), and co-localizes with CD28, CD45 and lipid rafts, similar to WT TCR. TCR:zeta did not closely associate with endogenous CD3epsilon, despite its co-presence in immune synapses, and TCR:zeta showed enhanced synaptic accumulation in T cells negative for surface-expressed TCR molecules. Notably, synaptic TCR:zeta demonstrated lowered densities when compared with TCR in dual TCR T cells, a phenomenon that was related to both extracellular and intracellular CD3zeta domains present in the TCR:zeta molecule and responsible for enlarged synapse areas
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Adoptive Transfer
Antigens
Antigens,CD28
Antigens,CD3
Antigens,CD45
Antigens,CD8
article
Biophysics
Cells
Flow Cytometry
Gene Therapy
genetics
Histocompatibility Antigens
Histocompatibility Antigens Class I
Human
Humans
Hungary
Immunity,Cellular
Immunological Synapses
immunology
In Vitro
Jurkat Cells
lipid raft
LIPID RAFTS
Membrane Microdomains
metabolism
physiology
Receptor-CD3 Complex,Antigen,T-Cell
Receptors,Antigen,T-Cell,alpha-beta
Research
Research Support
Support
Synapses
T-Lymphocytes
therapy
Transgenes
Megjelenés:European Journal of Immunology. - 41 : 5 (2011), p. 1288-1297. -
További szerzők:Sebestyén Zsolt Govers, Coen Guri, Yakir Szöőr Árpád (1984-) (orvos) Pályiné Krekk Zsuzsanna (1974-) (molekuláris biológus) Vereb György (1965-) (biofizikus, orvos) Nagy Péter (1971-) (biofizikus) Szöllősi János (1953-) (biofizikus) Debets, Reno
Internet cím:DOI
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7.

001-es BibID:BIBFORM010361
035-os BibID:(scopus)68849090496 (wos)000269333400005
Első szerző:Roszik János (biofizikus)
Cím:Evaluation of intensity-based ratiometric FRET in image cytometry-approaches and a software solution / Roszik, J., Lisboa, D., Szollosi, J., Vereb, G.
Dátum:2009
ISSN:1552-4922 (Print)
Megjegyzések:The intensity-based ratiometric FRET (fluorescence resonance energy transfer) method is a powerful technique for following molecular interactions in living cells. Since it is not based on irreversibly destroying the donor or the acceptor fluorophores, the time course of changes in FRET efficiency values can be monitored by this method. ImageJ, a sophisticated software tool for many types of image processing allows users to extend it with programs for various purposes. Implementing intensity-based ratiometric FRET with ImageJ vastly enhances the applicability of the FRET method. We developed an efficient ImageJ plugin, RiFRET, which calculates FRET efficiency on a pixel-by-pixel basis from ratiometric FRET images. It allows the user to correct for channel cross-talk (bleed-through) and to calculate FRET from image stacks, i.e., from 3D data sets. Semiautomatic processing for larger datasets is also included in the program. Furthermore, several options for calibrating FRET efficiency calculations were tested and their applicability to various expression systems is discussed. Although the ratiometric FRET method is widely applied, our plugin is the first freely available software for evaluating such FRET data. The program is user friendly and provides reliable, standardized results.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Cells
cytometry
Energy Transfer
Fluorescence
Fluorescence Resonance Energy Transfer
FRET
Image Processing
Software
time
Megjelenés:Cytometry. Part A. - 75A : 9 (2009), p. 761-767. -
További szerzők:Lisboa, Duarte (1982-) (biotechnológus) Szöllősi János (1953-) (biofizikus) Vereb György (1965-) (biofizikus, orvos)
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8.

001-es BibID:BIBFORM003489
035-os BibID:(scopus)54549105754 (wos)000260487500001
Első szerző:Roszik János (biofizikus)
Cím:AccPbFRET : an ImageJ plugin for semi-automatic, fully corrected analysis of acceptor photobleaching FRET images / Roszik János, Szöllősi János, Vereb György
Dátum:2008
Megjegyzések:The acceptor photobleaching fluorescence resonance energy transfer (FRET) method is widely used for monitoring molecular interactions in cells. This method of FRET, while among those with the simplest mathematics, is robust, self-controlled and independent of fluorophore amounts and ratios. RESULTS: AccPbFRET is a user-friendly, efficient ImageJ plugin which allows fully corrected, pixel-wise calculation and detailed, ROI (region of interest)-based analysis of FRET efficiencies in microscopic images. Furthermore, automatic registration and semi-automatic analysis of large image sets is provided, which are not available in any existing FRET evaluation software. CONCLUSIONS: Despite of the widespread applicability of the acceptor photobleaching FRET technique, this is the first paper where all possible sources of major errors of the measurement and analysis are considered, and AccPbFRET is the only program which provides the complete suite of corrections - for registering image pairs, for unwanted photobleaching of the donor, for cross-talk of the acceptor and/or its photoproduct to the donor channel and for partial photobleaching of the acceptor. The program efficiently speeds up the analysis of large image sets even for novice users and is freely available.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
acceptor photobleaching
FRET
CLSM
software
Megjelenés:BMC Bioinformatics. - 9 : 1 (2008), p. 346. -
További szerzők:Szöllősi János (1953-) (biofizikus) Vereb György (1965-) (biofizikus, orvos)
Internet cím:elektronikus változat
DOI
elektronikus változat
Borító:

9.

001-es BibID:BIBFORM022510
Első szerző:Váradi Tímea (okleveles vegyész)
Cím:ErbB protein modifications are secondary to severe cell membrane alterations induced by elisidepsin treatment / Váradi T., Roszik J., Lisboa D., Vereb G., Molina-Guijarro J. M., Galmarini C. M., Szöllosi J., Nagy P.
Dátum:2011
Megjegyzések:Elisidepsin is a marine-derived anti-tumor agent with unique mechanism of action. It has been suggested to induce necrosis associated with severe membrane damage. Since indirect evidence points to the involvement of ErbB receptor tyrosine kinases and lipid rafts in the mechanism of action of elisidepsin, we investigated the effect of the drug on the distribution of ErbB proteins and systematically compared the elisidepsin sensitivity of cell lines overexpressing ErbB receptors. Stable expression of a single member of the ErbB family (ErbB1-3) or co-transfection of ErbB2 and ErbB3 did not modify the elisidepsin sensitivity of CHO and A431 cells. However, elisidepsin induced the redistribution of ErbB3 and two GPI-anchored proteins (transfected GPI-anchored eGFP and placental alkaline phosphatase) from the plasma membrane to intracellular vesicles without comparable effects on ErbB1 and ErbB2. Elisidepsin increased the binding of a conformational sensitive anti-ErbB3 antibody without modifying the binding of other ErbB2 or ErbB3 antibodies, and it decreased the homoassociation of both ErbB2 and ErbB3. We also found that elisidepsin decreased the fluorescence anisotropy of a membrane specific fluorescent probe and induced a blue shift in the emission spectrum of Laurdan pointing to significant changes in the order of the plasma membrane possibly associated with the formation of liquid ordered domains. Although the distribution of ErbB proteins is preferentially altered by elisidepsin, our data question their role in determining sensitivity to the drug. We assume that induction of liquid ordered domains is the primary action of elisidepsin leading to all the other observed changes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Elisidepsin
ErbB proteins
Liquid ordered domain
FRET
Megjelenés:European Journal of Pharmacology 667 : 1-3 (2011), p. 91-99. -
További szerzők:Roszik János (1979-) (biofizikus) Lisboa, Duarte (1982-) (biotechnológus) Vereb György (1965-) (biofizikus, orvos) Molina-Guijarro, J. M. Galmarini, Carlos M. Szöllősi János (1953-) (biofizikus) Nagy Péter (1971-) (biofizikus)
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