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1.

001-es BibID:BIBFORM004861
035-os BibID:(scopus)14644392200 (wos)000227768400023
Első szerző:Diermeier, Simone
Cím:Epidermal growth factor receptor coexpression modulates susceptibility to Herceptin in HER2/neu overexpressing breast cancer cells via specific erbB-receptor interaction and activation / Diermeier, S., Horvath, G., Knuechel-Clarke, R., Hofstaedter, F., Szollosi, J., Brockhoff, G.
Dátum:2005
ISSN:0014-4827
Megjegyzések:Growth factors and Herceptin specifically and differentially modulate cell proliferation of tumor cells. However, the mechanism of action on erbB-receptor level is incompletely understood. We evaluated Herceptin's capacity to modulate erbB-receptor activation and interaction on the cell surface level and thereby potentially impair cell proliferation of HER2/neu (c-erbB2) overexpressing breast cancer cells, both in the presence and absence of relevant growth factors. METHODS: BT474 and SK-BR-3 breast cancer cell lines were treated with Epidermal Growth Factor (EGF), Heregulin, and with Herceptin in different combinations. Kinetics of cell proliferation were evaluated flow cytometrically based on BrdU-labeling. Fluorescence Resonance Energy Transfer, ELISAs and phosphorylation site specific Western Blotting was performed to investigate erbB-receptor interaction and activation. RESULTS: EGF induced EGFR/EGFR and EGFR/c-erbB2 interactions correlate with stimulation of cell proliferation in BT474 cells. Both homo- and heterodimerization are considerably less pronounced in SK-BR-3 cells and heterointeraction is additionally reduced by EGF treatment, causing inhibition of cell proliferation. Heregulin stimulates cell proliferation extensively in both cell lines. Herceptin drives BT474 cells more efficiently into quiescence than it does with SK-BR-3 cells and thereby blocks cell cycle progress. In SK-BR-3 Herceptin treatment causes c-erbB2 phosphorylation of Y877 and Y1248, EGF induces Y877 and Y1112 phosphorylation. The Y1112 phosphorylation site, activated by EGF in SK-BR-3 cell, is bypassed in BT474. In addition the inhibitory capacity of Herceptin on BT474 and SK-BR-3 cell proliferation depends on the presence and absence of growth factors to a various extent. CONCLUSION: The growth inhibitory effect of Herceptin on c-erbB2 overexpressing breast cancer cells is considerably modulated by EGFR coexpression and consequently EGFR/c-erbB2 homo- and heterointeractions, as well as the presence or absence of growth factors. C-erbB2 overexpression alone is insufficient to predict the impact of growth factors and antibodies on cell proliferation. The optimization and specification of therapeutic approaches based on erbB-receptor targeting requires to account for EGFR coexpression as well as the potential presence of erbB-receptor relevant growth factors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Antibodies
Antibodies,Monoclonal
Antineoplastic Agents
Breast Neoplasms
Carcinoma
Cell Cycle
Cell Cycle Proteins
Cell Line
Cell Line, Tumor
Cell Proliferation
Cells
drug effects
Drug Resistance,Neoplasm
Drug Synergism
drug therapy
Energy Transfer
Epidermal Growth Factor
Female
Fluorescence
Fluorescence Resonance Energy Transfer
genetics
Growth Inhibitors
Humans
Kinetics
metabolism
methods
Neuregulin-1
pathology
pharmacology
Phosphorylation
physiology
Proteins
Receptor, Epidermal Growth Factor
Receptor, erbB-2
Receptors, Cell Surface
Research
Support
therapeutic use
Megjelenés:Experimental Cell Research. - 304 : 2 (2005), p. 604-619. -
További szerzők:Horváth Gábor (1974-) (biofizikus) Knuechel-Clarke, Ruth Hofstaedter, Ferdinand Szöllősi János (1953-) (biofizikus) Brockhoff, Gero
Internet cím:elektronikus változat
DOI
Borító:

2.

001-es BibID:BIBFORM003553
Első szerző:Kakuk Annamária (molekuláris biológus)
Cím:Nuclear and nucleolar localization signals and their targeting function in phosphatidylinositol 4-kinase PI4K230 / Kakuk A., Friedlander E., Vereb Gy. Jr., Lisboa, D., Bagossi P., Tóth G., Gergely P., Vereb Gy.
Dátum:2008
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
phosphatidylinositol 4-kinase
PI4K230
nuclear localization signal
NLS
nucleolar targeting
NTS
importins
permeabilized HeLa cells
import assay
Megjelenés:Experimental Cell Research. - 314 : 13 (2008), p. 2376-2388. -
További szerzők:Friedländer Elza (1980-) (biofizikus) Vereb György (1965-) (biofizikus, orvos) Lisboa, Duarte (1982-) (biotechnológus) Bagossi Péter (1966-2011) (biokémikus, vegyész) Tóth Gábor Gergely Pál (1947-) (biokémikus) Vereb György (1938-) (biokémikus, sejtbiológus)
Internet cím:elektronikus változat
DOI
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3.

001-es BibID:BIBFORM077512
Első szerző:Kristóf Endre (általános orvos)
Cím:Interleukin-6 released from differentiating human beige adipocytes improves browning / Endre Kristóf, Ágnes Klusóczki, Roland Veress, Abhirup Shaw, Zsolt Sándor Combi, Klára Varga, Ferenc Győry, Zoltán Balajthy, Péter Bai, Zsolt Bacso, László Fésüs
Dátum:2019
ISSN:0014-4827
Megjegyzések:Brown and beige adipocytes contribute significantly to the regulation of whole body energy expenditure and systemic metabolic homeostasis not exclusively by thermogenesis through mitochondrial uncoupling. Several studies have provided evidence in rodents that brown and beige adipocytes produce a set of adipokines ("batokines") which regulate local tissue homeostasis and have beneficial effects on physiological functions of the entire body. We observed elevated secretion of Interleukin (IL)-6, IL-8 and monocyte chemoattractant protein (MCP)-1, but not tumor necrosis factor alpha (TNFα) or IL-1β pro-inflammatory cytokines, by ex vivo differentiating human beige adipocytes (induced by either PPARγ agonist or irisin) compared to white. Higher levels of IL-6, IL-8 and MCP-1 were released from human deep neck adipose tissue biopsies (enriched in browning cells) than from subcutaneous ones. IL-6 was produced in a sustained manner and mostly by the adipocytes and not by the undifferentiated progenitors. Continuous blocking of IL-6 receptor by specific antibody during beige differentiation resulted in downregulation of brown marker genes and increased morphological changes that are characteristic of white adipocytes. The data suggest that beige adipocytes adjust their production of IL-6 to reach an optimal level for differentiation in the medium enhancing browning in an autocrine manner.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Experimental Cell Research. - 377 : 1-2 (2019), p. 47-55. -
További szerzők:Klusóczki Ágnes (1991-) (biotechnológus) Veress Roland (1992-) (molekuláris biológus) Shaw, Abhirup (1992-) Combi Zsolt Varga Klára Győry Ferenc (1969-) (kardiológus) Balajthy Zoltán (1957-) (biokémikus, sejtbiológus) Bai Péter (1976-) (biokémikus) Bacsó Zsolt (1963-) (biofizikus) Fésüs László (1947-) (orvos biokémikus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00006
GINOP
OTKA-NK105046
OTKA
OTKA-K123975
OTKA
ÚNKP-18-4
ÚNKP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM004735
Első szerző:Nagy Péter (biofizikus)
Cím:Small interfering RNAs suppress the expression of endogenous and GFP-fused epidermal growth factor receptor (erbB1) and induce apoptosis in erbB1-overexpressing cells / Nagy, P., Arndt-Jovin, D. J., Jovin, T. M.
Dátum:2003
ISSN:014-4827 (Print)
Megjegyzések:Deregulated and excessive expression of epidermal growth factor receptor (EGFR or erbB1), a transmembrane receptor tyrosine kinase specific for the epidermal growth factor (EGF), is a feature and/or cause of a wide range of human cancers, and thus inhibition of its expression is potentially therapeutic. In RNA interference (RNAi), duplexes of 21-nucleotide RNAs (small interfering RNA, siRNA) corresponding to mRNA sequences of particular genes are used to efficiently inhibit the expression of the target proteins in mammalian cells. Here we show that by using RNAi the expression of endogenous erbB1 can be specifically and extensively (90%) suppressed in A431 human epidermoid carcinoma cells. As a consequence, EGF-induced tyrosine phosphorylation was inhibited and cell proliferation was reduced due to induction of apoptosis. We established an inverse correlation between the level of expressed erbB1 and EGF sensitivity on a cell-by-cell basis using flow cytometry. A431 cells expressing endogenous erbB1 were transfected with erbB1 fused C-terminally to enhanced green fluorescent protein (EGFP). Selective inhibition of the expression of the fusion protein was achieved with an siRNA specific for the EGFP mRNA, whereas the erbB1-specific siRNAs inhibited the expression of both molecules. siRNA-mediated inhibition of erbB1 and other erbB tyrosine kinases may constitute a useful therapeutic approach in the treatment of human cancer.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Animals
Apoptosis
Carcinoma
Cell Cycle
Cell Line
Cell Proliferation
Cells
chemistry
Epidermal Growth Factor
Flow Cytometry
genetics
Green Fluorescent Proteins
Human
Humans
Indicators and Reagents
Luminescent Proteins
metabolism
Microscopy,Fluorescence
Phosphorylation
physiology
Proteins
Receptor, Epidermal Growth Factor
Recombinant Fusion Proteins
Research
RNA,Small Interfering
Support
Tyrosine
Megjelenés:Experimental Cell Research. - 285 : 1 (2003), p. 39-49. -
További szerzők:Arndt-Jovin, Donna J. Jovin, Thomas M.
Internet cím:DOI
elektronikus változat
Borító:

5.

001-es BibID:BIBFORM024098
Első szerző:Sejersen, Thomas
Cím:Similarities and differences in the regulation of N-myc and c-myc genes in murine embryonal carcinoma cells / Sejersen T., Rahm M., Szabo G., Ingvarsson S., Sumegi J.
Dátum:1987
Megjegyzések:c-myc and N-myc are closely related genes coding for putative DNA-binding proteins. The protein products of both genes have been implicated in the regulation of growth of normal and neoplastic cells. We compared the regulation of N-myc and c-myc expression under different growth conditions as well as in vitro differentiation of the murine EC lines F9 and PCC7. N-myc and c-myc expression was found to be regulated by distinct mechanisms, although similarities exist. Differences were found both at the transcriptional and at the post-transcriptional level. The two myc genes were regulated by mainly posttranscriptional mechanisms, but in PCC7 cells nuclear run-on assays indicated that c-myc was repressed at the level of transcription. N-myc and c-myc expression was negatively regulated at a post-transcriptional level in F9 and PCC7 cells during differentiation to visceral endoderm and nerve-like tissue, respectively. Serum stimulation of F9 cells for 4 h induced a sevenfold increase in c-myc transcripts but no significant elevation of N-myc transcripts. Mitogenic stimulation with insulin and transferrin also induced a marked elevation of c-myc but not of N-myc mRNA. In addition, the N-myc and c-myc genes differed in F9 cells with respect to (i) the kinetics of expression following induction of differentiation, c-myc undergoing quicker changes than N-myc; (ii) the response to cycloheximide inhibition of protein synthesis, indicating that c-myc but not N-myc is down-regulated by a short-lived protein; and (iii) the half-lives of the transcripts, estimated to be approximately 40 min of c-myc and 130 min for N-myc
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Animal
Carcinoma
carcinoma cell
Cell Differentiation
Cell Line
Cells
Comparative Study
cycloheximide
differentiation
DNA-Binding Proteins
Endoderm
Gene Expression Regulation
genetics
In Vitro
Insulin
Kinetics
Mice
Neoplasm Proteins
Neurons
nonhuman
protein synthesis
Proteins
proto oncogene
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-myc
Proto-Oncogenes
rna
Support,Non-U.S.Gov't
Teratoma
Transferrin
Tumor Cells,Cultured
Megjelenés:Experimental Cell Research. - 172 : 2 (1987), p. 304-317. -
További szerzők:Rahm, Magnus Szabó Gábor (1953-) (biofizikus) Ingvarsson, Sigurdur Sümegi János
Internet cím:elektronikus változat
Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

6.

001-es BibID:BIBFORM003392
Első szerző:Soóki-Tóth Ágnes
Cím:Cellular regulation of ADP-Ribosylation of proteins III. : selective augmentation of in vitro ADP-ribosylation of histone H3 in murine thymic cells after in vivo emetine treatment / Ágnes Soóki-Tóth, Gáspár Bánfalvi, János Szöllösi, Eva Kirsten, Maria Staub, Ferenc Antoni, Ernest Kun
Dátum:1989
Megjegyzések:Thymic cells were isolated at intervals of between 0 and 144 h from mice that received one intraperitoneal injection of emetine (33 mg/kg), and thymus weight, incorporation of [14C]leucine into proteins and [3H]thymidine into DNA in intact thymic cells, as well as initial rates of protein ADP-ribosylation in permeabilized cells [A. Sooki-Toth, F. Asghari, E. Kirsten, and E. Kun (1987) Exp. Cell Res. 170, 93] were simultaneously monitored. The effect of emetine as an inhibitor of protein synthesis [F. Antoni, N. G. Luat, I. Csuka, I. Olah, A. Sooki-Toth, and G. Banfalvi (1987) Int. J. Immunopharmacol. 9, 333] corresponds to the induction of sequential cellular events, such as cell exit and remigration, by other antimitotic agents [C. Penit and F. Vasseur (1988) J. Immunol. 140, 3315] and produces an activation of proliferation of cells reentering into this organ. Proliferation, as demonstrated by a large increase in DNA synthesis and entrance into S phase, was kinetically related to an apparent increase in poly(ADP-ribose) polymerase activity in thymic cells and a highly significant in vitro ADP-ribosylation of histone H3. Since no DNA fragmentation occurred in thymic cells, as tested by a fluorometric technique [C. Birnboim and J. J. Jevac (1981) Cancer Res. 41, 1889], it is probable that a selective activation of poly(ADP-ribose) polymerase may have been induced in cells that undergo differentiation and proliferation while repopulating the thymus.
Tárgyszavak:Természettudományok Orvostudományok Biológiai tudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
murine thymic cells
in vivo
emetine treatment
histon H3
Megjelenés:Experimental Cell Research. - 184 : 1 (1989), p. 44-52. -
További szerzők:Bánfalvi Gáspár (1943-) (sejtbiológus, gyógyszerész) Szöllősi János (1953-) (biofizikus) Kirsten, Eva Staub, Maria Antoni Ferenc Kun, Ernest
Internet cím:elektronikus változat
Borító:

7.

001-es BibID:BIBFORM024111
035-os BibID:(scopus)0028972652 (wos)A1995TH62300008
Első szerző:Szabó Gábor (biofizikus)
Cím:50-Kb Chromatin Fragmentation in the Absence of Apoptosis / Szabo G.
Dátum:1995
Megjegyzések:Treatment with ionic detergents of nuclei isolated from various continuously growing cell lines generally yields chromatin samples of high viscosity, Extensive treatment with nuclease-free proteinase K or pronase solubilized the viscous lysates with > 90% of the DNA migrating at similar to 50 kb. Freshly prepared human peripheral blood T cells also yield a substantial fraction of their DNA in an similar to 50- to 100-kb band, The cleavage sites may coincide with a class of DNase I-hypersensitive regions, since digestion of chromatin by DNase I at similar to 10 U/ml, without protease, also yields fragments of preferentially similar to 50-kb size, Occasionally, the oligonucleosomal ladder was also detected together with high molecular weight degradation products, Remarkably, all of these fragmentation patterns were seen in healthy, resting or proliferating cells, i.e., in the absence of apoptosis, Tritiated thymidine incorporation could be readily detected in the similar to 50-kb DNA fragments, The effect of an apoptotic intracellular milieu on the integrity of isolated chromatin is apparently imitated by the extensive protease treatment used in our DNA isolation protocol.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Apoptosis
blood
Cell Line
Cells
Chromatin
Detergents
Dna
Human
Molecular Weight
Thymidine
Viscosity
Megjelenés:Experimental Cell Research. - 221 : 2 (1995), p. 320-325. -
Internet cím:elektronikus változat
Intézményi repozitóriumban (DEA) tárolt változat
DOI
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8.

001-es BibID:BIBFORM024104
Első szerző:Szabó Gábor (biofizikus)
Cím:Inositol derivatives down-regulate c-myc inducing growth arrest without differentiation / G. Szabó, L. Székely, M. Schablik, G. Klein, J. Sümegi, G. Szabó
Dátum:1991
Megjegyzések:Cyclitol derivatives that are structurally related to myo-inositol induce growth arrest without differentiation in human promyelocytic leukemia (HL60) cells. An early effect is the rapid down-regulation of c-myc mRNA levels. This was observed also in several mouse and human lines carrying either normal or rearranged myc. The mRNA levels of a constitutive mouse myc construct transfected into HL60 were not affected at the same time. Uridine and thymidine incorporation were significantly decreased by the cyclitol treatment. These effects partly resemble those of certain differentiation inducers and those of hexachlorcyclohexane, another myo-inositol analogue. This new group of agents offers a novel approach to studying control mechanisms involving c-myc.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
differentiation
Megjelenés:Experimental Cell Research. - 193 : 2 (1991), p. 420-424. -
További szerzők:Székely László Schablik Marcella Klein, George Sümegi János Szabó G. (biológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:

9.

001-es BibID:BIBFORM024100
Első szerző:Szabó Gábor (biofizikus)
Cím:Independent variations of myc amplification, inducibility, maturation, and proliferation states in HL60 / Szabo G., Bunce C., Brown G., Klein G., Sumegi J.
Dátum:1988
Megjegyzések:We have investigated the possible relationship between c-myc gene activity and other variable traits in HL60. In a panel of variant lines, a good correlation was observed between myc gene copy number and the level of myc mRNA. There was no correlation between myc amplification or expression and the resistance of the lines to induction of terminal neutrophilic or monocytic differentiation. Therefore, myc mRNA level does not appear to determine the ability of the variant HL60 lines to respond to inducers of differentiation. Flow cytometric analyses of the expression of a differentiation antigen (AGF 4.36) revealed stable negative and positive subpopulations in growing HL60. myc amplification, expression, and inducibility were identical in these subpopulations, suggesting that variation of these traits in HL60 sublines and variants is not due to maturation state differences. myc gene copy number was also identical in transferrin receptor positive (proliferating) and negative (resting) populations. These data contradict the notion that myc amplification has been important in determining the in vitro biological properties of HL60
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Cell Culture
Cell Division
cell growth
cell strain hl 60
controlled study
Dimethyl Sulfoxide
Dna
Flow Cytometry
Fluorescent Antibody Technique
Gene Amplification
Gene Expression Regulation
gene induction
Human
human cell
In Vitro
Leukemia,Myelocytic,Acute
Nucleic Acid Hybridization
oncogene myc
phorbol 13 acetate 12 myristate
priority journal
Proteins
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-myc
Proto-Oncogenes
RNA,Messenger
Support, Non-U.S.Gov't
Support, U.S.Gov't,P.H.S.
Tumor Cells, Cultured
Megjelenés:Experimental Cell Research. - 175 : 2 (1988), p. 334-343. -
További szerzők:Bunce, Chris Brown, Geoffrey Klein, George Sümegi János
Internet cím:elektronikus változat
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

10.

001-es BibID:BIBFORM006002
035-os BibID:(scopus)0023112835 (wos)A1987G382700017
Első szerző:Szabó Gábor (biofizikus)
Cím:Overall changes in chromatin sensitivity to DNase I during differentiation / Gábor Szabó, Sandor Damjanovich, János Sümegi, George Klein
Dátum:1987
Megjegyzések:The DNase I sensitivity of total chromatin was studied in fixed cells and nuclei isolated from proliferating and terminally differentiated cells, by measuring the incorporation of labelled nucleotides into DNase-sensitive sites, and electrophoresis of DNA isolated from DNase-treated nuclei. The unfixed nuclei were sensitive to digestion at around 10 micrograms/ml, the fixed cells at 30 ng/ml DNase I concentration. Proliferating Rauscher leukemia cells were more digestible than normal spleen cells. The DNase I sensitivity of the human HL60 leukemia line decreased upon DMSO-induced differentiation but still exceeded the digestibility of nuclei from normal human peripheral blood. A novel flow-cytometric technique was developed to study DNase sensitivity at the cell level. It confirmed the relative resistance of differentiated cells to DNase I and ruled out the possibility that this could be due to an altered distribution of cell cycle phases. The overall DNase I sensitivity of chromatin was compared with the sensitivity of the c-myc gene and the myc-associated hypersensitive sites. The latter sites were detected at 1 microgram/ml DNase I in HL60 nuclei. They disappeared partially upon DMSO-induced differentiation. At 10 micrograms/ml, myc was degraded in both growing and differentiating HL60, but not in HPB cells. These data suggest that a progressive condensation of the chromatin occurs during terminal differentiation which gradually involves specific genes that need to be inactivated.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Animal
blood
Cell Cycle
Cell Differentiation
Cell Division
Cell Line
Chromatin
cytology
Deoxyribonuclease I
Dna
Flow Cytometry
Human
Leukemia,Erythroblastic,Acute
Leukemia,Experimental
metabolism
Mice
Mice,Inbred BALB C
pathology
Spleen
Support,Non-U.S.Gov't
Support,U.S.Gov't,P.H.S.
Translation,Genetic
ultrastructure
Megjelenés:Experimental Cell Research. - 169 : 1 (1987), p. 158-168. -
További szerzők:Damjanovich Sándor (1936-2017) (biofizikus) Sümegi János Klein, George
Internet cím:elektronikus változat
DOI
Borító:
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