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1.

001-es BibID:BIBFORM028732
Első szerző:Fésüs László (orvos biokémikus)
Cím:Probing the molecular program of apoptosis by cancer chemopreventive agents / Laszlo Fésüs, Zsuzsa Szondy, Ivan Uray
Dátum:1995
ISSN:0730-2312
Megjegyzések:This paper provides a rational molecular basis for studies intended to clarify the interactions between cancer chemopreventive agents and apoptosis, one of the natural forms of cell death that overlaps molecular mechanisms with other forms such as programmed cell death and specialized forms of physiological cell death. Molecular details of the process show the existence of distinct molecular pathways leading to the activation of critical effector elements (apoptosis gene products) functioning under the control of a network of negative regulatory elements. Dysregulation of either apoptosis or anti-apoptosis genes has a significant role in multistage carcinogenesis. Inhibition of apoptosis is one of the underlying mechanisms of the action of tumor promoters. The network of apoptosis and anti-apoptosis gene products provides multiple targets for compounds with cancer chemopreventive potential. Many data in the literature show initiating, potentiating or inhibitory effects of such compounds on apoptosis. However, the molecular mechanism of these effects is largely unknown. We initiated a series of studies using mouse thymocytes which undergo apoptosis through distinct molecular mechanisms after T-cell receptor activation (TCR pathway), following the addition of glucocorticoids (DEX pathway) or DNA damaging agents (p53 pathway). All trans-and 9-cis-retinoic acid induced apoptosis, elicited through the DEX pathway, inhibited the TCR pathway, and did not affect p53- initiated apoptosis. N-acetylcysteine can inhibit all forms. Sodium salicylate enhanced spontaneous cell death, decreased p53-dependent apoptosis, and did not affect the DEX and TCR pathways. These preliminary results, which show differential effects of the studied compounds on distinct molecular pathways of apoptosis, warrant further investigations in the effort to utilize the molecular elements of apoptosis in proper cancer chemoprevention, and find biochemical targets for apoptosis-related surrogate endpoint biomarker assays of chemoprevention.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Cellular Biochemistry. Supplement. - Suppl. 22 (1995), p. 151-161. -
További szerzők:Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus) Uray Iván Péter (1970-) (kutatóorvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM110245
035-os BibID:(cikkazonosító)217 (Scopus)85151110056 (WoS)000962544000005
Első szerző:Jambrovics Károly (biológus, gyógyszer-biotechnológus)
Cím:Transglutaminase 2 associated with PI3K and PTEN in a membrane-bound signalosome platform blunts cell death / Jambrovics Károly, Botó Pál, Pap Attila, Sarang Zsolt, Kolostyák Zsuzsanna, Czimmerer Zsolt, Szatmari Istvan, Fésüs László, Uray Iván P., Balajthy Zoltán
Dátum:2023
ISSN:2041-4889
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Cell Death & Disease. - 14 : 3 (2023), p. 1-10. -
További szerzők:Botó Pál (1986-) (molekuláris biológus) Pap Attila (1980-) (biológus) Sarang Zsolt (1976-) (mikrobiológus) Kolostyák Zsuzsanna Czimmerer Zsolt (1981-) (molekuláris biológus) Szatmári István (1971-) (biológus) Fésüs László (1947-) (orvos biokémikus) Uray Iván Péter (1970-) (kutatóorvos) Balajthy Zoltán (1957-) (biokémikus, sejtbiológus)
Pályázati támogatás:K129139
OTKA
K129218
OTKA
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM084074
035-os BibID:(cikkazonosító)648 (WoS)000530232300124 (Scopus)85081217936
Első szerző:Jambrovics Károly (biológus, gyógyszer-biotechnológus)
Cím:Benefits of Combined All-Trans Retinoic Acid and Arsenic Trioxide Treatment of Acute Promyelocytic Leukemia Cells and Further Enhancement by Inhibition of Atypically Expressed Transglutaminase 2 / Jambrovics Károly, Uray Iván P., Keillor Jeffrey W., Fésüs László, Balajthy Zoltán
Dátum:2020
ISSN:2072-6694
Megjegyzések:Randomized trials in acute promyelocytic leukemia patients have shown that treatment with a combination of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) is superior in efficacy to monotherapy, with significantly decreased mortality. So far, there are little data available to explain the success of the ATRA and ATO combination treatment in molecular terms. We showed that ATRA- and ATO-treated cells had the same capacity for superoxide production, which was reduced by two-thirds in the combined treatment. Secreted inflammatory biomarkers (monocyte chemoattractant protein-1 [MCP-1], interleukin-1 beta [IL-1?] and tumor necrosis factor-? [TNF-?]) were significantly decreased and were further reduced in a transglutaminase 2 (TG2) expressiondependent manner. The amount of secreted TNF-? in the supernatant of NB4 TG2 knockout cells was close to 50 times lower than in ATRA-treated differentiated wild-type NB4 cells. The irreversible inhibitor of TG2 NC9 not only decreased reactive oxygen species production 28-fold, but decreased the concentration of MCP-1, IL-1? and TNF-? 8-, 15- and 61-fold, respectively in the combined ATRA + ATO-treated wild-type NB4 cell culture. We propose that atypical expression of TG2 leads to the generation of inflammation, which thereby serves as a potential target for the prevention of differentiation syndrome.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Cancers. - 12 : 3 (2020), p. 648-. -
További szerzők:Uray Iván Péter (1970-) (kutatóorvos) Keillor, Jeffrey W. Fésüs László (1947-) (orvos biokémikus) Balajthy Zoltán (1957-) (biokémikus, sejtbiológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00020
GINOP
K129218
OTKA
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM077169
035-os BibID:(WoS)000460110400026 (Scopus)85063936796
Első szerző:Jambrovics Károly (biológus, gyógyszer-biotechnológus)
Cím:Transglutaminase 2 programs differentiating acute promyelocytic leukemia cells in all-trans retinoic acid treatment to inflammatory stage through NF-kB activation / Jambrovics Károly, Uray Iván P., Keresztessy Zsolt, Keillor Jeffrey W., Fésüs László, Balajthy Zoltán
Dátum:2019
ISSN:0390-6078
Megjegyzések:Differentiation syndrome is a life-threatening complication arising during retinoid treatment of acute promyelocytic leukemia. Administration of all-trans retinoic acid leads to significant changes in gene expression, among the most induced of which is transglutaminase 2, which is not normally expressed in neutrophil granulocytes. To evaluate the pathophysiological function of transglutaminase 2 in the context of immunological function and disease outcomes, such as excessive superoxide anion, cytokine, and chemokine production in differentiated NB4 cells, we used an NB4 transglutaminase knock-out cell line and a transglutaminase inhibitor, NC9, which inhibits both transamidase- and guanosine triphosphate-binding activities, to clarify transglutaminase's contribution to the development of potentially lethal differentiation syndrome during all-trans retinoic acid treatment of acute promyelocytic leukemia. We found that such treatment not only enhanced cell-surface expression of CD11b and CD11c but also induced high-affinity states; atypical transglutaminase 2 expression in NB4 cells activated the nuclear factor kappa-light-chain-enhancer of activated B cells pathway, driving pathogenic processes with an inflammatory cascade through the expression of numerous cytokines, including Tumor necrosis factor alpha, Interleukin 1 beta, and Monocyte chemoattractant protein 1. NC9 decreased the amount of transglutaminase 2, p65/RelA, and p50 in differentiated NB4 cells and their nuclei, leading to attenuated inflammatory cytokine synthesis. NC9 significantly inhibits transglutaminase 2 nuclear translocation but accelerates its proteasomal breakdown. This study demonstrates that transglutaminase 2 expression induced by all-trans retinoic acid treatment reprograms inflammatory signaling networks governed by nuclear factor kappa-light-chain-enhancer of activated B cells activation, resulting in over-expression of tumor necrosis factor alpha and Interleukin 1 beta in differentiating acute promyelocytic leukemia cells, suggesting that atypically expressed transglutaminase 2 is a promising target for leukemia treatment.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Haematologica-The Hematology Journal. - 104 : 3 (2019), p. 505-515. -
További szerzők:Uray Iván Péter (1970-) (kutatóorvos) Keresztessy Zsolt Keillor, Jeffrey W. Fésüs László (1947-) (orvos biokémikus) Balajthy Zoltán (1957-) (biokémikus, sejtbiológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00020
GINOP
TÁMOP-4.2.2.D-15/1/KONV-2015-0016
TÁMOP
EFOP-3.6.1-16-2016-00022
EFOP
GINOP-2.3.2-15-2016-00006
GINOP
NK105046
OTKA
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5.

001-es BibID:BIBFORM061539
Első szerző:Piredda, Lucia
Cím:Lack of 'tissue' transglutaminase protein cross-linking leads to leakage of macromolecules from dying cells : relationship to development of autoimmunity in MRLIpr/Ipr mice / Lucia Piredda, Alessandra Amendola, Vittorio Colizzi, Peter J. A. Davies, Maria Grazia Farrace, Maurizio Fraziano, Vittorio Gentile, Ivan Uray, Mauro Piacentini, Laszlo Fesus
Dátum:1997
ISSN:1350-9047
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cell Death and Differentiation 4 : 6 (1997), p. 463-472. -
További szerzők:Amendola, Alessandra Colizzi, Vittorio Davies, Peter J. A. Farrace, Maria Grazia Fraziano, Maurizio Gentile, Vittorio Uray Iván Péter (1970-) (kutatóorvos) Piacentini, Mauro Fésüs László (1947-) (orvos biokémikus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM056375
Első szerző:Sárvári Anitta Kinga (biológus)
Cím:Atypical antipsychotics induce both proinflammatory and adipogenic gene expression in human adipocytes in vitro / Anitta K. Sárvári, Zoltán Veréb, Iván P. Uray, László Fésüs, Zoltán Balajthy
Dátum:2014
ISSN:0006-291X
Megjegyzések:Schizophrenia requires lifelong treatment, potentially causing systemic changes in metabolic homeostasis. In the clinical setting, antipsychotic treatment may differentially lead to weight gain among individual patients, although the molecular determinants of such adverse effects are currently unknown. In this study, we investigated changes in the expression levels of critical regulatory genes of adipogenesis, lipid metabolism and proinflammatory genes during the differentiation of primary human adipose-derived stem cells (ADSCs). These cells were isolated from patients with body mass indices <25 and treated with the second-generation antipsychotics olanzapine, ziprasidone, clozapine, quetiapine, aripiprazole and risperidone and the first-generation antipsychotic haloperidol. We found that antipsychotics exhibited a marked effect on key genes involved in the regulation of cell cycle, signal transduction, transcription factors, nuclear receptors, differentiation markers and metabolic enzymes. In particular, we observed an induction of the transcription factor NF-KB1 and NF-KB1 target genes in adipocytes in response to these drugs, including the proinflammatory cytokines TNF-α, IL-1β, IL-8 and MCP-1. In addition, enhanced secretion of both IL8 and MCP-1 was observed in the supernatant of these cell cultures. In addition to their remarkable stimulatory effects on proinflammatory gene transcription, three of the most frequently prescribed antipsychotic drugs, clozapine, quetiapine and aripiprazole, also induced the expression of essential adipocyte differentiation genes and the adipocyte hormones leptin and adiponectin, suggesting that both glucose and fat metabolism may be affected by these drugs. These data further suggest that antipsychotic treatments in patients alter the gene expression patterns in adipocytes in a coordinated fashion and priming them for a low-level inflammatory state.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Biochemical and Biophysical Research Communications. - 450 : 4 (2014), p. 1383-1389. -
További szerzők:Veréb Zoltán (1980-) (immunológus, mikrobiológus, molekuláris biológus) Uray Iván Péter (1970-) (kutatóorvos) Fésüs László (1947-) (orvos biokémikus) Balajthy Zoltán (1957-) (biokémikus, sejtbiológus)
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7.

001-es BibID:BIBFORM060605
Első szerző:Uray Iván Péter (1970-)
Cím:Pharmacological separation of the expression of tissue transglutaminase and apoptosis after chemotherapeutic treatment of HepG2 cells / Iván P. Uray, Peter J. A. Davies, László Fésüs
Dátum:2001
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular pharmacology. - 59 : 6 (2001), p. 1388-1394. -
További szerzők:Davies, Peter J. A. Fésüs László (1947-) (orvos biokémikus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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