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1.

001-es BibID:BIBFORM047648
Első szerző:Bácsi Attila (immunológus)
Cím:Colostrinin-Driven Neurite Outgrowth Requires p53 Activation in PC12 Cells / Attila Bacsi, G. John Stanton, Thomas K. Hughes, Marian Kruzel, Istvan Boldogh
Dátum:2005
ISSN:0272-4340
Megjegyzések:1. Colostrinin (CLN) induces maturation and differentiation of murine thymocytes,promotes proliferation of peripheral blood leukocytes, induces immunomodulatorcytokines, and ameliorates oxidative stress-mediated activation of c-Jun NH2-terminalkinases.2. Here we report that upon treatment with CLN, medullary pheochromocytoma(PC12) cells ceased to proliferate and extend neurites.3. The arrest of CLN-treated PC12 cells in the G1 phase of the cell cycle was due toan increase in the phosphorylation of p53 at serine15 (p53ser15) and expression of p21WAF1.PC12 cells treated with inhibitory oligonucleotides to p53 lacked p53ser15 and p21WAF1expression, and did not show morphological changes after CLN exposure. Transfectionwith inhibitory oligonucleotides to p21WAF1 had no effect on p53 activation; however, cellsfailed to arrest or extend neurites. An oligonucleotide inhibiting luciferase expression hadno effect on CLN-mediated p53 activation, p21WAF1 expression, growth arrest, or neuriteoutgrowth.4. We conclude that CLN induces delicate cassettes of signaling pathways common tocell proliferation and differentiation, and mediates activities that are similar to those ofhormones and neurotrophins, leading to neurite outgrowth.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
colostrinin
pheochromocytoma cell
neurite outgrowth
p53 activation
Megjelenés:Cellular And Molecular Neurobiology. - 25 : 7 (2005), p. 1123-1139. -
További szerzők:Stanton, G. John Hughes, Thomas K. Kruzel, Marian L. Boldogh István
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2.

001-es BibID:BIBFORM014138
Első szerző:Bálint Bálint László (kutató orvos)
Cím:Arginine Methylation Provides Epigenetic Transcription Memory for Retinoid-Induced Differentiation in Myeloid Cells / Balint L. Balint, Attila Szanto, Andras Madi, Uta-Maria Bauer, Petra Gabor, Szilvia Benko, Laszlo G. Puskas, Peter J. A. Davies, Laszlo Nagy
Dátum:2005
ISSN:0270-7306
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular And Cellular Biology. - 25 : 13 (2005), p. 5648-5663. -
További szerzők:Szántó Attila (1976-) (orvos, biokémikus) Mádi András (1967-) (biológus) Bauer, Uta-Maria Gábor Petra Benkő Szilvia (1973-) (molekuláris biológus) Puskás László G. Davies, Peter J. A. Nagy László (1966-) (molekuláris sejtbiológus, biokémikus)
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3.

001-es BibID:BIBFORM065560
Első szerző:Bene László (biofizikus)
Cím:Depolarized FRET (depolFRET) on the cell surface : FRET control by photoselection / László Bene, Péter Gogolák, Tamás Ungvári, Miklós Bagdány, István Nagy, László Damjanovich
Dátum:2016
ISSN:0167-4889
Megjegyzések:Sensitivity of FRET in hetero- and homo-FRET systems on the photoselected orientation distribution of donors has been proven by using polarized and depolarized light for excitation. FRET as well as donor and acceptor anisotropies have been simultaneously measured in a dual emission-polarization scheme realized in a conventional flow cytometer by using single laser excitation and applying fluorophore-conjugated mAbs against the MHCI and MHCII cell surface receptors. Depolarization of the originally polarized light have been achieved by using crystal depolarizers based on Cornu's principle, a quarter-wave plate for circular polarization, and a parallel beam splitter acting as a diagonal-polarizer for dual-polarization excitation. Simultaneous analysis of intensity-based FRET efficiency and acceptor depolarization equivocally report that depolarization of light may increase FRET in an amount depending on the acceptor-to-donor concentration ratio. Acceptor depolarization turned to be more sensitive to FRET than donor hyper-polarization and even than intensity-based FRET efficiency. It can be used as a sensitive tool for monitoring changes in the dynamics of the donor-acceptor pairs. The basic observations of FRET enhancement and increased acceptor depolarization obtained for hetero-FRET are paralleled by analog observations of homo-FRET enhancements under depolarized excitation. In terms of the orientation factor for FRET, the FRET enhancements on depolarization in the condition of the macroscopically isotropic orientation distributions such as those of the cell surface bound fluorophores report on the presence of local orientation mismatches of the donor and acceptor preventing the optimal FRET in the polarized case, which may be eliminated by the excitation depolarization. A theory of fluorescence anisotropy for depolarized excitation is also presented.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Polarizationally structured light
Circularly polarized light
Diagonal-polarization
CORNU-depolarizer
Orientation factor for FRET
Homo-FRET
Megjelenés:Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. - 1863 : 2 (2016), p. 322-334. -
További szerzők:Gogolák Péter (1968-) (biológus, immunológus) Ungvári Tamás Bagdány Miklós Nagy István (1957-) (villamosmérnök) Damjanovich László (1960-) (általános sebész)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Sebészet Kutatócsoport
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4.

001-es BibID:BIBFORM020781
Első szerző:Boda Zoltán (belgyógyász, haematologus, klinikai onkológus)
Cím:Repeated application of autologous bone marrow-derived stem cell therapy in patients with severe Buerger's disease / Z. Boda, K. Razso, M. Szarvas, Zs. Olah, P. Ilonczai, Z. Vereb, É. Rajnavolgyi
Dátum:2011
ISSN:2161-6760
Megjegyzések:Stem cell therapy (SCT) is a promising and prospective approach in the treatment of patients with severe peripheral arterial disorders, primarily with Buerger's disease. However, very little is known about the duration of the effect of SCT, and to our best knowledge no data are available on the efficacy and safety of repeated SCT in patients with Buerger's disease. Here we report on two patients with severe Buerger's disease, who received repeated autologous bone marrow-derived stem cell therapy. Our results show that a second SCT, applied to a previously treated leg 30 or 36 months after the first treatment was efficient in both cases. After twelve months, the clinical state of the repeatedly treated lower limb improved spectacularly and non-healing ulcers healed more rapidly than after the first SCT. No severe adverse events were detected. Thus repeated SCT offers a safe and efficient treatment option for relapsing patients at the advanced stage of Buerger's disease.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Buerger's disease
non healing ulcer
repeated bone marrow-derived stem cell therapy
Open Access
Megjelenés:Stem Cell Discovery. - 1 : 1 (2011), p. 16-19. -
További szerzők:Molnárné Rázsó Katalin (1966-) (belgyógyász, haematológus, klinikai onkológus) Szarvas Mariann (1977-) Oláh Zsolt (1974-) (belgyógyász) Ilonczai Péter (1977-) (orvos, belgyógyász, haematológus szakorvos) Veréb Zoltán (1980-) (immunológus, mikrobiológus, molekuláris biológus) Rajnavölgyi Éva (1950-) (immunológus)
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5.

001-es BibID:BIBFORM035749
Első szerző:Chan, Betty
Cím:SAP couples Fyn to SLAM immune receptors / Chan Betty, Lanyi Arpad, Song Hyun Kyu, Griesbach Jan, Simarro-Grande Maria, Poy Florence, Howie Duncan, Sumegi Janos, Terhorst Cox, Eck Michael J.
Dátum:2003
ISSN:1465-7392
Megjegyzések:SAP (SLAM-associated protein) is a small lymphocyte-specific signalling molecule that is defective or absent in patients with X-linked lymphoproliferative syndrome (XLP). Consistent with its single src homology 2 (SH2) domain architecture and unusually high affinity for SLAM (also called CD150), SAP has been suggested to function by blocking binding of SHP-2 or other SH2-containing signalling proteins to SLAM receptors. Additionally, SAP has recently been shown to be required for recruitment and activation of the Src-family kinase FynT after SLAM ligation. This signalling 'adaptor' function has been difficult to conceptualize, because unlike typical SH2-adaptor proteins, SAP contains only a single SH2 domain and lacks other recognized protein interaction domains or motifs. Here, we show that the SAP SH2 domain binds to the SH3 domain of FynT and directly couples FynT to SLAM. The crystal structure of a ternary SLAM-SAP-Fyn-SH3 complex reveals that SAP binds the FynT SH3 domain through a surface-surface interaction that does not involve canonical SH3 or SH2 binding interactions. The observed mode of binding to the Fyn-SH3 domain is expected to preclude the auto-inhibited conformation of Fyn, thereby promoting activation of the kinase after recruitment. These findings broaden our understanding of the functional repertoire of SH3 and SH2 domains.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Nature Cell Biology. - 5 : 2 (2003), p. 155-160. -
További szerzők:Lányi Árpád (1962-) (biológus, immunológus) Song, Hyun Kyu Griesbach, Jan Simarro-Grande, Maria Poy, Florence Howie, Duncan Sümegi János Terhorst, Cox Eck, Michael J.
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6.

001-es BibID:BIBFORM005082
Első szerző:Detre, Cynthia
Cím:Death or survival : membrane ceramide controls the fate and activation of antigen-specific T-cells depending on signal strength and duration / Detre, C., Kiss, E., Varga, Z., Ludanyi, K., Paszty, K., Enyedi, A., Kovesdi, D., Panyi, G., Rajnavolgyi, E., Matko, J.
Dátum:2006
ISSN:898-6568 (Print)
Megjegyzések:Sphingomyelinase (SMase)-mediated release of ceramide in the plasma membrane of T-lymphocytes induced by different stimuli such as ligation of Fas/CD95, irradiation, stress, inflammation or anticancer drugs primarily involves mitochondrial apoptosis signaling, but under specific conditions non-apoptotic Fas-signaling was also reported. Here we investigated, using a quantitative simulation model with exogenous C2-ceramide (and SMase), the dependence of activation and fate of T-cells on the strength and duration of ceramide accumulation. A murine, influenza virus hemagglutinin-specific T-helper cell (IP12-7) alone or together with interacting antigen presenting B-cells (APC) was used. C2-ceramide induced apoptosis of TH cells above a 'threshold' stimulus (>25 microM in 'strength' or >30 min in duration), while below the threshold C2-ceramide was non-apoptotic, as confirmed by early and late apoptotic markers (PS-translocation, mitochondrial depolarization, caspase-3 activation, DNA-fragmentation). The modest ceramide stimuli strongly suppressed the calcium response and inhibited several downstream signal events (e.g. ERK1/2-, JNK-phosphorylation, CD69 expression or IL-2 production) in TH cells during both anti-CD3 induced and APC-triggered activation. Ceramide moderately affected the Ca2+ -release from internal stores upon antigen-specific engagement of TCR in immunological synapses, while the influx phase was remarkably reduced in both amplitude and rate, suggesting that the major target(s) of ceramide-effects are membrane-proximal. Ceramide inhibited Kv1.3 potassium channels, store operated Ca2+ -entry (SOC) and depolarized the plasma membrane to which contribution of spontaneously formed ceramide channels is possible. The impaired function of these transporters may be coupled to the quantitative, membrane raft-remodeling effect of ceramide and responsible, in a concerted action, for the suppressed activation. Our results suggest that non-apoptotic Fas stimuli, received from previously activated, FasL+ interacting lymphocytes in the lymph nodes, may negatively regulate subsequent antigen-specific T-cell activation and thus modulate the antigen-specific T-cell response.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
analogs and derivatives
Animals
Antigens,CD95
Apoptosis
B-Lymphocytes
Calcium
Caspase 3
Caspases
Cell Membrane
Cell Survival
Cells
DNA Fragmentation
Human
Humans
Hungary
immunology
Inflammation
Interleukin-2
Kv1.3 Potassium Channel
Lymph Nodes
Lymphocyte Activation
Lymphocytes
Membrane Potentials
metabolism
Mice
pharmacology
physiology
Potassium
Potassium Channels
Receptors,Antigen,T-Cell
Research
Signal Transduction
Sphingomyelin Phosphodiesterase
Sphingosine
Support
Synapses
T-Lymphocytes
T-Lymphocytes, Helper-Inducer
Time Factors
Megjelenés:Cellular Signalling. - 18 : 3 (2006), p. 294-306. -
További szerzők:Kiss Endre (Budapest) Varga Zoltán (1969-) (biofizikus, szakfordító) Ludányi Katalin (1975-) (immunológus) Pászty Katalin Enyedi Ágnes Kövesdi Dorottya Panyi György (1966-) (biofizikus) Rajnavölgyi Éva (1950-) (immunológus) Matkó János (1952-) (biológus)
Internet cím:elektronikus változat
DOI
Borító:

7.

001-es BibID:BIBFORM083852
035-os BibID:(WoS)000514846600012 (Scopus)85079416349
Első szerző:Dogra, Pranay
Cím:Tissue Determinants of Human NK Cell Development, Function, and Residence / Pranay Dogra, Chiara Rancan, Wenji Ma, Marta Toth, Takashi Senda, Dustin J. Carpenter, Masaru Kubota, Rei Matsumoto, Puspa Thapa, Peter A. Szabo, Maya Meimei Li Poon, Jacky Li, Janice Arakawa-Hoyt, Yufeng Shen, Lawrence Fong, Lewis L. Lanier, Donna L. Farber
Dátum:2020
ISSN:0092-8674
Megjegyzések:Immune responses in diverse tissue sites are critical for protective immunity and homeostasis. Here, we investigate how tissue localization regulates the development and function of human natural killer (NK) cells, innate lymphocytes important for anti-viral and tumor immunity. Integrating high-dimensional analysis of NK cells from blood, lymphoid organs, and mucosal tissue sites from 60 individuals, we identify tissue-specific patterns of NK cell subset distribution, maturation, and function maintained across age and between individuals. Mature and terminally differentiated NK cells with enhanced effector function predominate in blood, bone marrow, spleen, and lungs and exhibit shared transcriptional programs across sites. By contrast, precursor and immature NK cells with reduced effector capacity populate lymph nodes and intestines and exhibit tissue-resident signatures and site-specific adaptations. Together, our results reveal anatomic control of NK cell development and maintenance as tissue-resident populations, whereas mature, terminally differentiated subsets mediate immunosurveillance through diverse peripheral sites.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
NK cells
Megjelenés:Cell. - 180 : 4 (2020), p. 749-763. -
További szerzők:Rancan, Chiara Ma, Wenji Tóth Márta (1986-) (biológus) Senda, Takashi Carpenter, Dustin J. Kubota, Masaru Matsumoto, Rei Thapa, Puspa Szabó Péter András Li Poon, Maya Meimei Li, Jacky Arakawa-Hoyt, Janice Shen, Yufeng Fong, Lawrence Lanier, Lewis L. Farber, Donna L.
Pályázati támogatás:3.4.2-VEKOP-15-2015-00001
EFOP
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8.

001-es BibID:BIBFORM065606
Első szerző:Fekete Tünde (immunológus, molekuláris biológus, mikrobiológus)
Cím:Interferon gamma boosts the nucleotide oligomerization domain 2-mediated signaling pathway in human dendritic cells in an X-linked inhibitor of apoptosis protein and mammalian target of rapamycin-dependent manner / Tünde Fekete, Gabor Koncz, Brigitta Szabo, Andrea Gregus, Eva Rajnavölgyi
Dátum:2017
ISSN:1672-7681 2042-0226
Megjegyzések:The cytoplasmic nucleotide oligomerization domain 2 (NOD2) receptor recognizes the bacterial cell wall componentmuramyl dipeptide (MDP). NOD2 ligation initiates the nuclear factor kappa B and the mitogen-activated protein kinasecascades. However, administering MDP alone is insufficient to elicit strong cytokine responses in various immune cells,including dendritic cells (DCs). Because the simultaneous presence of various microbial products and cytokines ininflamed tissues modulates DC function, we initiated this study to examine how interferon gamma (IFNc), a centralmodulator of inflammation, affects the NOD2-mediated signaling pathway in human conventional DCs (cDCs).Synergistic stimulation of DCs with MDP and IFNc increased the expression of CD40, CD80, CD83, CD86, and humanleukocyte antigen DQ proteins and significantly elevated the production of pro-inflammatory cytokines IL-1b, IL-6, IL-12,and tumour necrosis factor (TNF), as well as anti-inflammatory cytokine IL-10. Furthermore, the simultaneous presenceofMDP and IFNc was necessary to decrease IkBa protein levels. By investigating various mechanisms implicated in MDPandIFNc-mediated signaling pathways, we revealed that the increased production of pro-inflammatory cytokines ishighly dependent on the X-linked inhibitor of apoptosis protein (XIAP) but not on cellular IAP1 and IAP2. We also foundthat the NOD2 signaling pathway is regulated by the mammalian target of rapamycin (mTOR) but is not affected byphosphatidylinositol-3 kinase or signal transducer and activator of transcription 1 inhibition. Our results demonstrate, forthe first time, that IFNc positively affects NOD2-mediated signaling in human cDCs, in a manner considerably dependenton XIAP and partially dependent on mTOR.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
dendritic cell
mTOR
NOD2
XIAP
Megjelenés:Cellular And Molecular Immunology 14 : 4 (2017), p. 380-391. -
További szerzők:Koncz Gábor (1970-) (biológus, immunológus) Szabó Brigitta Gregus Andrea (1980-) (biológus) Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:NN114423
OTKA
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9.

001-es BibID:BIBFORM065603
Első szerző:Kövesdi Dorottya
Cím:Antigen receptor-mediated signaling pathways in transitional immature B cells / Dorottya Kövesdi, Katalin Pászty, Ágnes Enyedi, Endre Kiss, János Matkó, Katalin Ludányi, Éva Rajnavölgyi, Gabriella Sármay
Dátum:2004
ISSN:0898-6568
Megjegyzések:Engagement of antigen receptors on immature B cells induces apoptosis, while at the mature stage, it stimulates cell activation and proliferation. The difference in B cell receptor (BCR)-mediated signaling pathways regulating death or survival of B cells is not fully understood. We aimed to characterize the pathway leading to BCR-driven apoptosis. Transitional immature B cells were obtained from the spleen of sublethally irradiated and auto-reconstituted mice. We have detected a short-lived BCR-driven activation of mitogen-activated protein kinases (ERK1/2 and p38 MAPK) and Akt/PKB in transitional immature B cells that correlated with the lack of c-Fos expression, reduced phosphorylation of Akt substrates and a susceptibility for apoptosis. Simultaneous signaling through BCR and CD40 protected immature B cells from apoptosis, however, without inducing Bcl-2 expression. The BCR-induced apoptosis of immature B cells is a result of the collapse of mitochondrial membrane potential and the subsequent activation of caspase-3.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Apoptosis
B lymphocytes
Development
Signal transduction
Transitional immature cells
Megjelenés:Cellular Signalling. - 16 : 8 (2004), p. 881-889. -
További szerzők:Pászty Katalin Enyedi Ágnes Kiss Endre (Budapest) Matkó János (1952-) (biológus) Ludányi Katalin (1975-) (immunológus) Rajnavölgyi Éva (1950-) (immunológus) Sármay Gabriella
Pályázati támogatás:T029535
OTKA
T034493
OTKA
T034536
OTKA
TS044711
OTKA
D38465
OTKA
FKFP 0155/200
Egyéb
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10.

001-es BibID:BIBFORM065602
Első szerző:Ludányi Katalin (immunológus)
Cím:Fine-tuning of helper T cell activation and apoptosis by antigen-presenting cells / Katalin Ludanyi, Peter Gogolak, Bence Rethi, Maria Magocsi, Cynthia Detre, Janos Matko Eva Rajnavolgyi
Dátum:2004
ISSN:0898-6568
Megjegyzések:The role of antigen-presenting cells (APC) in regulating helper T cell responses and activation-induced cell death (AICD) was investigated in vitro. T cell activation was monitored by measuring the early rise of intracellular free calcium [Ca+]ic, mRNA and cell surface expression of activation and apoptotic molecules, the production of cytokines and the activation of transcription factors. Our results demonstrate that the unique characteristics of a given APC can modify the threshold, kinetics and magnitude of the T cell response. The rapid and sustained rise of intracellular free calcium correlated well with the extent of cytokine production and the expression of activation molecules. Fas-dependent AICD could be induced by the most potent antigen-presenting cell (2PK3) only. Our results demonstrate that the response and fate of effector/memory CD4+ helper T lymphocytes is highly dependent on the individual properties of the APC they encounter.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
APC
Antigen presentation
TCR
Co-stimulation
T cell signaling
Antigen-specific activation
Helper T cell
AICD
Megjelenés:Cellular Signalling. - 16 : 8 (2004), p. 939-950. -
További szerzők:Gogolák Péter (1968-) (biológus, immunológus) Réthi Bence (1973-) (biológus, immunológus) Magócsi Mária Detre, Cynthia Matkó János (1952-) (biológus) Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:T043420
OTKA
NKFP 00088/2001
Egyéb
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11.

001-es BibID:BIBFORM079160
035-os BibID:(PMID)31273921 (WoS)000475292400001 (Scopus)85071501758
Első szerző:Markovics Arnold (molekuláris biológus)
Cím:Nicotinic acid suppresses sebaceous lipogenesis of human sebocytes via activating hydroxycarboxylic acid receptor 2 (HCA2) / Arnold Markovics, Kinga Fanni Tóth, Katalin Eszter Sós, József Magi, Adrienn Gyöngyösi, Zoltán Benyó, Christos C. Zouboulis, Tamás Bíró, Attila Oláh
Dátum:2019
Megjegyzések:Nicotinic acid (NA) activates hydroxycarboxylic acid receptor 2 (HCA2), and it is widely used in treating dyslipidemias. Since its side effects include skin dryness, whereas its deficiency can be accompanied by dyssebacia, characterized by sebaceous gland enlargement, we asked if HCA2 is expressed on human sebocytes, and if NA influences sebocyte functions. By using human immortalized SZ95 sebocytes, we found that non-cytotoxic (?100 ?M; MTT-assay) concentrations of NA had no effect on the homeostatic sebaceous lipogenesis (SLG; Nile Red), but normalized excessive, acne-mimicking SLG induced by several lipogenic agents (arachidonic acid, anandamide, linoleic acid+testosterone; Nile Red; 48-hr treatments). Moreover, it exerted significant anti-proliferative actions (CyQUANT-assay), and increased [Ca2+]IC (Fluo-4 AM-based Ca2+-measurement). Although NA did not prevent the lipopolysaccharide-induced pro-inflammatory response (up-regulation [Q-PCR] and release [ELISA] of several pro-inflammatory cytokines) of the sebocytes, collectively, these data support the concept that NA may be effective in suppressing sebum production in vivo. While exploring the mechanism of the sebostatic actions, we found that sebocytes express HCA2 (Q-PCR, immunofluorescent labeling), siRNA-mediated silencing of which prevented the NA-induced Ca2+-signal and the lipostatic action. Collectively, our data introduce NA, and HCA2 activators in general, as novel, potent, and most likely safe sebostatic agents, with possible anti-acne potential.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
acne
HCA2
nicotinic acid
sebocyte
seborrhea
Megjelenés:Journal of Cellular and Molecular Medicine. - 23 : 9 (2019), p. 6203-6214. -
További szerzők:Tóth Kinga Fanni (1992-) (molekuláris biológus, élettanász) Sós Katalin Magi József Gyöngyösi Adrienn (1982-) (biológus) Benyó Zoltán Zouboulis, Christos C. (1960-) (bőrgyógyász) Bíró Tamás (1968-) (élettanász) Oláh Attila (1984-) (élettanász)
Pályázati támogatás:NKFIH 120552
Egyéb
NKFIH 121360
Egyéb
NKFIH 125055
Egyéb
GINOP-2.3.2-15-2016-00050
GINOP
NVKP_16-1-2016-0042
Egyéb
EU Horizon 2020 739593
Egyéb
Bolyai János Kutatási Ösztöndíj
MTA
ÚNKP-18-4-DE-247
Egyéb
NTP-NFTÖ-18-B-0168
Egyéb
Galderma Acne and rosacea basic research award 2015
Egyéb
Internet cím:DOI
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12.

001-es BibID:BIBFORM083079
035-os BibID:(cikkazonosító)860 (WoS)000497971600005 (Scopus)85074933970
Első szerző:Molnár Tamás (molekuláris biológus)
Cím:Current translational potential and underlying molecular mechanisms of necroptosis / Molnár Tamás, Mázló Anett, Tslaf Vera, Szöllősi Attila Gábor, Emri Gabriella, Koncz Gábor
Dátum:2019
ISSN:2041-4889
Megjegyzések:Cell death has a fundamental impact on the evolution of degenerative disorders, autoimmune processes, inflammatory diseases, tumor formation and immune surveillance. Over the past couple of decades extensive studies have uncovered novel cell death pathways, which are independent of apoptosis. Among these is necroptosis, a tightly regulated, inflammatory form of cell death. Necroptosis contribute to the pathogenesis of many diseases and in this review, we will focus exclusively on necroptosis in humans. Necroptosis is considered a backup mechanism of apoptosis, but the in vivo appearance of necroptosis indicates that both caspase-mediated and caspase-independent mechanisms control necroptosis. Necroptosis is regulated on multiple levels, from the transcription, to the stability and posttranslational modifications of the necrosome components, to the availability of molecular interaction partners and the localization of receptor-interacting serine/threonine-protein kinase 1 (RIPK1), receptor-interacting serine/threonine-protein kinase 3 (RIPK3) and mixed lineage kinase domain-like protein (MLKL). Accordingly, we classified the role of more than seventy molecules in necroptotic signaling based on consistent in vitro or in vivo evidence to understand the molecular background of necroptosis and to find opportunities where regulating the intensity and the modality of cell death could be exploited in clinical interventions. Necroptosis specific inhibitors are under development, but >20 drugs, already used in the treatment of various diseases, have the potential to regulate necroptosis. By listing necroptosis-modulated human diseases and cataloging the currently available drug-repertoire to modify necroptosis intensity, we hope to kick-start approaches with immediate translational potential. We also indicate where necroptosis regulating capacity should be considered in the current applications of these drugs
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Cell Death & Disease. - 10 : 11 (2019), p. 1-21. -
További szerzők:Türk-Mázló Anett (1989-) (molekuláris biológus) Tslaf Vera Szöllősi Attila Gábor (1982-) (élettanász) Emri Gabriella (1972-) (bőrgyógyász, allergológus, onkológus) Koncz Gábor (1970-) (biológus, immunológus)
Pályázati támogatás:125224
OTKA
2.3.2-15-2016-00005
GINOP
128034
NKFIH
125224
NKIFH
ÚNKP-18-3
Egyéb
ÚNKP19-4-DE-142
Egyéb
Internet cím:Szerző által megadott URL
DOI
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