17 results on '"leukaemic cells"'
Search Results
2. Dielectrophoretic investigations of haematological cells : procedures and applications
- Author
-
Haigh, Teresa
- Subjects
571.4 ,Leukaemic cells ,Image analysis ,Erythrocytes - Published
- 1995
3. Distinct effects of novel naphtoquinone-based triazoles in human leukaemic cell lines.
- Author
-
Coulidiati, Tangbadioa H., Dantas, Bruna B., Faheina‐Martins, Glaucia V., Gonçalves, Juan C. R., Nascimento, Wilson S., Oliveira, Ronaldo N., Camara, Celso A., Oliveira, Eduardo J., Lara, Aline, Gomes, Eneas R., and Araújo, Demetrius A. M.
- Subjects
- *
TRIAZOLES , *CELL lines , *CANCER cells , *REACTIVE oxygen species , *MONOCYTES , *BAX protein - Abstract
Objectives The aim of this study was to investigate the cytotoxic effect of new 1,4-naphthoquinone- 1,2,3-triazoles, named C2 to C8 triazole derivatives, towards human cancer cell lines. Methods The effect on cell viability was assessed by MTT and propidium iodide assays. The cytotoxic effect of C2 and C3 in K562 and HL-60 cells were analyzed by flow cytometry, DNA fragmentation and reactive oxygen species (ROS) production. Western blot and q-PCR procedures were also performed. Key findings C2 and C3 inhibited both K562 and HL-60 cells growth in a concentration-dependent manner. C2 presented the highest cytotoxic activity with an IC50 of approximately 14 µm and 41 µm for HL-60 and K562 cells, respectively, while being less toxic to normal peripheral blood monocyte cells. Both derivatives induced cellular changes in HL-60 cells, characteristic of apoptosis, such as mitochondrial membrane depolarization, phosphatidylserine externalization, increasing sub-G1 phase, DNA fragmentation, downregulating Bcl-2 protein and upregulating Bax protein. In K562 cells, C2 and C3 induced S-phase arrest of cell cycle, which was associated with upregulation of p21. The effect of these derivatives in HL-60 cells can be related to the ROS intracellular level. Conclusion Taken together our results showed that C2 and C3 triazole derivatives presented the best potential for drug design. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
4. Nuclear organization of PML bodies in leukaemic and multiple myeloma cells
- Author
-
Krejčí, Jana, Harničarová, Andrea, Kůrová, Jana, Uhlířová, Radka, Kozubek, Stanislav, Legartová, Soňa, Hájek, Roman, and Bártová, Eva
- Subjects
- *
B cell lymphoma , *MULTIPLE myeloma , *MONOCLONAL gammopathies , *PLASMACYTOMA , *ANEMIA , *BLOOD diseases , *APLASTIC anemia - Abstract
Abstract: The nuclear arrangement of promyelocytic leukaemia nuclear bodies (PML NBs) was studied in vitro after the cell treatment by clinically used agents such as all-trans retinoic acid (RA) in human leukaemia and cytostatics or gamma radiation in multiple myeloma cells. In addition, the influence of phorbol ester (PMA) on PML NBs formation was analyzed. A reduced number of PML bodies, which led to relocation of PML NBs closer to the nuclear interior, mostly accompanied RA- and PMA-induced differentiation. Centrally located PML NBs were associated with transcriptional protein RNAP II and SC35 regions, which support importance of PML NBs in RNA processing that mostly proceeds within the nuclear interior. Conversely, the quantity of PML NBs was increased after cytostatic treatment, which caused re-distribution of PML NBs closer to the nuclear envelope. Here we showed correlations between the number of PML NBs and average Centre-to-PML distances. Moreover, a number of cells in S phase, especially during differentiation, influenced number of PML NBs. Studying the proteins involved in PML compartment, such as c-MYC, cell-type specific association of c-MYC and the PML NBs was observed in selected leukaemic cells undergoing differentiation, which was accompanied by c-MYC down-regulation. [Copyright &y& Elsevier]
- Published
- 2008
- Full Text
- View/download PDF
5. Ffar2 expression regulates leukaemic cell growth in vivo
- Author
-
Laure B. Bindels, Audrey M. Neyrinck, Sarah Ducastel, Evelyne M. Dewulf, Patrice D. Cani, Martina Sboarina, Paolo E. Porporato, Olivier Feron, Pierre Sonveaux, Sophie Lestavel, Nathalie M. Delzenne, Bart Staels, UCL - SSS/LDRI - Louvain Drug Research Institute, and UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique
- Subjects
Male ,0301 basic medicine ,Cancer Research ,Apoptosis ,Free fatty acid receptor ,Inbred C57BL ,Receptors, G-Protein-Coupled ,Small hairpin RNA ,Mice ,0302 clinical medicine ,Receptors ,Propionate ,Tumor Cells, Cultured ,Receptor ,Inbred BALB C ,Cell proliferation ,Mice, Inbred BALB C ,Tumor ,Leukemia ,Cultured ,GPR43 ,FFA2 ,Tumor Cells ,3. Good health ,Oncology ,Biochemistry ,030220 oncology & carcinogenesis ,leukaemic cells ,free fatty acid receptor ,Female ,Leukaemic cells ,short-chain fatty acids ,cell proliferation ,CMTB ,propionate ,Animals ,Biomarkers, Tumor ,Leukemia, Experimental ,Mice, Inbred C57BL ,Cell Proliferation ,Biology ,Experimental ,G-Protein-Coupled ,Short-chain fatty acids ,03 medical and health sciences ,In vivo ,Free fatty acid receptor 2 ,Cell growth ,In vitro ,030104 developmental biology ,Cancer cell ,Cancer research ,Translational Therapeutics ,Biomarkers - Abstract
BACKGROUND: Activation of free fatty acid receptor 2 (FFAR2) by microbiota-derived metabolites (e.g., propionate) reduces leukaemic cell proliferation in vitro. This study aims to test whether Ffar2 expression per se also influences leukaemia cell growth in vivo. METHODS: Bcr-Abl-expressing BaF cells were used as a leukaemia model and the role of Ffar2 was evaluated in Balb/c mice after lentiviral shRNA transduction. RESULTS: Our data formally establish that reduced leukaemic cell proliferation is associated with increased Ffar2 expression in vivo and in vitro. Going beyond association, we point out that decreasing Ffar2 expression fosters cancer cell growth in vitro and in vivo. CONCLUSIONS: Our data demonstrate the role of Ffar2 in the control of leukaemic cell proliferation in vivo and indicate that a modulation of Ffar2 expression through nutritional tools or pharmacological agents may constitute an attractive therapeutic approach to tackle leukaemia progression in humans.
- Published
- 2017
- Full Text
- View/download PDF
6. An in vitro system for testing leucocyte and leukaemic cell line adhesion to synthetic fibres.
- Author
-
Barbe, Laurent L., Boval, Bernadette M., Wautier, Marie-Paule S., and Wautier, Jean-Luc T.
- Subjects
- *
LEUKEMIA , *LEUCOCYTES , *BLOOD filtration - Abstract
Leucocyte adhesion is an important phenomenon in antimicrobial defence, inflammation and immunological mechanisms and has been shown to be dependent upon specialized adhesion molecules. To prevent side-effects related to blood transfusion (e.g. anti-human leucocyte antigen immunization and transmission of infectious agents) leucocyte reduction of blood products is now systematically performed in various countries. The most common system used for leucoreduction is blood filtration. For further understanding of the mechanisms responsible for the interaction between leucocytes and the fibres present in filters we used a flow chamber to study the adhesion of leucocytes and leukaemic cell lines to different types of fibre. Adhesion was quantified using video-microscopy and computer image analysis. Our results demonstrate that adhesion to filter fibres was dependent on the expression of β2-integrins CD11–-CD18 and was inhibited by anti-CD18. The amount of fibres present, their spatial arrangement and the physicochemical characteristics of the fibres were important factors in leucocyte adhesion. Leucocyte adhesion was the highest to polyethylene terephthalate (PET) and polyimide fibres. Lymphocytes or lymphocytic cell lines were poorly adherent to PET fibres. The retaining capacity of leucocyte filters can be improved by taking into account the different parameters for the design of new filters. [ABSTRACT FROM AUTHOR]
- Published
- 2001
- Full Text
- View/download PDF
7. p53-Independent caspase-mediated apoptosis in human leukaemic cells is induced by a DNA minor groove binder with antineoplastic activity.
- Author
-
Marchini, S., Ciro', M., and Broggini, M.
- Abstract
Treatment of HL60 and Jurkat leukaemic cell lines, both not expressing p53, with the new non-covalent DNA minor groove binder α-bromoacryloyl-distamycin (PNU 151807), induces apoptosis as shown either morphologically or by DNA laddering formation. We evaluated the p53-independent mechanisms of activation of apoptosis in these cell systems, by determining the levels of different caspases at different times after treatment with PNU 151807. Through Western blotting analysis we could measure the cleavage of the 110 Kd form of PARP in both HL60 and Jurkat cells and correspondingly the activation of CPP32-caspase 3. The levels of caspase-1 did not change at any time after drug treatment. By using the tetrapeptidic sequence recognized by caspase-3 (DEVD-AMC) or by caspase-1 (YVAD-AMC) linked to fluorogenic substrate, we also demonstrated that only the DEVD sequence was recognized and cleaved after drug treatment, while no significant changes were found for YVAD peptides. PNU 151807-induced DNA fragmentation and DEVD-cleavage were both inhibited by concomitant treatment with the specific inhibitor DEVD-CHO, but not by YVAD-CHO, clearly demonstrating the direct activation of caspase-3-like caspases in the induction of programmed cell death in these cell lines after minor groove binder exposure. [ABSTRACT FROM AUTHOR]
- Published
- 1999
- Full Text
- View/download PDF
8. Membrane associated events during proliferative inhibition of granulocyte precursors.
- Author
-
Benestad, Haakon and Heikkilä, Reino
- Abstract
A new way of assessing the significance of intracellular signals that may regulate cellular proliferation, would be to analyze possible 'second messengers' when proliferation is slowed down, rather than stimulated. Therefore, we examined proliferating mononuclear blood cells from leukaemic patients which had been exposed to an inhibitory ox leucocyte extract. The extract decreased H-thymidine incorporation in leukaemic cells in short-term cultures. The inhibition was not cell-line specific, but was nevertheless non-toxic and not due to endotoxin. The K flux into the leukaemic cells was assessed with Rb, a K analogue. An inverse relationship was found between Rb uptake and H-thymidine incorporation. The increased Rb influx was probably due to leakage or exchange mechanisms other than the Na/K membrane pump, as suggested by ouabain inhibition experiments. However, the long lag time (>45 min) between addition of inhibitor and a marked increase in Rb uptake does not support a role for the K flux as an early mediator of the inhibitory signal. [ABSTRACT FROM AUTHOR]
- Published
- 1986
- Full Text
- View/download PDF
9. Apoptosis and Bcl-2 protein changes in L1210 leukaemic cells exposed to oxidative stress.
- Author
-
Zimowska, W., Motyl, T., Skierski, J., Balasinska, B., Ploszaj, T., Orzechowski, A., and Filipecki, M.
- Abstract
The aim of this study was to explore the dose- and time-dependent effects of hydrophilic peroxyl radical initiator 2,2'azobis(2amidinopropane)dihydrochloride (AAPH) on apoptosis, and on expression of Bcl-2 in L1210 leukaemic cells. We observed a progressive increase of intracellular concentration of oxygen free radicals (OFR), manifested by the rise of 6-carboxy-2', 7'-dichlorodihydrofluorescein diacetate, di(acetoxymethyl ester) oxidation, during 24 h of cells exposure to AAPH. Oxidative stress was associated with peroxidation of cellular lipids, which was demonstrated by the measurement of thiobarbituric acid-reactive substances and conjugated dienes. Analysis of cell viability by the use of trypan blue exclusion method revealed that AAPH reduced the ability of L1210 cells to multiply or survive. AAPH increased the number of leukaemic cells with typical features of apoptosis like condensation of chromatin, pyknosis and fragmentation of nucleus, followed by secondary necrosis. A characteristic internucleosomal DNA cleavage, visualized as a DNA ‘ladder’ consisting of fragments that are multiples of 180-200 bp was also observed. The intensity of apoptosis was dependent on AAPH concentration, time of cell exposure and the availability of growth factors and nutrients in extracellular environment (FCS concentration). The novel observation is the increase of Bcl-2 level in L1210 leukaemic cells surviving an oxidative stress. The level of Bcl-2 protein significantly rose with increasing AAPH concentration, and time of cell exposure to this oxidant. This phenomenon could be the result of: (1) negative selection of cells with the lowest expression of bcl-2, being more susceptible to oxidative stress and (2) increased synthesis and/or decreased degradation of Bcl-2 protein as an adaptation to continuous OFR loading. In contrast to growth-promoting medium (10% FCS/RPMI), the maintenance medium (2% FCS/RPMI) did not cover cell requirements for progressive Bcl-2 increase at the highest AAPH concentration (2 mM) applied in this study. Several observations indicate that the increased Bcl-2 level in surviving L1210 leukaemic cells exposed to oxidative stress is a symptom of their natural defence against cellular lipids peroxidation and apoptosis. [ABSTRACT FROM AUTHOR]
- Published
- 1997
- Full Text
- View/download PDF
10. Studies on the mechanism of synthesis and release of the procoagulant activity from leukaemic cells.
- Author
-
Mohanty, Dipika, Ghosh, K., and Das, K.
- Abstract
The synthesis and release of procoagulant activity (PCA) from leukaemic leucocytes was studied in an in vitro culture system stimulated by endotoxin. Puromycin, actinomycin-D, vinblastine, colchicine, dibutyryl cyclic AMP and ouabaln were added to the culture system to study some of the metabolic processes of these cells in relation to synthesis and release of PCA. It was found that production of PCA is an active process and depends on new protein synthesis. The release of PCA from cells can be inhibited by vinblastine, an inhibitor of microfilament and microtubules in the cell. The optimal release of PCA occurs at pH 7.2 -@#@ 7.4 at 37°C and is not inhibited by the ATPase inhibitor ouabaln. Dibutyryl cyclic AMP inhibits the release/synthesis of PCA. Gram negative septicaemia and endotoxinaemia are capable of increased production and release of PCA from leukaemic cells and could contribute to the coagulation fallure seen in this disease. [ABSTRACT FROM AUTHOR]
- Published
- 1991
- Full Text
- View/download PDF
11. Cellular pharmacokinetics of daunorubicin: Uptake by leukaemic cells in vivo and fate.
- Author
-
Trillet, V., Lakhal, M., Lang, J., Perrin-Fayolle, E., Timour Chah, Q., Fière, D., and Faucon, G.
- Abstract
In 6 patients with acute myeloblastic leukaemia, daunorubicin was assayed in leukaemic cells from peripheral blood or bone marrow. The cells were separated from red blood cells and granulocytes by centrifugation on a Ficoll-Isopac gradient. The assay was performed by high performance liquid chromatography. Daunorubicin concentrations in peripheral leukaemic cells, 2 hours after the end of the infusion, were much higher than in plasma, the cell/plasma concentration ratio reaching about 350 and rising to almost 700 at 24 h. At that time, drug concentrations were even higher in the bone marrow leukaemic cells. The value of the assay of daunorubicin in cells as method for monitoring therapy is discussed. [ABSTRACT FROM AUTHOR]
- Published
- 1985
- Full Text
- View/download PDF
12. Fluorescence Probe and Biochemical Characterization of Leukaemic Cells
- Author
-
Lajtha, L. G., Bessis, Marcel, editor, and Brecher, George, editor
- Published
- 1975
- Full Text
- View/download PDF
13. The p38 MAP kinase inhibitor SB203580 enhances nuclear factor-kappa B transcriptional activity by a non-specific effect upon the ERK pathway
- Subjects
p38 and ERK kinases ,C-JUN ,ACTIVATED PROTEIN-KINASE ,HUMAN MONOCYTES ,SIGNAL-TRANSDUCTION ,OKADAIC ACID ,SB203580 ,CELLULAR STRESSES ,nuclear factor kappaB ,ALPHA ,MYELOBLASTIC-LEUKEMIA CELLS ,leukaemic cells ,PHOSPHORYLATION ,transcriptional activity ,TUMOR-NECROSIS-FACTOR - Abstract
1 In the present study we investigated a possible role for the p38 mitogen-activated protein (MAP) kinase pathway in mediating nuclear factor-kappa B (NF-kappa B) transcriptional activity in the erythroleukaemic cell line TF-1. 2 TF-1 cells stimulated with the phosphatase inhibitor okadaic acid (OA) demonstrated enhanced NF-kappa B and GAL4p65-regulated transcriptional activity which was associated with elevated p38 phosphorylation. However, pretreatment with the p38 MAPK specific inhibitor SB203580 (1 mu M) or overexpression of kinase-deficient mutants of MKK3 or MKK6 did not affect OA-enhanced NF-kappa B transcriptional potency, as determined in transient transfection assays. In fact, 5 and 10 mu M SB203580 enhanced rather than inhibited NF-kappa B-mediated promoter activity by 2 fold, which was independent of phosphorylation of the p65 subunit. 3 The SB203580-mediated increase in NF-kappa B transcriptional activity was associated with enhanced phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and c-Jun N-terminal kinase (JNK), but not p38 kinase. 4 Overexpression of kinase-deficient mutants belonging to the ERK1/2, JNK, and p38 pathways showed that only dominant-negative Raf-l abrogated SB203580-enhanced NF-kappa B activity. This would implicate the involvement of the ERK1/2 pathway in the enhancing effects of SB203580 on NF-kappa B-mediated gene transcription. 5 This study demonstrates that the p38 MAP kinase pathway is not involved in the OA-induced activation of NF-kappa B. SB203580 at higher concentrations activates the ERK pathway, which subsequently enhances NF-kappa B transcriptional activity.
- Published
- 2000
14. Bcl-2 overexpression blocks caspase activation and downstream apoptotic events instigated by photodynamic therapy
- Author
-
Huijun Jiang, M T An, David W. C. Hunt, Julia G. Levy, David J. Granville, and Bruce M. McManus
- Subjects
Cancer Research ,Programmed cell death ,Porphyrins ,caspase ,medicine.medical_treatment ,HL-60 Cells ,Caspase 3 ,Photodynamic therapy ,Caspase 6 ,Proto-Oncogene Mas ,resistance ,medicine ,Humans ,Bcl-2 ,Caspase ,biology ,Hydrolysis ,apoptosis ,Regular Article ,DNA, Neoplasm ,Caspase Inhibitors ,Verteporfin ,Enzyme Activation ,Cell killing ,Photochemotherapy ,Proto-Oncogene Proteins c-bcl-2 ,photodynamic therapy ,Oncology ,Apoptosis ,Caspases ,leukaemic cells ,biology.protein ,Cancer research ,medicine.drug - Abstract
Treatment with the photosensitizer benzoporphyrin derivative monoacid ring A (BPD-MA, verteporfin) followed by irradiation with visible light induces apoptosis in human acute myelogenous leukaemia HL-60 cells. Photoactivation of BPD-MA induces procaspase 3 (CPP32/Yama/apopain) and procaspase 6 (Mch2) cleavage into their proteolytically active subunits in these cells. The Bcl-2 proto-oncogene product has been shown to protect cells from a number of proapoptotic stimuli. In the present study, the influence of Bcl-2 overexpression on cellular resistance to photoactivation of BPD-MA was studied. Overexpression of Bcl-2 in HL-60 cells prevented apoptosis-related events including caspase 3 and 6 activation, poly(ADP-ribose) polymerase cleavage and the formation of hypodiploid DNA produced by BPD-MA (0–200 ng ml−1) and light. However, Bcl-2 overexpression was less effective at preventing cell death that occurred after photoactivation at high levels (50–100 ng ml−1) compared with lower doses (10–25 ng ml−1) of BPD-MA. These results indicate that caspase 3 and 6 activation and their regulation by Bcl-2 may play important roles in photodynamic therapy (PDT)-induced cell killing. © 1999 Cancer Research Campaign
- Published
- 1998
- Full Text
- View/download PDF
15. The effect of the Fas/FasL pathway during chemotherapeutic drug-induced apoptosis of leukameic cells
- Author
-
Ping, Zou, Zhongwen, Liu, and Juan, Xiao
- Published
- 2001
- Full Text
- View/download PDF
16. Proteasomes are a target of the anti-tumour drug vinblastine
- Author
-
Marco PICCININI, Ornella TAZARTES, Caterina MEZZATESTA, Emanuela RICOTTI, Stefano BEDINO, Franca GROSSO, Umberto DIANZANI, Pier-Angelo TOVO, Michael MOSTERT, Alberto MUSSO, and Maria T. RINAUDO
- Subjects
proteolysis ,ubiquitin conjugates ,cytostatic agents ,leukaemic cells ,Cell Biology ,Molecular Biology ,Biochemistry - Abstract
Proteasomes, the proteolytic machinery of the ubiquitin/ATP-dependent pathway, have a relevant role in many processes crucial for cell physiology and cell cycle progression. Proteasome inhibitors are used to block cell cycle progression and to induce apoptosis in certain cell lines. Here we examine whether proteasomal function is affected by the anti-tumour drug vinblastine, whose cytostatic action relies mainly on the disruption of mitotic spindle dynamics. The effects of vinblastine on the peptidase activities of human 20S and 26S proteasomes and on the proteolytic activity of 26S proteasome were assessed in the presence of specific fluorogenic peptides and 125I-lysozyme–ubiquitin conjugates respectively. The assays of ubiquitin–protein conjugates and of inhibitory κBα (IκBα), which are characteristic intracellular proteasome substrates, by Western blotting on lysates from HL60 cells incubated with or without vinblastine, illustrated the effects of vinblastine on proteasomes in vivo. We also evaluated the effects of vinblastine on the signal-induced degradation of IκBα. Vinblastine at 3–110μM reversibly inhibited the chymotrypsin-like activity of the 20 S proteasome and the trypsin-like and peptidyl-glutamyl-peptide hydrolysing activities of both proteasomes, but only at 110μM vinblastine was the chymotrypsin-like activity of the 26S proteasome inhibited; furthermore, at 25–200μM the drug inhibited the degradation of ubiquitinated lysozyme. In HL60 cells exposed for 6h to 0.5–10μM vinblastine, the drug-dose-related accumulation of polyubiquitinated proteins, as well as that of a high-molecular-mass form of IκBα, occurred. Moreover, vinblastine impaired the signal-induced degradation of IκBα. Cell viability throughout the test was approx. 95%. Proteasomes can be considered to be a new and additional vinblastine target.
- Published
- 2001
17. The p38 MAP kinase inhibitor SB203580 enhances nuclear factor-kappa B transcriptional activity by a non-specific effect upon the ERK pathway
- Author
-
Birkenkamp, KU, Tuyt, LML, Lummen, C, Wierenga, LTJ, Kruijer, W, Vellenga, E, Groningen Biomolecular Sciences and Biotechnology, Guided Treatment in Optimal Selected Cancer Patients (GUTS), and Stem Cell Aging Leukemia and Lymphoma (SALL)
- Subjects
p38 and ERK kinases ,C-JUN ,ACTIVATED PROTEIN-KINASE ,HUMAN MONOCYTES ,SIGNAL-TRANSDUCTION ,OKADAIC ACID ,SB203580 ,CELLULAR STRESSES ,nuclear factor kappaB ,ALPHA ,MYELOBLASTIC-LEUKEMIA CELLS ,leukaemic cells ,PHOSPHORYLATION ,transcriptional activity ,TUMOR-NECROSIS-FACTOR - Abstract
1 In the present study we investigated a possible role for the p38 mitogen-activated protein (MAP) kinase pathway in mediating nuclear factor-kappa B (NF-kappa B) transcriptional activity in the erythroleukaemic cell line TF-1. 2 TF-1 cells stimulated with the phosphatase inhibitor okadaic acid (OA) demonstrated enhanced NF-kappa B and GAL4p65-regulated transcriptional activity which was associated with elevated p38 phosphorylation. However, pretreatment with the p38 MAPK specific inhibitor SB203580 (1 mu M) or overexpression of kinase-deficient mutants of MKK3 or MKK6 did not affect OA-enhanced NF-kappa B transcriptional potency, as determined in transient transfection assays. In fact, 5 and 10 mu M SB203580 enhanced rather than inhibited NF-kappa B-mediated promoter activity by 2 fold, which was independent of phosphorylation of the p65 subunit. 3 The SB203580-mediated increase in NF-kappa B transcriptional activity was associated with enhanced phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and c-Jun N-terminal kinase (JNK), but not p38 kinase. 4 Overexpression of kinase-deficient mutants belonging to the ERK1/2, JNK, and p38 pathways showed that only dominant-negative Raf-l abrogated SB203580-enhanced NF-kappa B activity. This would implicate the involvement of the ERK1/2 pathway in the enhancing effects of SB203580 on NF-kappa B-mediated gene transcription. 5 This study demonstrates that the p38 MAP kinase pathway is not involved in the OA-induced activation of NF-kappa B. SB203580 at higher concentrations activates the ERK pathway, which subsequently enhances NF-kappa B transcriptional activity.
- Published
- 2000
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.