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  1. 23 Archivum Immunologiae et Therapiae Experimentalis

  2. 9 Folia Histochemica et Cytobiologica

  3. 5 Acta Biochimica Polonica

  4. 5 Journal of Physiology and Pharmacology

  5. 3 Cellular and Molecular Biology Letters

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  1. 3 Bigda J.

  2. 3 Kandefer-Szerszen M.

  3. 2 Grzela T.

  4. 2 Krejner A.

  5. 2 Litwiniuk M.

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  1. 2 2020

  2. 2 2019

  3. 2 2018

  4. 2 2017

  5. 1 2016

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1

The expression of HSP 27, HSP 70 and HSP 90 in U937 sublines exhibiting different patterns of sensitivity to TNF

100%
Pierzchalski A., Sychowska D., Bartczak M., Bigda J.
Cellular and Molecular Biology Letters
|
2002
|
tom 07
|
nr Suppl.
2

Exogenous nitric oxide inhibits shedding of ADAM17 substrates

75%
Bzowska M., Stalinska K., Mezyk-Kopec R., Wawro K., Duda K., Das S., Bereta J.
Acta Biochimica Polonica
|
2009
|
tom 56
|
nr 2
325-335
 Both ADAM17, the secretase responsible for the shedding of ectodomains of numerous membrane proteins including TNF and its receptors, as well as nitric oxide synthesized by inducible nitric oxide synthase play regulatory roles in inflammation and tumor progression. We analyzed the effect of endogenous and exogenous nitric oxide on the expression and activity of ADAM17 in murine endothelial cells and a monocyte/macrophage cell line. We found that endogenous nitric oxide influenced neither ADAM17 mRNA level nor the shedding of two ADAM17 substrates, TNF and TNFR1. Exogenous NO significantly diminished the release of TNF and TNFR1 without affecting the ADAM17 transcript level. Our data seem contrary to a previous report that showed the activation of ADAM17 by nitric oxide (Zhang et al., 2000, J Biol Chem 275: 15839-15844). We discuss potential mechanisms of NO-mediated inhibition of ectodomain shedding and possible reasons of discrepancy between our results and the previous report.
3

Modulation of CD40L antigen expression in Jurkat cells: involvement of protein kinase C activity

75%
Lisowska K., Bryl E., Soroczynska M., Witkowski J. M.
Folia Histochemica et Cytobiologica
|
2003
|
tom 41
|
nr 4
4

Manipulating B cell homeostasis: a key component in the advancement of targeted strategies

75%
Treml L. S., Quinn III W. J., Treml J. F., Scholz J. L., Cancro M. P.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
tom 56
|
nr 3
5

The ability of Candida spp. strains to induce production of tumor necrosis factor and interleukin-6 by whole blood cells

75%
Nawrot U., Grzybek-Hryncewicz K., Czarny A.
Acta Microbiologica Polonica
|
2003
|
tom 52
|
nr 1
6

Environmental stress increases plasma tumor necrosis factor and decreases interferon gamma levels in rats

63%
Wrona D., Zander A., Slominska L., Grembecka B.
Acta Biologica Cracoviensia. Series Zoologia
|
2008
|
tom 50
29-36
7

Role of osteopontin in systemic lupus erythematosus

63%
Kaleta B.
Archivum Immunologiae et Therapiae Experimentalis
|
2014
|
tom 62
|
nr 6
8

Prolonged treatment with inhaled corticosteroids does not normalize high activity of matrix metalloproteinase-9 in exhaled breath condensates of children with asthma

63%
Grzela K., Zagorska W., Krejner A., Litwiniuk M., Zawadzka-Krajewska A., Banaszkiewicz A., Kulus M., Grzela T.
Archivum Immunologiae et Therapiae Experimentalis
|
2015
|
tom 63
|
nr 3
9

Effect of granulocyte-macrophage colony-stimulating growth factor on interferon and tumor necrosis factor production in whole blood cell cultures of patients with acute myelogenous leukemia

63%
Kaminska T., Hus I., Dmoszynska A., Kandefer-Szerszen M.
Archivum Immunologiae et Therapiae Experimentalis. Supplement
|
2001
|
tom 49
|
nr 2
83-87
10

Specific T-cell subsets can predict the efficacy of anti-TNF treatment in inflammatory bowel diseases

63%
Dulic S., Toldi G., Sava F., Kovacs L., Molnar T., Milassin A., Farkas K., Rutka M., Balog A.
Archivum Immunologiae et Therapiae Experimentalis
|
2020
|
tom 68
|
nr 2
11

Two Gln187 mutants of human soluble APRIL inhibit proliferation of lung carcinoma A549 cells

63%
Dai S., Zheng Y., Chen B., Gao M., Zhang Y., Zhang L., Gong W., He F.
Acta Biochimica Polonica
|
2009
|
tom 56
|
nr 4
703-710
 Soluble APRIL (sAPRIL), the active form of a proliferation-inducing ligand (APRIL), is implicated in the proliferation of tumor cells. Suppressing APRIL function has been considered as a potential strategy for the therapy of APRIL-associated tumors. In the present study, we generated human sAPRIL and its two mutants, Gln187-D-sAPRIL (Gln187 deleted) and Gly187-sAPRIL (Gln187 replaced by Gly). In vitro experiments showed that the two mutants had similar specific binding capacity to lung carcinoma A549 cells compared to the wild-type sAPRIL, and both, especially Gly187-sAPRIL, exhibited significant antagonistic effect on sAPRIL-induced tumor cell proliferation in a dose-dependent manner, which might be predominantly mediated by blocking sAPRIL-induced MEK and ERK phosphorylation but not p38MAPK or JNK signaling. In vivo experiments with nude mice bearing A549 cell-derived xenograft tumor showed that only the Gly187-sAPRIL mutant could significantly suppress the tumor growth. These results suggest that Gln187 may be a crucial amino acid in APRIL-mediated tumor cell proliferation via the MEK-ERK signaling pathway and that the sAPRIL mutants may serve as novel potential antagonists of APRIL for the therapy of APRIL-associated cancers.
12

A proliferation-inducing ligand regulation in polymorphonuclear neutrophils by Panax ginseng

63%
Ratajczak-Wrona W., Wawrusiewicz-Kurylonek N., Garley M., Kretowski A. J., Jablonska E.
Archivum Immunologiae et Therapiae Experimentalis
|
2020
|
tom 68
|
nr 6
13

Interferon and tumour necrosis factor production in bovine aorta endothelial cells aging in vitro. The influence of culture conditions on age-dependent phenotypic changes

63%
Paduch R., Zdzisinska B., Rzeski W., Wrobel M., Kandefer-Szerszen M.
Annales Universitatis Mariae Curie-Sklodowska. Sectio C, Biologia
|
2001
|
tom 56
14

Sera of lung cancer patients affect the release of TH1, TH2 and monocyte-derived cytokines, and the expression of IL-2Ralpha by normal, stimulated mononuclear cells

63%
Chechlinska M., Duma A., Swierkowska A., Kaminska J., Steffen J.
Cellular and Molecular Biology Letters
|
2004
|
tom 09
|
nr 1
We have shown that the sera of lung cancer patients affect the response of ConA-stimulated normal peripheral blood mononuclear cells by decreasing the expression of IL-2Rα and inhibiting the release of IL-1β and IL-2. A tendency to enhance the release of IL-6 was also observed. We conclude that an imbalance in the Th1/Th2 cytokine response, typical for cancer patients, may at least partly be related to soluble factors circulating in the patients’ blood. We discuss a putative role of serum IL-10, IL-1ra, and soluble IL-2Rα in the effects observed.
15

The importance of abrogation of G2-phase arrest in combined effect of TRAIL and ionizing radiation

63%
Rezacova M., Vavrova J., Vokurkova D., Tichy A., Knizak J., Psutka J.
Acta Biochimica Polonica
|
2005
|
tom 52
|
nr 4
Background: In this work we studied the relationship between the enhanced expression of DR5 receptor and the effect of combination of TRAIL and ionizing radiation on cell cycle arrest and apoptosis induction in human leukemia cell line HL-60. Material and methods: DR5, APO2.7 and cell cycle were analyzed by flow cytometry. Proteins Bid and Mcl-1 were analyzed by Western-blotting. For clonogenic survival, colony assay on methylcellulose was used. Results: Ionizing radiation caused significantly enhanced positivity of DR5 receptors 24 h after irradiation with high doses (6 and 8 Gy). An increase of DR5 receptor positivity after a dose of 2 Gy was not statistically significant and application of TRAIL 48 h after irradiation did not increase the apoptosis induction. However, a decrease of radiation-induced G2 phase arrest and an increase of apoptosis were observed when TRAIL was applied 16 h before irradiation with the dose of 2 Gy. Incubation with 6 µg/l TRAIL for 16 h reduced D0 value from 2.9 Gy to 1.5 Gy. The induction of apoptosis by TRAIL was accompanied by Bid cleavage and a decrease of antiapoptotic Mcl-1 16 h after incubation with TRAIL. Conclusion: TRAIL in concentration of 6 µg/l applied 16 h before irradiation by the dose of 1.5 Gy caused the death of 63% of clonogenic tumor cells, similarly as the dose of 2.9 Gy alone, which is in good correlation with the enhanced apoptosis induction.
16

The dynamic and complex role of mast cells in allergic disease

63%
Kulka M., Befus A. D.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
tom 51
|
nr 2
17

Anti-tumor action of tumor necrosis factor against Bomirski Ab melanoma in hamsters

63%
Koszalka P., Szmit E., Mysliwski A., Bigda J.
Archivum Immunologiae et Therapiae Experimentalis
|
2007
|
tom 55
|
nr 4
18

Fast perinuclear clustering of mitochondria in oxidatively stressed human choriocarcinoma cells

63%
Hallmann A., Milczarek R., Lipinski M., Kossowska E., Spodnik J. H., Wozniak M., Wakabayashi T., Klimek J.
Folia Morphologica
|
2004
|
tom 63
|
nr 4
Mitochondrial dysfunction plays a crucial role in cell types that exhibit necrosislike death after activation of their death program. Tumour necrosis factor (TNF) induces abnormal, perinuclear clustering of mitochondria from an evenly spread distribution throughout the cytoplasm. The mitochondria withdraw from the cell periphery and aggregate in a unipolar perinuclear cluster. TNF-induced mitochondrial clustering is caused by impaired kinesin-mediated transportation of mitochondria. In this report, we describe a novel activity of menadione (MEN), namely the induction of an altered spatial distribution of mitochondria in the choriocarcinoma JAR cells. Strikingly, 2 hours of cell exposition to menadione did not disrupt the integrity of the plasma membrane, while the intracellular ATP level significantly decreased. Control (untreated) cells displayed a typically scattered distribution of filamentary mitochondria inside the cell. After 2 hours of MEN treatment the spatial distribution of the mitochondria was markedly altered to an asymmetric perinuclear clustered distribution. Menadione-stressed cells displayed a highly asymmetrical perinuclear clustered distribution of the mitochondria. The exposure of cells to MEN also results in a change in shape of the mitochondria into a population of enlarged granular structures. The results of our study demonstrate that in JAR cells menadione causes mitochondria to translocate from the cell periphery into the perinuclear region several hours before disruption of cell membrane integrity and cell death.
19

Is it wise to target the late cistimulatory molecule OX40 as a therapeutic target?

63%
Cavanagh M. M., Hussell T.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
tom 56
|
nr 5
20

New biodefense strategies by neutrophils

63%
Ishikawa F., Miyazaki S.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
tom 53
|
nr 3
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