Gotowe bibliografie tematyczne / Interferon-gamma/biosynthesis

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Gotowa bibliografia na temat „Interferon-gamma/biosynthesis”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Interferon-gamma/biosynthesis"

Boeve, Christine M. A., and Marc De Ley. "Modulation of Human Interferon-Gamma; Biosynthesis by Antisense Oligodeoxynucleotides." Molecular Biotechnology 14, no. 2 (2000): 157–64. http://dx.doi.org/10.1385/mb:14:2:157.

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Werner, E. R., G. Werner-Felmayer, D. Fuchs, A. Hausen, G. Reibnegger та H. Wachter. "Parallel induction of tetrahydrobiopterin biosynthesis and indoleamine 2,3-dioxygenase activity in human cells and cell lines by interferon-γ". Biochemical Journal 262, № 3 (1989): 861–66. http://dx.doi.org/10.1042/bj2620861.

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In all of eight tested human cells and cell lines with inducible indoleamine 2,3-dioxygenase (EC 1.13.11.17) tetrahydrobiopterin biosynthesis was activated by interferon-gamma. This was demonstrated by GTP cyclohydrolase I (EC 3.5.4.16) activities and intracellular neopterin and biopterin concentrations. Pteridine synthesis was influenced by extracellular tryptophan. In T 24-cell extracts, submillimolar concentrations of tetrahydrobiopterin stimulated the indoleamine 2,3-dioxygenase reaction.

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Boeve, C. M., A. V. Wyngaerd, and M. De Ley. "Inhibition of human interferon-gamma biosynthesis by an antisense RNA-expressing vector." Molecular Pharmacology 49, no. 1 (1996): 58–62. https://doi.org/10.1016/s0026-895x(25)08693-6.

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Reginato, A. M., C. Sanz-Rodriguez, A. Diaz, R. M. Dharmavaram та S. A. Jimenez. "Transcriptional modulation of cartilage-specific collagen gene expression by interferon γ and tumour necrosis factor α in cultured human chondrocytes". Biochemical Journal 294, № 3 (1993): 761–69. http://dx.doi.org/10.1042/bj2940761.

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To examine the possibility that cytokines produced in inflamed joint tissues may contribute to the loss of articular cartilage by causing inhibition of synthesis of cartilage-specific matrix macromolecules, we studied the effects of interferon gamma (IFN gamma) and tumour necrosis factor alpha (TNF alpha), alone and in combination, on the expression of the genes for types-II, -IX and -XI collagens in cultured human chondrocytes. Chondrocytes isolated from human fetal epiphyseal cartilage by sequential enzymic digestions were cultured in the presence of IFN gamma (30 pM), TNF alpha (15 pM) or a

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Luedke, C. E., and A. Cerami. "Interferon-gamma overcomes glucocorticoid suppression of cachectin/tumor necrosis factor biosynthesis by murine macrophages." Journal of Clinical Investigation 86, no. 4 (1990): 1234–40. http://dx.doi.org/10.1172/jci114829.

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Finbloom, D. S. "Regulation of cell-surface receptors for human interferon-γ on the human histiocytic lymphoma cell line U937". Biochemical Journal 274, № 3 (1991): 775–80. http://dx.doi.org/10.1042/bj2740775.

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Interferon-gamma (IFN gamma) binds to high-affinity receptors on monocytes and is rapidly internalized. This study investigates the ability of the human monocyte-like cell line, U937, to regulate the cell-surface expression of the IFN gamma receptor (IFN gamma R) during endocytosis of ligand. Recombinant IFN gamma was radiolabelled to high specific radioactivity with Bolton-Hunter reagent and used to enumerate IFN gamma R on treated U937 cells. Cells which had internalized IFN gamma for up to 3 h displayed maximal levels of IFN gamma R at all time points tested after all unlabelled IFN gamma h

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Kurzrock, R., M. F. Rohde, J. R. Quesada, et al. "Recombinant gamma interferon induces hypertriglyceridemia and inhibits post-heparin lipase activity in cancer patients." Journal of Experimental Medicine 164, no. 4 (1986): 1093–101. http://dx.doi.org/10.1084/jem.164.4.1093.

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Animals suffering from malignancy or chronic infection develop characteristic metabolic abnormalities, including a well-defined hypertriglyceridemic state. These abnormalities have been attributed to release of one or more mediators from activated macrophages. We report that cancer patients receiving RIFN-gamma, a potent macrophage activator, at doses of greater than or equal to 0.25 mg/m2/d i.m. show marked increases in triglyceride but not in cholesterol levels (pretreatment triglyceride level of 180 +/- 190 mg/dl [mean +/- SD] vs. a day-14 level of 370 +/- 242 mg/dl, n = 23, p less than 0.0

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BASHAM, TERESA Y., BRIAN J. NICKOLOFF, THOMAS C. MERIGAN, and VERA B. MORHENN. "Recombinant Gamma Interferon Differentially Regulates Class II Antigen Expression and Biosynthesis on Cultured Normal Human Keratinocytes." Journal of Interferon Research 5, no. 1 (1985): 23–32. http://dx.doi.org/10.1089/jir.1985.5.23.

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Drouet, C., A. Reboul, and M. Colomb. "Identification of a human non-interferon lymphokine activating monocyte complement biosynthesis." Biochemical Journal 263, no. 1 (1989): 157–64. http://dx.doi.org/10.1042/bj2630157.

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A monocyte-stimulating activity produced by mitogen-induced mononuclear cells has been defined by its ability to enhance the synthesis in vitro of complement C1 subcomponents, C2 and C3. A lymphokine responsible for this activity was purified from culture supernatants of peripheral blood mononuclear cells activated by staphylococcal enterotoxin A. From 0.5 litre of supernatant the purification procedure [(NH4)2SO4 precipitation, phenyl-Sepharose chromatography and preparative electrofocusing] yielded about 100 pmol of purified lymphokine. Its pI is 7.9 and its Mr, estimated by SDS/polyacrylami

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Patston, PA, RL Medcalf, Y. Kourteva, and M. Schapira. "C1-inhibitor-serine proteinase complexes and the biosynthesis of C1- inhibitor by Hep G2 and U 937 cells." Blood 82, no. 11 (1993): 3371–79. http://dx.doi.org/10.1182/blood.v82.11.3371.3371.

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Abstract The biosynthesis of the serpin alpha 1-proteinase inhibitor is regulated by a feedback mechanism whereby complexes between alpha 1- proteinase inhibitor and serine proteinases bind to liver cells and monocytes, a reaction that activates alpha 1-proteinase-inhibitor gene transcription. Such a mechanism may form the basis for the development of new therapeutic strategies for serpin deficiency states with reduced levels of otherwise normally functioning serpins. This issue was addressed for C1-inhibitor, the missing serpin in hereditary angioedema. C1-inhibitor biosynthesis by Hep G2 hep

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Rozprawy doktorskie na temat "Interferon-gamma/biosynthesis"

Millward, Jason Michael 1976. "Interferon-gamma and the regulation of neuroinflammation." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115699.

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Inflammation of the central nervous system (CNS) is important in many human diseases, and is regulated by a multitude of factors, including the cytokine interferon-gamma (IFNgamma). The importance of IFNgamma is highlighted in experimental autoimmune encephalomyelitis (EAE), an animal model of CNS inflammation. Mice lacking IFNgamma show exaggerated disease, with a different pattern of chemokine expression than the wild-type. We administered IFNgamma to the CNS using intrathecal injection of a replication-defective adenoviral vector to ask about direct actions of IFNgamma on chemokine expressi

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