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Oncostatin M signal...
Oncostatin M signaling in human glioma cell lines.
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- Krona, Annika, 1973 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för laboratoriemedicin , Avdelningen för patologi,Institute of Laboratory Medicine, Dept of Pathology
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- Järnum, Sofia (författare)
- Lund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Department of Experimental Medical Science,Faculty of Medicine
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- Salford, Leif (författare)
- Lund University,Lunds universitet,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine
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- Widegren, Bengt (författare)
- Lund University,Lunds universitet,Biologiska institutionen,Naturvetenskapliga fakulteten,Department of Biology,Faculty of Science
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- Åman, Pierre, 1953 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för laboratoriemedicin , Avdelningen för patologi,Institute of Laboratory Medicine, Dept of Pathology
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(creator_code:org_t)
- 2005
- 2005
- Engelska.
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Ingår i: Oncology reports. - 1021-335X .- 1791-2431. ; 13:5, s. 807-11
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Abstract
Ämnesord
Stäng
- We have recently found that oncostatin M (OSM) is overexpressed in most human brain tumors. The effects of OSM are unclear with conflicting reports of growth stimulatory or inhibitory effects in various cell types. The aim of this study was to investigate the effects of OSM in 5 glioma cell lines and 7 short-term cultures of human gliomas and in normal cultured human astrocytes. None of the cell lines and short-term cultured tumor cells expressed OSM in vitro. OSM signals through a gp130 containing receptor complex over the JAK/STAT pathway. Immunofluorescence and RT-PCR analysis showed that the tumor cells express gp130 and the other receptor components, LIFRbeta and OSMRbeta. OSM treatment induced phosphorylation of STAT3 and STAT1 indicating presence of a functional JAK/STAT pathway. No OSM effect on proliferation was observed. OSM gave no protective effects against tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-induced cytotoxicity.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Cancer and Oncology (hsv//eng)
Nyckelord
- Apoptosis Regulatory Proteins
- Astrocytes
- cytology
- drug effects
- Base Sequence
- Cell Line
- Tumor
- Cell Survival
- drug effects
- Cells
- Cultured
- Cytokines
- pharmacology
- DNA Primers
- Glioma
- physiopathology
- Humans
- Membrane Glycoproteins
- pharmacology
- Oncostatin M
- Peptides
- genetics
- pharmacology
- Receptors
- Cytokine
- genetics
- Receptors
- Oncostatin M
- Reverse Transcriptase Polymerase Chain Reaction
- Signal Transduction
- drug effects
- TNF-Related Apoptosis-Inducing Ligand
- Tumor Necrosis Factor-alpha
- pharmacology
- cytotoxicity
- STAT3
- proliferation
- oncostatin M
- astrocytoma
- brain tumor
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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