130 results on '"Rossner M"'
Search Results
102. Cloning of a novel neuronally expressed orphan G-protein-coupled receptor which is up-regulated by erythropoietin, interacts with microtubule-associated protein 1b and colocalizes with the 5-hydroxytryptamine 2a receptor.
- Author
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Maurer MH, Grünewald S, Gassler N, Rossner M, Propst F, Würz R, Weber D, Kuner T, Kuschinsky W, and Schneider A
- Subjects
- Amino Acid Sequence, Animals, Brain drug effects, Brain metabolism, Cloning, Molecular, Humans, Mice, Mice, Transgenic, Microtubule-Associated Proteins genetics, Molecular Sequence Data, Multigene Family, Nerve Tissue Proteins metabolism, Neurons drug effects, Organ Specificity, Rats, Sequence Homology, Amino Acid, Two-Hybrid System Techniques, Up-Regulation drug effects, Up-Regulation genetics, Erythropoietin pharmacology, Microtubule-Associated Proteins metabolism, Nerve Tissue Proteins genetics, Neurons metabolism, Receptor, Serotonin, 5-HT2A metabolism, Receptors, G-Protein-Coupled genetics, Receptors, G-Protein-Coupled metabolism
- Abstract
G-protein-coupled receptors (GPCRs) are the largest group of cell surface molecules involved in signal transduction and are receptors for a wide variety of stimuli ranging from light, calcium and odourants to biogenic amines and peptides. It is assumed that systematic genomic data-mining has identified the overwhelming majority of all remaining GPCRs in the genome. Here we report the cloning of a novel orphan GPCR which was identified in a search for erythropoietin-induced genes in the brain as a strongly up-regulated gene. This unknown gene coded for a protein which had a seven-transmembrane topology and key features typical of GPCRs of the A family but a low overall identity to all known GPCRs. The protein, coded ee3, has an unusually high evolutionary conservation and is expressed in neurons in diverse areas of the CNS with relation to integrative functions or motor tasks. A yeast two-hybrid screen for interacting proteins revealed binding to the microtubule-associated protein (MAP) 1b. Coupling to MAP1a has been described for another cognate GPCR, the 5-hydroxytryptamine (5HT) 2a receptor. Surprisingly, we found complete colocalization of ee3 and the 5HT2a receptor. The interaction with MAP1b proved to be critical for the stability or folding of ee3 as in mice lacking MAP1b the ee3 protein was undetectable by immunohistochemistry, although messenger RNA levels remained unchanged. We propose that ee3 is a highly interesting new orphan GPCR with potential connections to erythropoietin and 5HT2a receptor signalling.
- Published
- 2004
- Full Text
- View/download PDF
103. Tumor necrosis factor-like weak inducer of apoptosis-induced neurodegeneration.
- Author
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Potrovita I, Zhang W, Burkly L, Hahm K, Lincecum J, Wang MZ, Maurer MH, Rossner M, Schneider A, and Schwaninger M
- Subjects
- Animals, Antibodies administration & dosage, Antibodies pharmacology, Apoptosis Regulatory Proteins, Brain Ischemia complications, Brain Ischemia metabolism, Brain Ischemia pathology, Carrier Proteins antagonists & inhibitors, Cell Death genetics, Cell Death physiology, Cells, Cultured, Cerebral Infarction genetics, Cerebral Infarction pathology, Cerebral Infarction prevention & control, Cytokine TWEAK, Disease Models, Animal, Gene Expression Profiling, Humans, I-kappa B Kinase, Male, Mice, Mice, Inbred Strains, Mice, Knockout, NF-kappa B biosynthesis, NF-kappa B genetics, Nerve Degeneration etiology, Nerve Degeneration pathology, Neurons pathology, Protein Serine-Threonine Kinases metabolism, RNA biosynthesis, RNA genetics, Receptors, Tumor Necrosis Factor biosynthesis, Receptors, Tumor Necrosis Factor genetics, Recombinant Fusion Proteins genetics, Recombinant Fusion Proteins metabolism, Stroke complications, Stroke pathology, TWEAK Receptor, Transfection, Tumor Necrosis Factors, Up-Regulation genetics, Carrier Proteins genetics, Carrier Proteins metabolism, Nerve Degeneration metabolism, Neurons metabolism, Stroke metabolism
- Abstract
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a member of the tumor necrosis factor (TNF) family of cytokines. It has proangiogenic and proinflammatory properties in vivo and induces cell death in tumor cell lines. TWEAK effects are mediated by the membrane receptor Fn14. In a systematic search for genes regulated in a murine stroke model with the tag-sequencing technique massively parallel signature sequencing, we have identified TWEAK as an induced gene. After 24 hr of focal cerebral ischemia in vivo or oxygen glucose deprivation in primary cortical neurons, both TWEAK and its receptor Fn14 were significantly upregulated. TWEAK induced cell death in primary neurons. Transfection of a nuclear factor (NF)-kappaB-luciferase fusion gene demonstrated that TWEAK stimulated transcriptional activity of NF-kappaB through Fn14 and the IkappaB kinase. Inhibition of NF-kappaB reduced TWEAK-stimulated neuronal cell death, suggesting that NF-kappaB mediates TWEAK-induced neurodegeneration at least in part. Intraperitoneal injection of a neutralizing anti-TWEAK antibody significantly reduced the infarct size after 48 hr of permanent cerebral ischemia. In summary, our data show that TWEAK induces neuronal cell death and is involved in neurodegeneration in vivo.
- Published
- 2004
- Full Text
- View/download PDF
104. What's in a picture? The temptation of image manipulation.
- Author
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Rossner M and Yamada KM
- Subjects
- Ethics, Publishing, Research Design, Software, Image Processing, Computer-Assisted methods
- Published
- 2004
- Full Text
- View/download PDF
105. Identification of regulated genes during permanent focal cerebral ischaemia: characterization of the protein kinase 9b5/MARKL1/MARK4.
- Author
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Schneider A, Laage R, von Ahsen O, Fischer A, Rossner M, Scheek S, Grünewald S, Kuner R, Weber D, Krüger C, Klaussner B, Götz B, Hiemisch H, Newrzella D, Martin-Villalba A, Bach A, and Schwaninger M
- Subjects
- Alternative Splicing, Amino Acid Sequence, Animals, Cell Survival genetics, Cloning, Molecular, Disease Models, Animal, Gene Expression Profiling, Mice, Molecular Sequence Data, Organ Specificity, Phosphorylation, Protein Serine-Threonine Kinases metabolism, Sequence Homology, Sequence Homology, Amino Acid, Brain Ischemia enzymology, Brain Ischemia genetics, Gene Expression Regulation, Protein Serine-Threonine Kinases genetics
- Abstract
Cerebral ischaemia induces transcriptional changes in a number of pathophysiologically important genes. Here we have systematically studied gene expression changes after 90 min and 24 h of permanent focal ischaemia in the mouse by an advanced fragment display technique (restriction-mediated differential display). We identified 56 transcriptionally altered genes, many of which provide novel hints to ischaemic pathophysiology. Particularly interesting were two pro-apoptotic genes (Grim19 and Tdag51), whose role in cerebral ischaemia and neuronal cell death has not been recognized so far. Among the unknown sequences, we identified a gene that was rapidly and transiently up-regulated. The encoded protein displayed high homology to the MARK family of serine-threonine protein kinases and has recently been described as MARKL1/MARK4. Here we demonstrate that this protein is a functional protein kinase with the ability to specifically phosphorylate a cognate peptide substrate for the AMP-kinase family. Upon overexpression in heterologous cells, the functional wild-type protein, but not its kinase-dead mutant, led to decreased cell viability. We conclude that the up-regulation of this kinase during focal ischaemia may represent an interesting new target for pharmacological intervention.
- Published
- 2004
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- View/download PDF
106. Restriction-mediated differential display (RMDD) identifies pip92 as a pro-apoptotic gene product induced during focal cerebral ischemia.
- Author
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Schneider A, Fischer A, Weber D, von Ahsen O, Scheek S, Krüger C, Rossner M, Klaussner B, Faucheron N, Kammandel B, Goetz B, Herrmann O, Bach A, and Schwaninger M
- Subjects
- Animals, COS Cells, DNA Fragmentation, Gene Expression Regulation, Immediate-Early Proteins, Infarction, Middle Cerebral Artery, Mice, Neurons cytology, Neurons physiology, Oligonucleotide Array Sequence Analysis, Proteins genetics, Time Factors, Apoptosis, Brain Ischemia physiopathology, Gene Expression Profiling methods, Proteins metabolism
- Abstract
Studies of gene expression changes after cerebral ischemia can provide novel insight into ischemic pathophysiology. Here we describe application of restriction-mediated differential display to screening for differentially expressed genes after focal cerebral ischemia. This method combines the nonredundant generation of biotin-labeled fragment sets with the excellent resolution of direct blotting electrophoresis, reliable fragment recovery, and a novel clone selection strategy. Using the filament model in mouse with 90 minutes MCA occlusion followed by 2, 6, and 20 hours reperfusion, we have compared gene expression in sham-operated animals to both the ipsi- and contralateral forebrain hemisphere of ischemic mice. Our screening method has resulted in the identification of 70 genes differentially regulated after transient middle cerebral artery occlusion (MCAO), several of which represent unknown clones. We have identified many of the previously published regulated genes, lending high credibility to our method. Surprisingly, we detected a high degree of correspondent regulation of genes in the nonischemic hemisphere. A high percentage of genes coding for proteins in the respiratory chain was found to be up-regulated after ischemia, potentially representing a new mechanism involved in counteracting energy failure or radical generation in cerebral ischemia. One particularly interesting gene, whose upregulation by ischemia has not been described before, is pip92; this gene shows a rapid and long-lasting induction after cerebral ischemia. Here we demonstrate that pip92 induces cell death in primary neurons and displays several hallmarks of pro-apoptotic activity upon overexpression, supporting the notion that we have identified a novel pathophysiological player in cerebral ischemia. In summary, restriction-mediated differential display has proven its suitability for screening complex samples such as brain to reliably identify regulated genes, which can uncover novel pathophysiological mechanisms.
- Published
- 2004
- Full Text
- View/download PDF
107. The JCB will let your data shine in RGB.
- Author
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Rossner M and O'Donnell R
- Subjects
- Image Enhancement, Photography standards, Photomicrography standards, Software standards, Periodicals as Topic standards, Publishing standards
- Published
- 2004
- Full Text
- View/download PDF
108. The "CMT Rat": Peripheral Neuropathy and Dysmyelination Caused by Transgenic Overexpression of PMP22.
- Author
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Niemann S, Sereda MW, Rossner M, Stewart H, Suter U, Meinck HM, Griffiths IR, and Nave KA
- Abstract
We have generated a transgenic rat model of Charcot-Marie-Tooth disease type 1A (CMT1A) providing formal proof that this neuropathy can be caused by increased expression of peripheral myelin protein-22 (PMP22). Heterozygous PMP22-transgenic rats develop muscle weakness and gait abnormalities as well as reduced nerve conduction velocities and EMG abnormalities, which closely resemble recordings in patients with CMT1A. Dys- and demyelination, Schwann cell hypertrophy, and "onion bulb" formation are also similar to findings in humans. When bred to homozygosity, transgenic rats completely fail to elaborate myelin, but all myelin-forming Schwann cells segregate with axons in the normal one-to-one ratio. Although arrested at this "promyelin" stage, differentiation proceeds in homozygous rats at the molecular level, as demonstrated by high-level expression of myelin structural genes. Intracellular trafficking of the wild-type protein is not visibly impaired, even when strongly overexpressed, suggesting that PMP22 blocks myelin assembly in a late Golgi/cell membrane compartment of the affected Schwann cell.
- Published
- 1999
- Full Text
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109. Neuronal basic helix-loop-helix proteins (NEX, neuroD, NDRF): spatiotemporal expression and targeted disruption of the NEX gene in transgenic mice.
- Author
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Schwab MH, Druffel-Augustin S, Gass P, Jung M, Klugmann M, Bartholomae A, Rossner MJ, and Nave KA
- Subjects
- Aging metabolism, Animals, Animals, Newborn growth & development, Animals, Newborn metabolism, Basic Helix-Loop-Helix Transcription Factors, Brain metabolism, Cell Differentiation physiology, Embryonic and Fetal Development physiology, Gene Expression physiology, Helix-Loop-Helix Motifs genetics, Mice, Neurons cytology, Neuropeptides genetics, Rats, Rats, Sprague-Dawley, Mice, Transgenic genetics, Nerve Tissue Proteins genetics, Nerve Tissue Proteins metabolism, Neurons metabolism, Neuropeptides metabolism
- Abstract
Basic helix-loop-helix (bHLH) genes have emerged as important regulators of neuronal determination and differentiation in vertebrates. Three putative neuronal differentiation factors [NEX for neuronal helix-loop-helix protein-1 (mammalian atonal homolog-2), neuroD (beta-2), and NDRF for neuroD-related factor (neuroD2)] are highly homologous to each other in the bHLH region and comprise a new bHLH subfamily. To study the role of NEX, the first bHLH protein identified in this group, we have disrupted the NEX gene by homologous recombination. NEX-deficient mice have no obvious developmental defect, and CNS neurons appear fully differentiated. To investigate further whether the absence of NEX is compensated for by neuroD and NDRF, we compared the spatiotemporal expression of all three genes. We demonstrate, by in situ hybridization, that the transcription patterns of NEX, neuroD, and NDRF genes are highly overlapping in the developing CNS of normal rats between embryonic day 12 and adult stages but are not strictly identical. The most prominent transcription of each gene marks the dorsal neuroepithelium of the telencephalon in early development and is sustained in the adult neocortex, hippocampus, and cerebellum. In general, neuroD provides the earliest marker of neuronal differentiation in any given region compared with NDRF or NEX. Whereas a few CNS regions are specific for neuroD, no region was detected in which solely NEX or NDRF is expressed. This suggests that the function of the mutant NEX gene in neuronal differentiation is compensated for by neuroD and NDRF and that, in analogy with myogenic bHLH proteins, neuronal differentiation factors are at least in part equivalent in function.
- Published
- 1998
110. SHARPs: mammalian enhancer-of-split- and hairy-related proteins coupled to neuronal stimulation.
- Author
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Rossner MJ, Dörr J, Gass P, Schwab MH, and Nave KA
- Subjects
- Amino Acid Sequence, Animals, Animals, Newborn, Basic Helix-Loop-Helix Transcription Factors, DNA-Binding Proteins physiology, Embryo, Mammalian, Gene Expression Regulation, Developmental drug effects, Helix-Loop-Helix Motifs genetics, Insect Proteins physiology, Kainic Acid pharmacology, Male, Molecular Sequence Data, Multigene Family, Nerve Growth Factors pharmacology, Neuropeptides biosynthesis, Neuropeptides genetics, PC12 Cells, Rats, Rats, Sprague-Dawley, Repressor Proteins physiology, Transcription Factors biosynthesis, Transcription Factors genetics, Drosophila Proteins, Helix-Loop-Helix Motifs physiology, Homeodomain Proteins, Neurons physiology, Neuropeptides physiology, Transcription Factors physiology
- Abstract
In the mammalian central nervous system, a diverse group of basic helix-loop-helix (bHLH) proteins is involved in the determination of progenitor cells and, subsequently, in regulating neuronal differentiation. Here we report the identification of a novel subfamily of bHLH proteins, defined by two mammalian enhancer-of-split- and hairy-related proteins, termed SHARP-1 and SHARP-2. In contrast to known bHLH genes, detectable transcription of SHARP genes begins at the end of embryonic development marking differentiated neurons that have reached a final position, and increases as postnatal development proceeds. In the adult, SHARP genes are expressed in subregions of the CNS that have been associated with adult plasticity. In PC12 cells, a model system to study neurite outgrowth, SHARP genes can be induced by NGF with the kinetics of an immediate-early gene. Similarly, within 1 h after the administration of kainic acid in vivo, SHARP-2 is induced in neurons throughout the rat cerebral cortex. This suggests that neuronal bHLH proteins are also involved in the "adaptive" changes of mature CNS neurons which are coupled to glutamatergic stimulation.
- Published
- 1997
- Full Text
- View/download PDF
111. Murine flt3 ligand protects M1 leukemic cells from LIF-induced differentiation and suppression of self-renewal.
- Author
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Begley CG, Rasko JE, Curtis D, Takagi K, Metcalf D, Hilton D, Roberts B, Nicola NA, and Rossner MT
- Subjects
- Animals, Base Sequence, Blotting, Northern, Cell Differentiation drug effects, Cell Line, Chlorocebus aethiops, DNA Primers, Fetus, Hematopoiesis, Hematopoietic Stem Cells drug effects, Hematopoietic Stem Cells physiology, Humans, Leukemia Inhibitory Factor, Leukemia, Myeloid, Acute, Liver metabolism, Macrophage Colony-Stimulating Factor pharmacology, Membrane Proteins physiology, Mice, Molecular Sequence Data, Polymerase Chain Reaction, RNA, Messenger analysis, RNA, Messenger biosynthesis, Recombinant Proteins biosynthesis, Templates, Genetic, Transfection, Tumor Cells, Cultured, Growth Inhibitors pharmacology, Hematopoietic Stem Cells cytology, Interleukin-6, Lymphokines pharmacology, Membrane Proteins biosynthesis
- Abstract
Self-renewing cell divisions are an important characteristic exhibited by both normal hematopoietic stem cells and leukemic cell populations. We have examined the action of flt3/flk2 ligand (FL) on physiologic suppression of self-renewal during growth factor-induced differentiation of M1 leukemic cells. Unstimulated M1 cells expressed high levels of flt3 receptor mRNA and protein, with approximately 20,000 molecules present at the cell surface. Consistent with data obtained from normal macrophage populations, expression of both mRNA and protein for flt3 receptor was suppressed as cells were induced to differentiate into mature macrophages in response to leukemia inhibitory factor (LIF). Although FL alone had no detectable action on unstimulated M1 cells, an effect was revealed during LIF-induced differentiation. FL overcame LIF-induced suppression in clonal cultures of M1 cells, prevented morphologic changes associated with macrophage differentiation and interfered with the LIF-induced responsiveness of M1 cells to macrophage colony-stimulating factor (M-CSF). This action of FL was evident on both parental M1 cells and M1 cells whose differentiation program was perturbed by enforced expression of the transcription factor SCL. The action of FL was most striking in clone transfer experiments in which FL rescued M1 cells from LIF-induced suppression of self-renewal. The ability of FL to maintain self-renewal characteristics satisfies one of the criteria predicted for a stem-cell-active molecule and contrasts with the action of FL in stimulating proliferation and differentiation of normal hematopoietic cells.
- Published
- 1996
112. A transgenic rat model of Charcot-Marie-Tooth disease.
- Author
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Sereda M, Griffiths I, Pühlhofer A, Stewart H, Rossner MJ, Zimmerman F, Magyar JP, Schneider A, Hund E, Meinck HM, Suter U, and Nave KA
- Subjects
- Animals, Animals, Genetically Modified, Base Sequence, DNA Primers chemistry, Demyelinating Diseases genetics, Disease Models, Animal, Gene Expression, Homozygote, Humans, Molecular Sequence Data, Neural Conduction, Rats, Schwann Cells cytology, Charcot-Marie-Tooth Disease genetics, Myelin Proteins genetics
- Abstract
Charcot-Marie-Tooth disease (CMT) is the most common inherited neuropathy in humans and has been associated with a partial duplication of chromosome 17 (CMT type 1A). We have generated a transgenic rat model of this disease and provide experimental evidence that CMT1A is caused by increased expression of the gene for peripheral myelin protein-22 (PMP22, gas-3). PMP22-transgenic rats develop gait abnormalities caused by a peripheral hypomyelination, Schwann cell hypertrophy (onion bulb formation), and muscle weakness. Reduced nerve conduction velocities closely resemble recordings in human patients with CMT1A. When bred to homozygosity, transgenic animals completely fail to elaborate myelin. We anticipate that the CMT rat model will facilitate the identification of a cellular disease mechanism and serve in the evaluation of potential treatment strategies.
- Published
- 1996
- Full Text
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113. The flt3/flk-2 ligand: receptor distribution and action on murine haemopoietic cell survival and proliferation.
- Author
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Rasko JE, Metcalf D, Rossner MT, Begley CG, and Nicola NA
- Subjects
- Animals, Cell Division, Cell Survival, Clone Cells, Hematopoiesis, Ligands, Mice, Recombinant Proteins metabolism, fms-Like Tyrosine Kinase 3, Bone Marrow metabolism, Hematopoietic Stem Cells metabolism, Proto-Oncogene Proteins metabolism, Receptor Protein-Tyrosine Kinases metabolism
- Abstract
In this study the distribution and quantitation of the flt3/flk-2 receptor was examined on bone marrow cells and defined haemopoietic subpopulations. Undifferentiated cells expressed the greatest numbers of flt3/flk-2 receptors: 19% of primitive lin-kit+sca-1+ bone marrow cells and 16% of fetal liver lin-aa4.1+ cells exhibited over 15 000 receptors per cell as determined by binding of the radiolabeled cognate ligand (flt3/flk-2 ligand, FL). Moderate binding was demonstrated on early B lymphocyte subsets (4400 receptors per cell) and very low levels were detected on monocytes. Binding was not detected on promyelocytes, myelocytes, promonocytes, metamyelocytes, polymorphonuclear cells, eosinophils or nucleated erythroid cells. FL enhanced the survival of primitive lin kit+sca-1+ cells with an efficacy s with an efficacy equivalent to stem cell factor (SCF). FL stimulated predominantly blast and granulocyte-macrophage colony formation in cultures of bone marrow cells by both direct and indirect mechanisms. Marked synergistic effects of FL with combinations of colony stimulating factors (CSFs) or interleukin-6 occurred in the proliferation of primitive lin-kit+sca-1+ cells, but not lin-kit+sca-1- progenitor cells. Surprisingly, recloning experiments revealed that FL plus IL-3 increased the generation of progenitor cells by lin-kit a-1- cells compared with SCF plus IL-3. Thus FL functions as a factor with both direct and indirect stimulatory activities directed to the expansion, maintenance of clonogenic potential, and possibly limited self-renewal, of early haemopoietic cells.
- Published
- 1995
114. Fms-like tyrosine kinase 3 catalytic domain can transduce a proliferative signal in FDC-P1 cells that is qualitatively similar to the signal delivered by c-Fms.
- Author
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Rossner MT, McArthur GA, Allen JD, and Metcalf D
- Subjects
- Animals, Brain Chemistry, Cell Differentiation drug effects, Cell Division, Cell Line, Cloning, Molecular, Genes, fms genetics, Granulocyte-Macrophage Colony-Stimulating Factor pharmacology, Macrophage Colony-Stimulating Factor pharmacology, Mice, Organ Specificity, Proto-Oncogene Proteins genetics, RNA, Messenger biosynthesis, Receptor Protein-Tyrosine Kinases genetics, Receptor, Macrophage Colony-Stimulating Factor genetics, Receptors, Cell Surface genetics, Recombinant Fusion Proteins biosynthesis, Sequence Analysis, DNA, Transcription, Genetic, fms-Like Tyrosine Kinase 3, Hematopoietic Stem Cells cytology, Proto-Oncogene Proteins physiology, Receptor Protein-Tyrosine Kinases physiology, Receptor, Macrophage Colony-Stimulating Factor physiology, Receptors, Cell Surface physiology, Signal Transduction physiology
- Abstract
A full length clone of murine fms-like tyrosine kinase 3 [flt3, also known as fetal liver kinase 2 (flk2)] was constructed from sequences obtained from a brain complementary DNA (cDNA) library and from cDNA prepared from the cell line Tikaut. In the absence of a ligand to study the function of Flt3, a chimeric molecule was constructed comprising the extracellular domain of murine c-Fms and the transmembrane and cytoplasmic domains of Flt3. A plasmid encoding the chimeric receptor was cotransfected along with a plasmid conferring neomycin resistance into FDC-P1 cells that do not normally express c-fms or flt3 and require granulocyte-macrophage colony-stimulating factor (GM-CSF) or interleukin 3 for growth. Two types of clones were obtained following selection in GM-CSF and G418. Two of seven clones had the capacity for M-CSF-dependent colony formation in semisolid medium, indicating that the cytoplasmic domain of Flt3 can transduce a proliferative signal. From the remaining clones, M-CSF-dependent clonogenic cells could be selected by prior bulk liquid culture in M-CSF. It has been shown previously that the GM-CSF-dependent proliferative capacity is strongly inhibited by M-CSF in FDC-P1 cells engineered to express full length c-fms. This phenomenon was also observed with FD/fms-flt3 cells that were clonogenic in M-CSF. Stimulation of FD/fms or FD/fms-flt3 cells in liquid culture by M-CSF caused differentiation of a small proportion of cells along the myelomonocytic pathway which was enhanced by the combination of M-CSF and GM-CSF.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1994
115. Receptor insertion into factor-dependent murine cell lines to develop specific bioassays for murine G-CSF and M-CSF and human GM-CSF.
- Author
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Metcalf D, Willson T, Rossner M, and Lock P
- Subjects
- Animals, DNA, Complementary analysis, Electroporation, Humans, Mice, Receptor, Macrophage Colony-Stimulating Factor analysis, Receptors, Colony-Stimulating Factor genetics, Receptors, Granulocyte Colony-Stimulating Factor analysis, Receptors, Granulocyte-Macrophage Colony-Stimulating Factor analysis, Biological Assay methods, Cell Line chemistry, Granulocyte Colony-Stimulating Factor physiology, Granulocyte-Macrophage Colony-Stimulating Factor physiology, Macrophage Colony-Stimulating Factor physiology, Receptors, Colony-Stimulating Factor analysis
- Abstract
cDNAs encoding the receptors for murine G-CSF, M-CSF or human GM-CSF were inserted into the murine hemopoietic continuous cell lines Ba/F3 or FDC-P1 and sublines selected that were then responsive to proliferative stimulation by these growth factors. When used in microwell assays the Ba/F3 G-CSF receptor-expressing cell line was able to detect 100 pg G-CSF per ml, the Ba/F3 M-CSF receptor-expressing cell line 100-400 pg M-CSF per ml and the FDC-P1 line expressing the alpha- and beta-chains of the human GM-CSF receptor detected 5-10 pg/ml of GM-CSF in test material. These cell lines appear satisfactory for use as selective bioassays for these colony stimulating factors in material potentially containing a mixture of growth factors.
- Published
- 1994
- Full Text
- View/download PDF
116. Review: hepatitis B virus X-gene product: a promiscuous transcriptional activator.
- Author
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Rossner MT
- Subjects
- Amino Acid Sequence, Animals, Gene Expression, Genes, Viral, Hepatitis B genetics, Humans, Molecular Sequence Data, Protein Processing, Post-Translational, Sequence Homology, Nucleic Acid, Viral Regulatory and Accessory Proteins, Hepatitis B virus genetics, Trans-Activators genetics
- Published
- 1992
- Full Text
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117. [Changes in psychodynamics of manic-depressive diseases through the long-term administration of lithium salts].
- Author
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König L and Rossner M
- Subjects
- Adolescent, Adult, Anxiety, Clinical Trials as Topic, Female, Humans, Lithium administration & dosage, Lithium pharmacology, Long-Term Care, Male, Middle Aged, Personality Disorders drug therapy, Social Adjustment, Time Factors, Bipolar Disorder drug therapy, Lithium therapeutic use, Personality drug effects
- Published
- 1974
- Full Text
- View/download PDF
118. [Phase-preventive long-term treatment with lithium of cyclic psychotic patients].
- Author
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König L, Rossner M, and Felber W
- Subjects
- Bipolar Disorder drug therapy, Coma chemically induced, Diarrhea chemically induced, Humans, Lithium administration & dosage, Lithium adverse effects, Nausea chemically induced, Time Factors, Tremor chemically induced, Vertigo chemically induced, Vomiting chemically induced, Bipolar Disorder prevention & control, Lithium therapeutic use
- Published
- 1974
119. [Neuroleptic long term care with extremely low doses in psychotic syndromes of paranoid-hallucination type].
- Author
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Rossner M and König L
- Subjects
- Dose-Response Relationship, Drug, Haloperidol administration & dosage, Humans, Long-Term Care, Trifluperidol administration & dosage, Hallucinations drug therapy, Paranoid Disorders drug therapy, Psychotic Disorders drug therapy, Tranquilizing Agents administration & dosage
- Abstract
About 30 patients with, in some cases, recurring paranoid or paranoid-hallucinatory psychoses underwent a long-term treatment--from 2--6 years according to individual cases--with very small doses of powerful neuroleptics (Haloperidol, Triperidol, and occasionally Trisedyl). Relapses, such as remanifestations, which occured in some cases, were easily controlled either in outpatients or in the day clinic. No extrapyramidal symptoms of pharmacogenic defect syndromes were observed. The rehabilitation successes were in part very good to exceptional.
- Published
- 1975
120. [Clinical experiences with noxiptilin].
- Author
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König L, Lange E, Rossner M, Liefke T, Uhlig B, Kursawe HK, and Lungwitz J
- Subjects
- Adjustment Disorders drug therapy, Adolescent, Adult, Aged, Ambulatory Care, Cyclothymic Disorder drug therapy, Dibenzocycloheptenes administration & dosage, Dibenzocycloheptenes adverse effects, Female, Humans, Intracranial Arteriosclerosis drug therapy, Male, Middle Aged, Neurocognitive Disorders drug therapy, Psychophysiologic Disorders drug therapy, Schizophrenia drug therapy, Depression drug therapy, Dibenzocycloheptenes therapeutic use
- Abstract
Noxiptilin (Elronon) proved to be a good bipolar thymoleptic agent in the clinical test at 3 special clinics. Its stimulating effect on the psychomotor function is more pronounced than its sedative action. Therefore, in cases with the anxious, agitated depressive syndrome the additional therapy with a neuroleptic agent or a sedative tranquilizer may be favourable. N. is well tolerated even at a higher age. The side effects are the same as those of other known thymoleptics.
- Published
- 1976
121. [Diagnostic problems of chronic misuse of barbiturate-free sedatives].
- Author
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Rossner M, Ficker F, and Sauermann W
- Subjects
- Diagnosis, Differential, Glutethimide, Humans, Mental Disorders diagnosis, Nervous System Diseases diagnosis, Pentanols, Hypnotics and Sedatives, Substance-Related Disorders diagnosis
- Abstract
Atypical neuropsychiatric disease pictures resulting from chronic abuse of barbiturate-free soporifics are often misinterpreted diagnostically. The problems of diagnosis are discussed on the basis of experience gathered by the authors and with due consideration of results reported in the literature.
- Published
- 1979
122. [Quantitative and qualitative changes in the course of manic-depressive illnesses under long term lithium treatment].
- Author
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König L and Rossner M
- Subjects
- Bipolar Disorder diagnosis, Female, Humans, Lithium administration & dosage, Long-Term Care, Male, Recurrence, Bipolar Disorder drug therapy, Lithium therapeutic use
- Published
- 1975
123. [Clomipramine (monochlorimipramine) produced in the GDR].
- Author
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Lange E, Rossner M, König L, and Ficker F
- Subjects
- Depression drug therapy, Germany, East, Humans, Clomipramine therapeutic use, Dibenzazepines
- Published
- 1978
124. An alpha 2-macroglobulinlike activity in the blood of chelicerate and mandibulate arthropods.
- Author
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Armstrong PB, Rossner MT, and Quigley JP
- Subjects
- Animals, Immunoassay, Molecular Weight, Peptide Fragments analysis, Species Specificity, Trypsin metabolism, Arthropods analysis, alpha-Macroglobulins analysis
- Abstract
The alpha 2-macroglobulins are large molecular weight proteinase-binding proteins that inhibit the ability of proteinases to hydrolyze protein substrates without suppressing activity against amide or ester substrates. They are also able to protect the active site of bound proteinases from active site inhibitors of suitably high molecular weight. The ability to protect the amidolytic activity of trypsin from the macromolecular active site inhibitor, soybean trypsin inhibitor, was used to demonstrate an alpha 2-macroglobulinlike activity in the blood of the horseshoe crab, Limulus polyphemus and the crustaceans Libinia emarginata (the spider crab) and Cancer borealis (the Jonah crab). The alpha 2-macroglobulinlike activities of L. polyphemus and L. emarginata are sensitive to methylamine, but that of C. borealis is relatively insensitive. The molecular weights (mw) of the trypsin-protecting proteins in L. emarginata and C. borealis, estimated from gelfiltration studies, are, respectively, 480 X 10(3) and 460 X 10(3), and are significantly smaller than that of L. polyphemus (Mr = 570 X 10(3)).
- Published
- 1985
- Full Text
- View/download PDF
125. [Operative castration in sexual delinquency--a survey of topical literature and an attempt at forming an opinion].
- Author
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Rossner M
- Subjects
- Androgen Antagonists therapeutic use, Humans, Hypothalamus surgery, Male, Paraphilic Disorders drug therapy, Paraphilic Disorders therapy, Psychotherapy, Stereotaxic Techniques, Castration psychology, Sex Offenses
- Abstract
An attempt is made to form an opinion regarding the indication of operative castration for sexual delinquents, from a survey of recent literature dealing with methods of treatment for cases of sexual deviation/sexual delinquency (operative/medicinal castration, combined psychotherapy and medicinal castration, stereotactic operation on the hypothalamus).
- Published
- 1979
126. [Treatment of depression with chlorimipramine. Review of literature and personal clinical experiences].
- Author
-
Rossner M and Ficker F
- Subjects
- Adult, Aged, Antidepressive Agents adverse effects, Blood Pressure drug effects, Dibenzazepines adverse effects, Evaluation Studies as Topic, Exanthema chemically induced, Fatigue chemically induced, Female, Humans, Male, Middle Aged, Nausea chemically induced, Pruritus chemically induced, Sweating drug effects, Vomiting chemically induced, Antidepressive Agents therapeutic use, Depression drug therapy, Dibenzazepines therapeutic use
- Published
- 1972
127. [Delirious condition of excitation after meprobamate intoxication--intoxication effect or inanition delirium?].
- Author
-
Lange E and Rossner M
- Subjects
- Humans, Male, Delirium chemically induced, Meprobamate poisoning, Starvation complications, Substance-Related Disorders
- Published
- 1966
128. [Contribution on the clinical picture and etiology of Adie's syndrome].
- Author
-
Rossner M and Lange E
- Subjects
- Accommodation, Ocular, Achilles Tendon physiopathology, Adie Syndrome diagnosis, Adolescent, Adult, Child, Diagnosis, Differential, Dysautonomia, Familial complications, Encephalitis complications, Female, Humans, Male, Mydriatics, Patella, Pupil physiopathology, Reflex, Stretch, Tendons physiopathology, Adie Syndrome etiology
- Published
- 1969
129. [Head injuries with suicidal intent. Case reports and studies of the psychology of suicide].
- Author
-
Rossner M
- Subjects
- Adjustment Disorders, Aged, Depressive Disorder, Major, Female, Guilt, Humans, Middle Aged, Paranoid Disorders, Sleep Initiation and Maintenance Disorders, Craniocerebral Trauma, Suicide
- Published
- 1972
130. [Economic and social aspects in relation to the long term prevention of relapses in manic-depressive psychoses using lithium salts].
- Author
-
Rossner M, König L, and Lange E
- Subjects
- Bipolar Disorder prevention & control, Chronic Disease, Humans, Long-Term Care, Socioeconomic Factors, Bipolar Disorder drug therapy, Lithium administration & dosage
- Published
- 1971
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