Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:BIOD00035 (CSF)
 30,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

SSPE patients characteristically have high complement-fixing (CF) and neutralizing (N) antibody titers against measles virus in their sera, CSF, and brain. However, using SSPE patients' sera, the immunoperoxidase (IP) labeling of smooth nucleocapsids in SSPE or measles virus infected Vero cells or measles virions has not been achieved using conventional EM fixatives. Using the periodate-lysine-paraformaldehyde (PLP) fixative developed by McLean and Nakane (1974), and the indirect IP technique, antibodies against smooth nucleocapsids in SSPE and measles virus infected Vero cell cultures have been detected in serum from SSPE patients and normal individuals with high measles antibody titers.
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PMID:Antibody in SSPE serum and brain igG against measles virus smooth nucleocapsids detected by immunoelectron microscopy. 33 49

The authors present here the published values of lysine in some biological fluids, plasma, urine, CSF, amniotic fluid, aqueous humor, sweat. The plasma levels are lower in newborn infants than in adult subjects. The urinary excretion of lysine is high in the first pregnancy, the lysine concentration of amniotic fluid decreases progressively. A sex difference has been described in CSF: values higher in men. Changes occur in lysine concentrations when samples are not prepared for analysis immediately after collection and certain drugs interfere with analysis.
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PMID:[Lysine in human biologic fluids and tissues: reference values, physiologic variations and interferences]. 190 99

TCR-gamma delta+ CTL clones were generated from CD4-CD8- T cells that were stimulated twice with the cell line JY. Either IL-2 or IL-4 was used as growth factor. A number of TCR-gamma delta+ clones were found to lyse the stimulator cell line JY. Two of these clones secreted N alpha-benzyloxycarbonyl-L-lysine thiobenzyl ester serine esterase activity after stimulation with JY cells. The cytotoxic activity of these two clones was blocked by a mAb specific for HLA-A2. Moreover, these two TCR-gamma delta+ clones selectively lysed human fibroblast line M1 and murine P815 cells transfected with DNA fragments encoding HLA-A2 but not those transfected with HLA-B7 encoding DNA, indicating that these clones recognize HLA-A2. Analysis of the recognition of HLA-A2 by using target cells transfected with mutated HLA-A2 encoding genes revealed that the nature of the amino acid at position 152 of the molecule is critical for recognition of the TCR-alpha beta+ as well as the TCR-gamma delta+ CTL clones since replacement of Val for Ala at that position resulted in abrogation of recognition of one TCR-gamma delta+ and one TCR-alpha beta+ clone and substitution of Val for Glu affected recognition of all clones. Substitution of Leu for Trp at position 156 abrogated recognition by one TCR-gamma delta+ and one TCR-alpha beta+ T cell clone, but recognition by the other clones was not changed. All clones were able to secrete IL-2, IFN-gamma, and GM-CSF but not IL-4 after activation.
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PMID:Cytotoxic activity and lymphokine production of T cell receptor (TCR)-alpha beta+ and TCR-gamma delta+ cytotoxic T lymphocyte (CTL) clones recognizing HLA-A2 and HLA-A2 mutants. Recognition of TCR-gamma delta+ CTL clones is affected by mutations at positions 152 and 156. 211 41

Ligand-induced tyrosine phosphorylation of the human colony-stimulating factor 1 receptor (CSF-1R) could involve either an intra- or intermolecular mechanism. We therefore examined the ability of a CSF-1R carboxy-terminal truncation mutant to phosphorylate a kinase-defective receptor, CSF-1R[met 616], that contains a methionine-for-lysine substitution at its ATP-binding site. By using an antipeptide serum that specifically reacts with epitopes deleted from the enzymatically competent truncation mutant, cross-phosphorylation of CSF-1R[met 616] on tyrosine was demonstrated, both in immune-complex kinase reactions and in intact cells stimulated with CSF-1. Both in vitro and in vivo, CSF-1R[met 616] was phosphorylated on tryptic peptides identical to those derived from wild-type CSF-1R, suggesting that receptor phosphorylation on tyrosine can proceed via an intermolecular interaction between receptor monomers. When expressed alone, CSF-1R[met 616] did not undergo ligand-induced down modulation, but its phosphorylation in cells coexpressing the kinase-active truncation mutant accelerated its degradation.
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PMID:Ligand-induced phosphorylation of the colony-stimulating factor 1 receptor can occur through an intermolecular reaction that triggers receptor down modulation. 215 38

Replacement of leucine 301 in the human colony stimulating factor 1 receptor (CSF-1R) by serine, threonine, glutamic acid, or proline induced ligand-independent transforming activity in mouse NIH3T3 cells, whereas substitution by phenylalanine, methionine, cysteine, or lysine did not. Serine, glutamic acid, and proline mutations were more potent than threonine in inducing cell transformation. The growth of cells transformed by CSF-1R [S301] and [T301] was further stimulated by human recombinant CSF-1, but cells expressing CSF-1R [E301] responded poorly to the growth factor. The transforming efficiency of mutant receptors was also enhanced by the presence of a phenylalanine for tyrosine mutation at codon 969 near the receptor carboxylterminus. Like the v-fms oncogene product, receptors containing S301 or E301 mutations were partially inhibited in their intracellular transport to the plasma membrane, whereas non-transforming variants were transported normally. However, CSF-1R [T301] was processed as efficiently as the wild-type glycoprotein, indicating that the properties of altered transport and cell transformation could be at least partially dissociated. Expression of CSF-1 receptors bearing activating mutations led to increased phosphorylation of cellular substrates on tyrosine, suggesting that cell transformation resulted from constitutive receptor kinase activity. We conclude that only particular mutations at codon 301 mimic an effect of ligand on CSF-1R so as to constitutively activate its growth promoting activity.
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PMID:Transforming activities of human CSF-1 receptors with different point mutations at codon 301 in their extracellular domains. 215 80

We studied anti-oligodendrocyte antibody in sera and CSF from patients with multiple sclerosis (MS) and other neurological diseases (OND) by enzyme-linked immunosorbent assay (ELISA). Oligodendrocytes were isolated by percoll density gradient from brains of 4 week-old rat and cultured in poly-1-lysine-coated 96 well microwell plate. After overnight culture, oligodendrocytes were fixed in 0.5% glutaraldehyde and stored at -20 degrees C. ELISA was performed using peroxidase-conjugated goat anti-human IgG (Fab')2 as usual. Serum and CSF were examined at dilution of 1:400 and 1:2 respectively, and O.D. was read at 490 nM. In sera from patients with MS and OND, the titer of anti-oligodendrocyte antibody was significantly higher than those from normal controls. However, there was no significant difference between MS and OND. Significantly higher titer of anti-oligodendrocyte antibody was observed in CSF from patients with meningoencephalitis and polyradiculoneuropathy. However, comparing CSF anti-oligodendrocyte antibody per CSF IgG, there was no significant difference among each group. There was no significant correlation between the cytotoxicity index of sera and anti-oligodendrocyte antibody level. There might be additional cytotoxic factor other than anti-oligodendrocyte antibody. Our data support the idea anti-oligodendrocyte antibody is not specific to MS, and the role of anti-oligodendrocyte antibody in the pathogenesis of MS is secondary.
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PMID:[The study of anti-oligodendrocyte antibody in sera, and CSF of patients with multiple sclerosis]. 236 27

The morphology and projections of neurons in the paraventricular organ (PVO) were studied by means of silver impregnation after intraocular application of cobaltous lysine in the lungfish Protopterus dolloi. Cobalt-labeled neurons were found exclusively in the PVO in the dorsal and infundibular hypothalamus. These bipolar neurons possess one CSF-contacting process that protrudes into the ventricular lumen with a club-shape ending and a thick, ramifying process directed into the hypothalamic neuropil; the ependymofugal processes form intra- and extrahypothalamic projections. Impregnated fibers from paraventricular neurons cross in infundibular and hypothalamic commissures, the commissure of the posterior tuberculum, the postoptic, the habenular, and the anterior commissures. Projections to the infundibulum and the median eminence are relatively sparse; no fibers are labeled in the pituitary gland. Ascending projections to the forebrain are extensive. Major targets include the dorsal hypothalamus, the periventricular preoptic nuclei, the habenula, the subhabenular region, the anterodorsal thalamus, and the medial telencephalic hemisphere (septum). Most ascending fibers follow the medial forebrain bundle; others course in the fasciculus retroflexus and terminate in rostral parts of the ipsilateral habenula. Descending fibers run caudally along the ventral floor of the brainstem. They terminate in the neuropil of the mesencephalic tegmentum, ventral tectum, isthmic region, ventral portions of the reticular formation throughout the rhombencephalon, and extend into the spinal cord. Intraocular application of cobaltous lysine results in selective impregnation of neurons in the PVO and their ascending and descending projections, presumably via uptake of tracer from vascular circulation. These projections do not represent retinofugal or retinopetal projections. We provide conclusive evidence for the existence of a PVO in Protopterus. On the basis of PVO location and acetylcholinesterase histochemistry, we propose subdivisions of the infundibular hypothalamus corresponding to those in amphibians. Ascending PVO projections appear to be particularly well developed in lungfish compared with other species and may be related to specialized endocrine mechanisms in this group of vertebrates.
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PMID:Paraventricular organ of the lungfish Protopterus dolloi: morphology and projections of CSF-contacting neurons. 239 40

Compared to healthy controls, unmedicated schizophrenic patients had significantly higher plasma concentrations of taurine, methionine, valine, isoleucine, leucine, phenylalanine, and lysine. Except for taurine, these amino acids share the L-transport system for neutral amino acids. In the patients, homovanillic (HVA) acid levels in CSF were decreased and the plasma levels of the amino acids competing with tyrosine and tryptophan for transport into the brain, were all negatively correlated to the CSF concentrations of HVA and 5-HIAA. These findings could be explained by a change in the affinity of the L-system or by a decrease in its overall capacity in schizophrenia. Raised plasma levels of the competing amino acids may limit the brain uptake of tyrosine, leading to a diminished dopamine turnover, and resulting in a compensatory development of supersensitive dopamine receptors.
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PMID:Plasma amino acids in relation to cerebrospinal fluid monoamine metabolites in schizophrenic patients and healthy controls. 241 98

Five patients from two unrelated pedigrees are affected by an inherited form or forms of mitochondrial encephalomyopathy in which the exact site of the block in the respiratory chain has yet to be identified. All five patients regularly exhibit an unusual aminoacidopathy evident both in fasting plasma and in CSF. Alanine concentrations are elevated, reflecting high tissue pyruvate and lactate levels. Concentrations of the four essential amino acids threonine, methionine, tryptophan and lysine are substantially reduced, as are those of citrulline, ornithine and arginine. This pattern of amino-acid deficiency is apparently not due to failure to absorb the dibasic amino acids, to any abnormality of the urea cycle, to excessive synthesis and turnover of creatine, or to protein malnutrition. The aminoacidopathy presumably is a metabolic consequence of one or more impairments in the electron transport chain in mitochondria. A detailed explanation of its aetiology needs to be sought.
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PMID:An unusual aminoacidopathy associated with mitochondrial encephalomyopathy. 250 79

The turnover of the colony-stimulating factor 1 receptor (CSF-1R), the c-fms proto-oncogene product, is accelerated by ligand binding or by activators of protein kinase C (PKC), such as the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA). The mechanisms of ligand- and TPA-induced downmodulation were shown to differ by the following criteria. First, in cells in which PKC was downmodulated, CSF-1R reexpressed at the cell surface remained sensitive to ligand but was refractory to TPA-induced degradation. Second, a kinase-defective receptor containing a methionine-for-lysine substitution at amino acid 616 at its ATP-binding site failed to undergo ligand-induced downmodulation but remained responsive to TPA. Following CSF-1 stimulation, no intermediates of receptor degradation could be immunoprecipitated with polyvalent antisera to CSF-1R. In contrast, TPA induced specific proteolytic cleavage of the receptor near its transmembrane segment, resulting in the release of the extracellular ligand-binding domain from the cell and the generation of an intracellular fragment containing the kinase domain. Two-dimensional phosphopeptide mapping demonstrated no new sites of phosphorylation in response to TPA in either the residual intact receptor or the intracellular proteolytic fragment. Therefore, PKC appears not to trigger downmodulation by directly phosphorylating the receptor but, rather, activates a protease which recognizes CSF-1R as a substrate.
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PMID:Ligand and protein kinase C downmodulate the colony-stimulating factor 1 receptor by independent mechanisms. 252 80


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