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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polysaccharides and other complex carbohydrates were released by proteolysis of the chloroform-methanol insoluble residue of 10 day-old worms and eggs of Hymenolepis diminuta. Gas-liquid chromatographic analysis of alditol acetate derivatives of monosaccharides released from the polysaccharides by hydrolysis revealed that in the 10 day-old worm, glucose was the most abundant sugar, followed by galactose, glucosamine, galactosamine, fucose and possibly rhamnose. Mannose was least abundant and xylose was absent. In the egg, glucose and galactose were equally abundant, followed by the same sugars found in 10 day-old worms, and xylose was present. Uronic acid was detected in both fractions by specific chemical tests. None of the saccharide material from eggs and worms was susceptible to degradation by Streptomyces hyaluronidase, chondroitinase AC, and slightly susceptible to chondroitinase ABC, as shown by electrophoretic analysis on composite 2.2% acrylamide-agarose slab gels and 4.5/12.5% polyacrylamide gels before and after enzymatic treatment. One of the gel-separable bands, however, was degradable by both nitrous acid and Flavobacterium heparinase. Both bands from eggs were degradable by nitrous acid. These results suggest that eggs contain heparin and/or heparan sulfate and perhaps dermatan sulfate and that 10 day-old worms also have these polyglycans but possibly not chondroitin sulfate or hyaluronic acid.
Mol Biochem Parasitol 1984 Jan
PMID:Characterization of polysaccharides of the eggs and adults of Hymenolepis diminuta. 653 86

The glycosaminoglycan (GAG) contents of hypertrophic scars, normal scars, and human skin from cadavers of matched ages were compared. Cellulose acetate electrophoresis, chondroitinase digestions, and reaction product and infrared analyses were used to characterize the component GAGs. DEAE-cellulose chromatography was used to separate hyaluronic acid (HA) and sulfated GAGs. Chondroitinase analysis was improved under these conditions. HA was determined enzymatically. Results showed an elevation of HA in hypertrophic scar. Dermatan sulfate was the major GAG in both scars and a slightly greater quantity was observed in the hypertrophic scar. Small amounts of chondroitin 4-sulfate and chondroitin 6-sulfate disaccharide constituents were also detected by the chondroitinase assay method and these were also elevated in hypertrophic scar. These results suggest that the GAGs of hypertrophic scar differ from normal scar and normal skin.
Exp Mol Pathol 1984 Feb
PMID:Glycosaminoglycans of normal and hypertrophic human scar. 669

Arylsulfatases A and B were measured in the liver of mice infected with Schistosoma mansoni. The increase of total arylsulfatases paralleled enlargement of the granulomas. It began at 7 weeks after infection and reached a maximum at 10 to 14 weeks when the enzyme activity became about 2.5 times that of normal liver. The elevated enzyme activity was due to granulomatous tissue, because when granulomas were separated from hepatic cells, the former contained the increased activity but the latter did not. Arylsulfatase A, arylsulfatase B, and arylsulfatase Bv, in both normal liver and granulomas, were separated by anion-exchange column chromatography and differences in net charges of these enzymes were demonstrated by polyacrylamide gel electrophoresis. Biochemical properties were indistinguishable between arylsulfatase B and arylsulfatase Bv while they differed from arylsulfatase A. Granulomas at 8 weeks after infection showed 3.0-, 3.5-, and 5.0-fold increases in activity for arylsulfatase A, B, and Bv, respectively. As the granulomas enlarged, by 12 weeks, arylsulfatases B and Bv activities further increased but the arylsulfatase A value remained the same as that of 8 weeks. The finding suggests that arylsulfatases are involved in granuloma development and arylsulfatases B and Bv activities may reflect functions of macrophages and other cells including fibroblasts.
Exp Mol Pathol 1984 Feb
PMID:Biochemical characterization of arylsulfatases detected in granulomatous inflammation. 669 6

Ruthenium red and toluidine blue O precipitates were described associated with lathyritic elastic fibers in aortas of chickens treated with beta-aminopropionitrile fumarate (I. Pasquali-Ronchetti, C. Fornieri, I. Castellani, G. M. Bressan, and D. Volpin (1981). Alterations of the connective tissue components induced by beta-aminopropionitrile. Exp. Mol. Pathol. 35, 42-56). In this report evidence is given that these precipitates reveal the presence of proteoglycans, as they are completely removed by 5 M guanidine-HCl incubation and by specific enzymatic digestions. In particular, proteoglycans associated with the poorly cross-linked lathyritic elastin can be removed by testicular hyaluronidase, chondroitinase ABC, heparitinase, and nitrous acid treatments, whereas they are rather resistant to streptococcal hyaluronidase and chondroitinase AC. On the contrary, proteoglycans of the matrix or associated with collagen fibers are particularly sensitive to these latter enzymatic treatments. The conclusion is reached that glycosaminoglycans associated with beta-aminopropionitrile-induced lathyritic elastin (i) are different from those of the matrix or associated with collagen, and (ii) include mainly dermatan and heparan sulfates.
Exp Mol Pathol 1984 Apr
PMID:Elastin fiber-associated glycosaminoglycans in beta-aminopropionitrile-induced lathyrism. 670 93

Determination of hyperplastic and hypertrophic changes of mucus-secreting cells in animal airways has been performed in the past by using histologic, immunologic, and/or molecular biologic approaches. Histologic techniques are tedious and time-consuming. The other approaches require specific antibodies and cDNA probes that have proved difficult to develop. Described here is a method for the rapid estimation of hyperplastic and hypertrophic changes of secretory epithelial cells in rat airways. The assay specifically measures acidic and neutral mucoproteins in a linear fashion from 0.5 microgram to at least 10 micrograms. Male Sprague-Dawley rats were exposed to metabisulfite mist (10% wt/vol) for 5 days/wk for 3 wk. The lungs were removed and homogenized in a phosphate-buffered solution containing reducing agents and protease inhibitors. The particulate matter was removed by centrifugation, and the soluble extract was applied to a column packed with Sepharose CL-6B. The material eluting in the void volume was applied to a PVDF membrane and stained for either acidic or neutral mucosubstances using Alcian blue or periodic acid-Schiff (PAS) staining, and the absorbance was read using a 96-well plate reader. Lungs from sodium metabisulfite-exposed animals showed a 7-fold and 3.5-fold increase in PAS-positive and Alcian blue-positive material, respectively. The increase in both PAS and Alcian blue staining was hyaluronidase and chondroitinase insensitive. The observed changes are consistent with morphometric measurements of mucus-containing cells in histologic sections of the tissues. This assay may be useful in determining which neurohumoral mediators might be involved in mucus cell hypertrophy and hyperplasia in animal models of chronic obstructive pulmonary disease.
Am J Respir Cell Mol Biol 1994 Jun
PMID:Hypertrophic and hyperplastic changes of mucus-secreting epithelial cells in rat airways: assessment using a novel, rapid, and simple technique. 751 72

The purpose of this study was to determine the biochemical and molecular characteristics of mucin synthesized by cystic fibrosis cells (CFPAC-1), a pancreatic cancer cell line derived from a patient with cystic fibrosis, and pancreatic cancer (SW-1990) cell lines. High molecular weight glycoproteins (HMG) were quantified by [3H]-glucosamine labeling and chromatography on sepharose CL-4B. Mucin gene expression was determined by using cDNA probes for 2 distinct intestinal mucins (MUC2 and MUC3) and one stomach mucin (MUC1). The specific mucin core epitopes were confirmed by immunoblots using antibodies that recognize T, Tn, sialosyl Tn, MUC1, MUC2, and MUC3. The results of these experiments demonstrate that CFPAC-1 cells contained 1.25 fold and 1.4 fold more HMG in the membrane and cytosolic fractions, however, secreted 4-fold more HMG into the medium compared to SW-1990 cells. The HMG of SW-1990 was found to be mucinous in nature and not proteoglycans, as it was not susceptible to hyalurinidase, heparinase and chondroitinase ABC. The HMG of CFPAC-1 was also predominantly (80%) mucinous but with small amounts of proteoglycans. mRNA and immunoblot analysis suggest that these CFPAC-1 and SW-1990 cells predominantly express MUC1 apomucin, small amounts of MUC2 apomucin, and no MUC3. Pulse chase labeling and immunoprecipitation of MUC1 type mucin using the 139H2 monoclonal antibody demonstrated that different sizes of mucin gene product were present in both cell lines, corresponding to the known length polymorphism of this mucin. Both T and Tn antigens were significantly higher in CFPAC-1 and SW-1990 cells as compared to sialosyl Tn antigen. These findings were associated with the increased activities of polypeptidyl N-acetylgalactosaminyl transferase and b1,3-galactosyltransferase. These investigations demonstrate for the first time that cystic fibrosis cells (CFPAC-1) secrete and synthesize high amounts of mucin which is associated with high levels of MUC1 mRNA, low levels of MUC2 mRNA and non detectable MUC3 mRNA.
Biochem Mol Biol Int 1995 Feb
PMID:Cystic fibrosis and pancreatic cancer cells synthesize and secrete MUC1 type mucin gene product. 754 50

This paper describes low-density mucus glycoconjugates released from feline trachea by dirhamnolipid (DRL), a toxin from Pseudomonas aeruginosa. Mucus glycoconjugates in feline tracheas were radiolabeled in vivo with 3H-proline and 14C-glucose. Control mucus and that released by 200 micrograms/ml DRL were dissolved in guanidine hydrochloride buffer (GuHCl) and chromatographed on Sepharose CL-2B. Molecules eluting in the void volume (V0) of the column were isolated by isopycnic density gradient centrifugation in CsCl/GuHCl. All samples gave peaks of radiolabeled and periodic acid/Schiff (PAS)-reactive material at rho = approximately 1.50 and approximately 1.60 g/ml, but DRL-stimulated samples contained low-density material (rho < 1.32 g/ml), also PAS-reactive and radiolabeled. Control secretions incubated with DRL in vitro did not form low-density material. In Triton X-100 (1% vol/vol), a nonionic detergent, low-density material behaved as smaller molecules, running in the partially included volume (Vi) of the column of Sepharose CL-2B, but still in the V0 of Sephacryl S-300. Incubation with chondroitinase ABC, heparinase II and III, and keratanase failed to change its elution profile on S-300, evidence against glycosaminoglycans; but proteolysis with trypsin or proteinase K gave two peaks, peptide fragments near the totally included volume of the column and glycopeptides in V0. The V0 glycopeptides banded between 1.50 and 1.55 g/ml in a CsCl gradient and eluted as a single peak in the Vi of Sephacryl S-400, suggesting a distinct homogeneous glycopeptide, smaller than those from normal mucins. The main 14C-labeled sugars in this glycopeptide were fucose, glucosamine, galactosamine, and galactose, consistent with a mucin. Thus, DRL releases stable but noncovalent complexes containing one or more distinct mucinlike glycoconjugates, probably combined with lipids and peptides. We discuss their possible relevance to airway diseases, including cystic fibrosis.
Am J Respir Cell Mol Biol 1995 Mar
PMID:Mucus glycoconjugate complexes released from feline trachea by a bacterial toxin. 787 96

Cell adhesion to extracellular matrix molecules such as fibronectin involves complex transmembrane signaling processes. Attachment and spreading of primary fibroblasts can be promoted by interactions of cell surface integrins with RGD-containing fragments of fibronectin, but the further process of focal adhesion and stress fiber formation requires additional interactions. Heparin-binding fragments of fibronectin can provide this signal. The COOH-terminal heparin-binding domain of fibronectin contains five separate heparin-binding amino acid sequences. We show here that all five sequences, as synthetic peptides coupled to ovalbumin, can support cell attachment. Only three of these sequences can promote focal adhesion formation when presented as multicopy complexes, and only one of these (WQPPRARI) retains this activity as free peptide. The major activity of this peptide resides in the sequence PRARI. The biological response to this peptide and to the COOH-terminal fragment may be mediated through cell surface heparan sulfate proteoglycans because treatment of cells with heparinase II and III, or competition with heparin, reduces the response. Treatment with chondroitinase ABC or competition with chondroitin sulfate does not.
Mol Biol Cell 1993 Jun
PMID:A synthetic peptide from the COOH-terminal heparin-binding domain of fibronectin promotes focal adhesion formation. 837 70

After in vivo administration of purified antibody against cultured mesangial cell (anti-MC IgG), glomerular basement membrane (GBM) was selectively bound. The glomerular bound anti-MC IgG exhibited a monospecificity for a 109-kDa antigen extracted from cultured mesangial cells and normal GBM. The antigen was not digestible by collagenase, heparitinase, or chondroitinase and was revealed by immunoelectron microscopy of a normal glomerular component to be predominantly distributed along the lamina rara externa of GBM and to be absent in mesangium. The ample expression of the antigen in puromycin aminonucleoside nephrosis implies that it represents a significant sclerotic material in glomerulonephritis. Abnormal production of GBM components by mesangial cells may play an important role in glomerulosclerosis.
Exp Mol Pathol 1995 Apr
PMID:Coexpression of a novel glomerular basement membrane matrix material in mesangial cell culture and glomerulosclerosis. 854 99

Tumor cells of glial origin express high levels of basic fibroblast growth factor (bFGF) which stimulates their proliferation in an autocrine manner. In the present study we examined bFGF receptor (FGFR) expression and 125I-bFGF binding and processing in a human glioma cell line. RT-PCR demonstrated the co-expression of bFGF and FGFR mRNAs in five glioma cell lines examined. The high-affinity FGFR was visualized in U87-MG glioma cells by crosslinking with 125I-bFGF and by Western blotting with anti-receptor antisera. Both techniques identified a discrete 110-kDa moiety associated with the cell membrane, consistent with the reported size of one of the FGFR-1 isoforms. Western blotting also identified an intracellular receptor pool which was not accessible with exogenous 125I-bFGF. Suramin treatment induced a 2-fold increase in immunoreactive FGFR and a 1.5-fold increase in 125I-bFGF binding sites, indicating that FGFRs are chronically down-regulated by endogenous bFGF in U87-MG cells. Removal of extracellular bFGF with heparin resulted in a rapid, cycloheximide-sensitive increase in high-affinity bFGF binding sites. At 37 degrees C, receptor-bound 125I-bFGF was internalized and subjected to limited proteolytic cleavage over 12 h. U87-MG cells also contained abundant low-affinity bFGF binding sites which were removed by digestion with heparinase III but not by chondroitinase ABC. The presence of heparin (25 micrograms/ml) in the binding reaction eliminated the association of 125I-bFGF with the heparin-like sites but did not prevent binding to the high-affinity receptor. Scatchard binding analysis in the presence of heparin revealed a single class of high-affinity sites in U87-MG cells (Kd = 4.9 +/- 0.9 pM; 10-12 x 10(3) sites per cell). Neither heparin nor heparinase digestion prevented the binding of 125I-bFGF to the detergent-extractable high-affinity receptor, although both treatments significantly reduced the extent of 125I-bFGF association with the receptor. These findings indicate that in U87-MG cells, heparan sulfate proteoglycans may be involved in presentation of bFGF to the high-affinity receptor, but are not essential for high-affinity binding to occur.
Mol Cell Endocrinol 1995 Oct 30
PMID:Basic fibroblast growth factor binding and processing by human glioma cells. 867 45


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