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31.
J. KRØLL 《Scandinavian journal of immunology》1983,17(S10):135-139
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The OPAR mouse monoclonal antibody (mAb) directed against rat hepatocytes was previously shown to inhibit adhesion of TA3/Ha mammary carcinoma cells to hepatocytes. The antigen is abundantly present at the surface of hepatocytes beneath the endothelium of liver capillaries where we have observed invasion of carcinoma cells to occur. The OPAR mAb reacted with three major bands on a Western blot of liver plasma membrane proteins. The same proteins were also seen upon immunoprecipitation from iodinated liver plasma membrane proteins. We have isolated OPAR antigens by lectin wheat germ agglutinin (WGA) and OPAR affinity chromatography. Amino acid sequence analysis revealed that two of the bands were 1-macroglobulin and C4-binding protein, which are serum components produced by hepatocytes. The presence of the epitope on distinct proteins and our previous observation that it can be detected in the Golgi apparatus but not in the endoplasmic reticulum, suggested that OPAR reacts with a liver-specific glycoconjugate. Loss of OPAR reactivity after neuraminidase and N-glycosidase F treatment showed that the epitope contains sialic acid residues on N-linked sugar moieties. OPAR also reacted with rat fibronectin, and inhibited adhesion of TA3/St cells to fibronectin. This explains the inhibition by the OPAR mAb of TA3/St cell adhesion to hepatocytes, which we have shown to be due mainly to interaction with hepatocyte surface-associated fibronectin. However, adhesion of the related TA3/Ha cells to hepatocytes, which is mediated by the 6P4 integrin, and does not involve binding to fibronectin, is also inhibited. This suggests that 64 on liver-metastasizing carcinoma cells binds to an OPAR epitope-carrying glycoprotein produced by hepatocytes. 相似文献
35.
Seelen MA Trouw LA van der Hoorn JW Fallaux-van den Houten FC Huizinga TW Daha MR Roos A 《Clinical and experimental immunology》2003,134(2):335-343
In systemic lupus erythematosus (SLE), autoantibodies directed against complement components of the classical pathway, especially against C1q, are associated with severe disease and are of prognostic value for flares of lupus nephritis. Mannose-binding lectin (MBL), the recognition unit of the MBL pathway of complement activation, has structural similarities to C1q. Deficiencies of MBL have been shown to predispose to the development of SLE and to influence the course of the disease. We hypothesized that the presence of autoantibodies to MBL, analogous to autoantibodies to C1q in patients with SLE, may contribute to disease development. The occurrence of anti-MBL autoantibodies was assessed by enzyme-linked immunosorbent assay (ELISA) of 68 serum samples from 20 patients with SLE and in serum from 70 healthy controls. Levels of antibodies directed against MBL were significantly higher in patients with SLE compared to healthy subjects. No significant difference was found between patients with active disease compared to those with inactive disease. While the occurrence of anti-C1q autoantibodies was associated with renal involvement, no such relationship was found for anti-MBL autoantibodies. A significant correlation was found between anti-MBL and anti-C1q antibody levels. The level of anti-MBL antibodies was negatively correlated with MBL-complex activity of circulating MBL. Anti-MBL autoantibodies were of the immunoglobulin G (IgG) isotype and the binding site of IgG anti-MBL was located in the F(ab')2 portion. We conclude that anti-MBL are present in sera from SLE patients and influence the functional activity of MBL. 相似文献
36.
G M de Boo A Tibben J B Lanser A Jennekens-Schinkel J Hermans M Vegter-van der Vlis R A Roos 《Journal of medical genetics》1997,34(7):564-568
Intelligence in 20 presymptomatic subjects with an increased risk (> 95%) for carrying the gene for Huntington's disease (HD) was studied in a prospective, case-control, single blind study. No significant differences between the groups were detected for intelligence indices and subtest scores (Wechsler Adult Intelligence Scale). The high level of the performance IQ and the significant discrepancy between performance IQ and verbal IQ found in both the high risk and the low risk groups contrasted with our expectations based on anamnestic information, general clinical opinion, and the results of previously conducted studies. We propose that psychosocial circumstances could explain the test results and discuss the consequences of our findings for clinical genetics practice. 相似文献
37.
Tumour necrosis factor-alpha stimulates invasiveness of T-cell hybridomas and cytotoxic T-cell clones by a pertussis toxin-insensitive mechanism.
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Tumour necrosis factor-alpha (TNF-alpha) stimulated invasion by mouse T-cell hybridomas and cytotoxic T-lymphocyte clones into rat embryo fibroblast monolayers. The effect on these highly invasive cells was limited: invasion was stimulated maximally to 130% of controls. However, when cells were pretreated with pertussis toxin (PT), which inhibits invasion to +/- 20% of controls, a clearcut effect was observed: 400 U TNF-alpha per ml stimulated invasion usually two- to threefold, and sometimes even up to 10-fold. Therefore, experiments were done with PT-pretreated cells. Stimulation was dose dependent and maximal at 200-400 U TNF-alpha per ml. An anti-TNF-alpha monoclonal antibody completely abolished TNF-alpha-induced invasion. The effect was maximal 30 min after addition of cells and TNF-alpha to the monolayer and then declined. TNF-alpha preincubation of T-cell hybridoma cells, but not of fibroblasts, had a similar stimulatory effect, which was also maximal after 30 min. This shows that TNF-alpha acts directly on the T-cell hybridoma cells. Invasive T-cell hybridomas colonize many tissues from the blood similarly as normal T cells. Our data thus suggest that TNF-alpha can stimulate migration of normal T lymphocytes into inflamed tissues and can promote metastasis of malignant T lymphomas. The signals involved are transmitted via a pertussis toxin-insensitive pathway. 相似文献
38.
Pernille Mathiesen Tørring Martin Jakob Larsen Charlotte Brasch-Andersen Lotte Nylandsted Krogh Maria Kibæk Lone Laulund Niels Illum Ulrike Dunkhase-Heinl Antje Wiesener Bernt Popp Giuseppe Marangi Tina Duelund Hjortshøj Jakob Ek Ida Vogel Naja Becher Laura Roos Marcella Zollino Christina Ringmann Fagerberg 《European journal of medical genetics》2019,62(2):129-136
Introduction
MED13L-related intellectual disability is characterized by moderate intellectual disability (ID), speech impairment, and dysmorphic facial features. We present 8 patients with MED13L-related intellectual disability and review the literature for phenotypical and genetic aspects of previously described patients.Materials and methods
In the search for genetic aberrations in individuals with ID, two of the patients were identified by chromosomal microarray analysis, and five by exome sequencing. One of the individuals, suspected of MED13L-related intellectual disability, based on clinical features, was identified by Sanger sequencing.Results
All 8 individuals had de novo MED13L aberrations, including two intragenic microdeletions, two frameshift, three nonsense variants, and one missense variant. Phenotypically, they all had intellectual disability, speech and motor delay, and features of the mouth (open mouth appearance, macroglossia, and/or macrostomia). Two individuals were diagnosed with autism, and one had autistic features. One had complex congenital heart defect, and one had persistent foramen ovale. The literature was reviewed with respect to clinical and dysmorphic features, and genetic aberrations.Conclusions
Even if most clinical features of MED13L-related intellectual disability are rather non-specific, the syndrome may be suspected in some individuals based on the association of developmental delay, speech impairment, bulbous nasal tip, and macroglossia, macrostomia, or open mouth appearance. 相似文献39.
de Pril R Fischer DF Maat-Schieman ML Hobo B de Vos RA Brunt ER Hol EM Roos RA van Leeuwen FW 《Human molecular genetics》2004,13(16):1803-1813
Polyglutamine diseases are characterized by neuronal intranuclear inclusions (NIIs) of expanded polyglutamine proteins, indicating the failure of protein degradation. UBB(+1), an aberrant form of ubiquitin, is a substrate and inhibitor of the proteasome, and was previously reported to accumulate in Alzheimer disease and other tauopathies. Here, we show accumulation of UBB(+1) in the NIIs and the cytoplasm of neurons in Huntington disease and spinocerebellar ataxia type-3, indicating inhibition of the proteasome by polyglutamine proteins in human brain. We found that UBB(+1) not only increased aggregate formation of expanded polyglutamines in neuronally differentiated cell lines, but also had a synergistic effect on apoptotic cell death due to expanded polyglutamine proteins. These findings implicate UBB(+1) as an aggravating factor in polyglutamine-induced neurodegeneration, and clearly identify an important role for the ubiquitin-proteasome system in polyglutamine diseases. 相似文献
40.
Viscosity measurements were carried out as a function of pressure and temperature with solutions of 8 wt.-% PVC (Mw ≈ 75 000) in ten thermodynamically good solvents by means of a Searle-type viscometer. A rollingxyhball viscometer was used for the investigation of the pure solvents. In all cases the viscosity increases in a more or less exponential manner when the pressure is raised. The viscosity ratio f1000 = η1000 bar/η1bar can be varied by the choice of the solvent from ca. 2 (tetrahydrofuran) to 3,0 (cyclohexanone) at 40°C. For a constant temperature of 40°C, the volumes of activation for the viscous flow of the solutions, V≠, or f1000 exceed that of the pure solvent, by typically 25%. The dependence of f1000 or V≠ upon temperature is not very pronounced. However, the greater the f1000-values, the more marked are the temperature effects. The theoretical analysis of the data, including earlier measurements with PS, indicates that three terms contribute to f1000: the basic value (f1000)s stemming from the pure solvent, the value (f1000)p which the polymer would contribute under athermal conditions, and finally a thermodynamic term, (f1000)pa, considering the pull-along effect (i.e. the specific forces a given segment exerts on other segments under variable thermodynamic conditions). 相似文献