Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To characterize macromolecules from intestinal epithelium known to be reactive with human disease sera, monoclonal antibodies (MAbs) were elicited to determine cell localization, organ-specificity and cross-reactivity of the immunodominant determinants. Eight MAbs, reactive with murine epithelial cell-associated components by enzyme-linked immunosorbent assay, immunoblotting and immunofluorescence, demonstrated binding by the same techniques to constituents in determinant-bearing epithelial macromolecules were glycoproteins of approximately 180,000 (human and 199,000 (murine) mol. wt. Pre-incubation of sera from patients with chronic inflammatory bowel disease (but not normal human sera or control protein) inhibited binding of the 199 K macromolecule by three MAbs elicited and characterized in this study.
Mol Immunol 1988 Mar
PMID:Shared and unique determinants on human and murine intestinal epithelium as established by monoclonal antibodies. 245 95

We describe a very rare case in which macroamylasemia was associated with ulcerative colitis of total colitis type. The patient's serum amylase isozyme pattern by electrophoresis showed a broad abnormal peak toward the side of the positive pole compared with regular salivary and pancreatic fractions. Sephadex G-200 column chromatography showed a sedimentation coefficient of 6.6 S. Amylase activity was bound to IgG. Double diffusion experiments demonstrated that amylase activity could be precipitated in gel by an antibody to the lambda chain. Although inflammatory bowel disease is occasionally associated with hyperamylasemia due to pancreatitis, we emphasize that, when hyperamylasemia is recognized in patients with inflammatory bowel disease, macroamylasemia also should be considered.
J Mol Med (Berl) 1995 Feb
PMID:Macroamylasemia associated with ulcerative colitis. 754 95

The purpose of this study was to better establish the morphologic basis of the early mucosal lesions of experimental inflammatory bowel disease because understanding the development of these lesions has important pathogenetic implications. Sprague-Dawley rats were given 1.5% hydrolyzed lambda-carrageenan orally for 30 days. This produced small intestinal lesions which were then evaluated. Light microscopy showed an increased amount of inflammatory cells in the gut wall with prominent Peyer's patches, microgranulomas, crypt abscesses, pin-point ulcerations, and a repair reaction. Scanning electron microscopy revealed pin-point ulcerations in relation to Peyer's patches. Transmission electron microscopy, in addition to the above findings, showed disruptions of enterocyte microvilli and terminal webs. Follicle-associated epithelium appeared to be a predictive site for the development of crypt abscesses and pin-point ulcerations. Enzyme-linked immunoadsorbent assays indicated that orally administered carrageenan elicited a systemic antibody response. Our results suggest that damage to enterocyte microvilli and terminal webs may be important early events in the morphogenesis of the lesions.
Exp Mol Pathol 1994 Apr
PMID:Development of the early mucosal lesions in experimental inflammatory bowel disease--implications for pathogenesis. 807 May 40

In the Western world, chronic inflammatory bowel disease (IBD) presents as two major clinical forms, Crohn's disease (CD) and ulcerative colitis (UC) [Targan, S.R. and Shanahan, F. (1994). In Retford, D.C (ed.), Inflammatory Bowel Disease: From Bench to Bedside. Williams and Wilkins, Baltimore]. Genetic epidemiological studies, the occurrence of rare syndromes associated with IBD, and animal models suggest that inherited factors play significant roles in the susceptibility to both forms of IBD [Yang, H.-Y. and Rotter, J.I. (1995) In Kirsner, J.B. and Shorter, R.G. (eds). Genetic Aspects of Idiopathic Inflammatory Bowel Disease. Williams and Wilkins, Baltimore, pp.301-331]. Recently, a genome-wide search on European families with multiple affected members with CD identified a putative susceptibility locus in the centromeric region of chromosome 16 [Hugot, J.-P. et al. (1996) Nature, 379, 821-823]. We have now tested this region in an independent set of US families, confirmed that this region is likely to contain a gene predisposing to CD, and further refined the chromosomal location of this gene. Most importantly with respect to this locus, our data also seem to indicate that there is heterogeneity both within the CD group, and between the CD and UC groups with respect to this locus. The susceptibility locus appears to be involved only in non-Jewish CD sibpairs and not in our Ashkenazi Jewish CD sibpairs. Additionally, we have tested sibpairs having either only UC or both UC and CD for involvement of this locus, and have found no evidence that this region predisposes to IBD in these patients.
Hum Mol Genet 1996 Oct
PMID:Susceptibility locus for inflammatory bowel disease on chromosome 16 has a role in Crohn's disease, but not in ulcerative colitis. 889 7

During the past decade nitric oxide has emerged as an important mediator of physiological and pathophysiological processes. Elevated nitric oxide bio-synthesis has been associated with nonspecific immune-mediated cellular cytotoxicity and the pathogenesis of chronic, inflammatory autoimmune diseases including rheumatoid arthritis, insulin-dependent diabetes, inflammatory bowel disease, and multiple sclerosis. Recent evidence suggests, however, that nitric oxide is also immunoregulatory and suppresses the function of activated proinflammatory macrophages and T lymphocytes involved in these diseases. This article reviews the role of nitric oxide in the biology of central nervous system glial cells (astrocytes and microglia) as it pertains to the pathogenesis of multiple sclerosis in humans and experimental allergic encephalitis, the animal model of this disease. Although nitric oxide has been clearly implicated as a potential mediator of microglia-dependent primary demyelination, a hallmark of multiple sclerosis, studies with nitric oxide synthase inhibitors in the encephalitis model have been equivocal. These data are critically reviewed in the context of what is know from clinical research on the nitric oxide pathway in multiple sclerosis. Specific recommendations for future preclinical animal model research and clinical research on the nitric oxide pathway in patients are suggested. These studies are necessary to further define the role of nitric oxide in the pathology of multiple sclerosis and to fully explore the potential for nitric oxide synthase inhibitors as novel therapeutics for this disease.
J Mol Med (Berl) 1997 Mar
PMID:The role of nitric oxide in multiple sclerosis. 910 72

Several annexins have been implicated in the pathogenesis of benign and malignant neoplasms of different origins. In some tumours a suppressive action of annexins has been shown, whereas studies of other tumours indicate an involvement of annexins in tumour progression. In the light of the expression of annexins at distinct episodes of fetal development these observations point towards a functional role of annexins in cellular development and differentiation. This view is supported by data that link certain annexins to distinct pathways of signal transduction. Auto-antibodies against several annexins have been detected in patients with autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis and inflammatory bowel disease. Until now it is unclear whether their presence reflects a relevant pathogenetic mechanism or merely represents an unspecific expression of a raised autoimmunity in these patients.
Cell Mol Life Sci 1997 Jun
PMID:Annexins in cancer and autoimmune diseases. 923 Sep 35

A rat model for human ulcerative colitis (UC) has been developed by using 1-hydroxyanthraquinone (1-HA) to cause severe inflammation of colonic mucosa. 1-HA also has synergistic effects on the carcinogenicity of methylazoxymethanol (MAM) acetate in the rat colon. In this study, four adenomas and 16 adenocarcinomas induced in male F344 rats by 1-HA and MAM acetate were examined for mutations in the entire coding regions and introns flanking coding exons of the APC gene by polymerase chain reaction (PCR)-single strand conformation polymorphism (SSCP) and PCR-restriction-SSCP analyses. No mutations were found. These results, together with our previous observations of a relative lack of Ki-ras gene mutations in the same tumors, are similar to those found in human UC-associated colon cancer, suggest a common pathway in these two systems, although they are different in their implication of p53 mutations. Therefore, this model may have some relevance and application to the study of colon cancer in human inflammatory bowel disease, which is not associated with APC mutations or with Ki-ras or p53 mutations.
Mol Carcinog 1997 Dec
PMID:No involvement of APC gene mutations in ulcerative colitis-associated rat colon carcinogenesis induced by 1-hydroxyanthraquinone and methylazoxymethanol acetate. 943 83

The cause of the inflammatory bowel diseases Crohn's disease and ulcerative colitis is unknown, but epidemiological evidence suggests that it is multifactorial with a strong genetic component. Several genetic loci probably contribute to disease susceptibility, accounting for the complex pattern of inheritance and heterogeneous clinical manifestations. The combination of candidate gene studies and, more recently, genome-wide searches has resulted in the identification of a number of putative susceptibility loci. With large-scale, fine-mapping studies under way, and accelerating progress in the physical mapping of the human genome, rapid progress is now being made towards the identification of the genes responsible for inflammatory bowel disease.
Mol Med Today 1997 Dec
PMID:Mapping susceptibility loci in inflammatory bowel disease: why and how? 944 26

Autoantigen-specific CD4+ T cells have been implicated as the causative cell type in: multiple sclerosis, rheumatoid arthritis, autoimmune uveitis, diabetes mellitus, inflammatory bowel disease and graft-versus-host disease. The pathology of a number of experimentally induced autoimmune diseases is also mediated by autoantigen-specific CD4+ T cells. Ideally, treatment of CD4+ T-cell-mediated diseases would eliminate the autoantigen-specific cells, while sparing the remainder of the T-cell repertoire. We have developed an effective therapy that deletes the autoreactive T cells at the site of autoimmune tissue destruction. This approach uses an antibody directed against a cell-surface protein (OX-40, also known as CD134) that is selectively upregulated on activated autoantigen-specific T cells within the inflamed tissue.
Mol Med Today 1998 Feb
PMID:Antibodies to OX-40 (CD134) can identify and eliminate autoreactive T cells: implications for human autoimmune disease. 954 94

The RT-PCR technique was adopted to amplify variable region of VP2 gene of infectious bursal disease virus using three different sets of primers. These primers could generate products of 643, 474 and 552 bp sizes. The authenticity of the amplicons was confirmed by their size in agarose gel, restriction enzyme digestion and by nested PCR. Out of total five clinical samples tested, IBD viral genomic RNA could be detected in four by RT-PCR. Restriction enzyme digestion of PCR products with StuI could differentiate clinical samples from an intermediate vaccine strain currently being used in India.
Biochem Mol Biol Int 1998 Jun
PMID:Detection of infectious bursal disease virus of poultry in clinical samples by RT-PCR. 967 52


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