Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

IgE binds to two types of Fc receptors, called Fc epsilon R1 (or high-affinity Fc epsilon R) and Fc epsilon R2 (or low-affinity Fc epsilon R). The Fc epsilon R1 is composed of four polypeptide chains, one alpha, one beta, and two gamma chains. The alpha chain contains the IgE binding site and is a member of the immunoglobulin supergene family. The Fc epsilon R2, also called CD23, consists of one polypeptide chain which shows homology to animal lectin receptors. Fc epsilon R1 are expressed on mast cells and basophils. Crosslinking of the Fc epsilon R1 induces immediate release of mediators of inflammation such as histamine and leukotrienes and delayed secretion of interleukins 4, 5, and 6. Fc epsilon R2 are expressed on resting mu delta + B cells, monocytes/macrophages (M phi), eosinophils, and platelets but rarely on T cells. Interleukin-4 upregulates Fc epsilon R2 expression on B cells and M phi. The functions of Fc epsilon R2 on the different cell types are not fully established and are controversial. Fc epsilon R2 on M phi, eosinophils, and platelets mediate cytotoxicity to schistosomules, enhance phagocytosis, and induce the release of granule enzymes. However, M phi from patients with atopic dermatitis expressing significantly more Fc epsilon R2 than M phi from normals do not release more leukotriene C4, prostaglandin E2, or beta-glucuronidase after incubation with aggregated IgE than normal monocytes. Furthermore, aggregated IgG1 is much more efficient than IgE in inducing mediator release from M phi and IgG1 antibodies are not known to induce immediate-type hypersensitivity reactions. Therefore, definitive proof that Fc epsilon R2 are involved in the pathogenesis of allergic disorders is still lacking. IL-4 appears to play a central role in immediate-type hypersensitivity. It induces human B cells to secrete IgE and IgG4, Ig isotypes typical for antibodies to helminthic parasites and allergens. IL-4 stimulates mast cell growth and upregulates Fc epsilon R2 expression. Interferon-gamma and IL-2 inhibit the IL-4-induced IgG4 and IgE secretion. Whether the abnormally high IgE antibody production in atopic patients is the result of overproduction of IL-4 or deficient IFN-gamma/IL-2 production is presently unknown.
J Invest Dermatol 1990 Jun
PMID:Fc receptors for IgE and interleukin-4 induced IgE and IgG4 secretion. 219 Oct 55

The exposure of murine skin to potent chemical carcinogens induced distinctive effects on the distribution of epidermal Langerhans cells (LC). Our previous finding that weekly applications of 7,12-dimethylbenz[a]anthracene deplete the numbers of adenosine triphosphatase (ATPase)-positive LC was extended to show that LC are also depleted on Ia and beta-glucuronidase staining. In contrast, application of the tobacco-derived carcinogen, benzo[a]pyrene (BP), caused a significant increase in Ia-positive LC density within 2 weeks and elevated levels were maintained for up to 6 months with continuous treatment. The tobacco-derived cocarcinogenic agent, catechol, also enhanced the numbers of epidermal LC. The LC in carcinogen treated epidermis were morphologically abnormal; after BP and catechol treatment LC appeared smaller with shorter dendrites, whereas in DMBA treated epidermis LC were enlarged with elongated dendrites. Application of the contact sensitizing agent, dinitrofluorobenzene, to skin treated with BP induced hyporesponsiveness rather than contact sensitivity upon subsequent antigen challenge. Hence, the function of the large number of morphologically altered LC in BP treated skin was impaired. We conclude that carcinogen-induced alterations of LC are associated with impaired immunocompetence, although different carcinogens probably operate via different mechanisms to induce such phenomena.
J Invest Dermatol 1989 Feb
PMID:Differential effects of benzo[a]pyrene and dimethylbenz[a]-anthracene on Langerhans cell distribution and contact sensitization in murine epidermis. 249 54

During chemical carcinogenesis Langerhans cells (LC) are depleted from the epidermis, disrupting the normal immunological functions of the skin. Tumor promotors but not initiators, have been shown to deplete adenosine triphosphatase (ATPase)-positive LC from the skin and therefore the cutaneous immune system may be impaired during tumor promotion but not initiation. The present study shows that the tumor promotor 12-O-tetradecanoylphorbol 13-acetate (TPA) but not the initiator urethane depletes Ia-positive LC from BALB/c murine ear epidermis, and beta-glucuronidase-positive LC from C57BL mouse tail skin. Sensitization with 2,4-dinitrofluorobenzene (DNFB) through urethane-treated skin resulted in a normal contact sensitivity response when the mice were challenged 5 days later. In contrast, tolerance resulted from sensitization through TPA-treated skin as a result of the generation of suppressor cells. In addition, TPA but not urethane-treated C57BL mouse tail skin survived for an extended time when grafted onto histoincompatible BALB/c mice. Therefore, impairment of the normal immunological functions of skin resulted from treatment with the tumor promotor TPA but not the tumor initiator urethane, which suggests that a loss of LC during tumor promotion may impair immunological protection against skin tumors.
J Invest Dermatol 1988 Mar
PMID:Suppressor cell activation and enhanced skin allograft survival after tumor promotor but not initiator induced depletion of cutaneous Langerhans cells. 296 90

Treatment of human polymorphonuclear leukocytes (PMN) with anthralin (0.2-50 micrograms/ml) results in dose-dependent inhibition of nondirected as well as directed migration (chemotaxis) against the synthetic tripeptide N-formyl-methionyl-leucyl-phenylalanine (FMLP), the complement fragment C5a and leukotriene B4. Polymorphonuclear leukocytes (PMN) pretreated with anthralin at concentrations which inhibit cell motility also show a dose-dependent inhibition of superoxide anion generation. In contrast to anthralin two derivatives (danthrone and anthralin dimer) were ineffective. Specific binding of [3H]FMLP to neutrophil membrane receptors was impaired by anthralin at concentrations 5-10 fold higher than those which were inhibitory for cell function. Release of beta-glucuronidase from azurophilic (lysosomal) granules provoked by various chemotaxins in the presence of cytochalasin B was not affected by anthralin over a wide range of concentrations. Also there were no signs of cytotoxicity e.g., leakage of cytoplasmatic lactate dehydrogenase (LDH) caused by anthralin, These data indicate that neutrophil functions may become substantially altered by anthralin. The effective dosages correspond to concentrations obtained in vivo after local application. Danthrone as well as anthralin dimer, known to be clinically ineffective, showed no effects upon PMN function. It is suggested that anthralin via a free radical mechanism alters sensitive sites at or in the cellular membrane including receptors.
J Invest Dermatol 1985 Jul
PMID:Multifunctional inhibition by anthralin in nonstimulated and chemotactic factor stimulated human neutrophils. 298 75

Three fluorescein-labeled lectins were shown to bind differentially to cell surfaces in different epithelial layers of rat oral mucosa regardless of the age or the site of origin of the tissue. Griffonia simplicifolia (GS-1-B4), specific for alpha-D-galactosyl end groups, labeled basal cells only; Ulex europeus (Ulex 1) specific for alpha-L-fucosyl groups labeled spinous cells; and Bandeiraea simplicifolia (BSII), specific for N-acetyl-D-glucosamine, labeled cornified cells. Pretreatment of sections with alpha-galactosidase completely abolished the staining of basal cells by GS-1-B4, but had no effect on the staining of spinous cells by Ulex 1. In contrast, alpha-fucosidase abolished the staining of spinous cells by Ulex 1 and caused staining of both basal and spinous cells by GS-1-B4. Neuraminidase and chondroitinase ABC produced results similar to one another, with staining of basal cells by GS-1-B4 and labeling of both basal and spinous cells with Ulex 1. beta-galactosidase, beta-glucuronidase, and testicular hyaluronidase did not affect the staining pattern of GS-1-B4 or Ulex 1, whereas chymotrypsin completely abolished any staining with either lectin. The results demonstrate a complex arrangement of cell surface carbohydrates in the epithelium of rat oral mucosa. The findings indicate a possible simplification in the spatial arrangements of cell surface carbohydrates during the differentiation of basal to spinous cells.
J Invest Dermatol 1985 Dec
PMID:Preferential lectin binding to specific layers of rat oral epithelium and modification by enzyme pretreatment. 299 51

Scales from patients with nonpustular psoriasis were investigated for the presence of peptides capable of activating functional activities in human polymorphonuclear leukocytes (PMNL). Two compounds with similar molecular weight (12,500 and 15,000) were isolated which markedly stimulated PMNL functional activities including chemotaxis, generation of superoxide radical anion (O-2), and liberation of beta-glucuronidase as a marker enzyme. As revealed by ion-exchange and subsequent radioimmunoassay followed by chromatofocusing, one peptide proved to be the desarginated form of the complement split product C5ades arg. No C5a was detectable. As a second psoriatic scale chemotaxin we isolated an anionic neutrophil-activating peptide (ANAP) which shows a single isoelectric point at pH 6.8. This peptide shares some of the characteristics of epidermal cell-derived thymocyte-activating factor and interleukin 1 and, as shown by deactivation experiments, it cross-reacts with a monocyte-derived cytokine. The 2 newly described neutrophil-activating peptides (C5ades arg and ANAP) may play an important role in the psoriatic tissue reaction.
J Invest Dermatol 1986 Jul
PMID:Identification of C5ades arg and an anionic neutrophil-activating peptide (ANAP) in psoriatic scales. 301 8

In 14 patients with progressive systemic sclerosis (PSS) the activities of acid lysosomal glycosidases (alpha-, beta-galactosidase, beta-glucosidase, beta-glucuronidase, and beta-N-acetyl-glucosaminidase) were determined fluorometrically in serum, leukocytes, and skin tissue. The beta-galactosidase was the only enzyme which exhibited a significantly elevated activity in PSS serum and skin but not leukocytes, as compared to the control. The activity patterns of the studied glycosidases in serum were similar to those found in skin, but differ from the distribution of glycosidase activities in leukocytes. In cultured dermal fibroblasts derived from PSS patients, an elevated intracellular activity of beta-galactosidase was detected. These results suggest that the increased beta-galactosidase activity in the serum originates from the skin fibroblasts.
Arch Dermatol Res 1987
PMID:Origin of the enhanced activity of lysosomal beta-galactosidase in serum and skin in progressive systemic sclerosis. 311 93

A spontaneous, hypomelanotic variant (MI) of the highly melanotic transplantable hamster melanoma of Bomirski (Ma) is the subject of this report. Tyrosinase activity is 2-3 times higher, but melanin content significantly lower than in the parental Ma melanotic melanoma. Acid phosphatase activity is similar in both, but beta-glucuronidase and aryl-sulfatase A are 2-3 times higher in the hypomelanotic variant. Transplanted MI melanomas grow more slowly than the parental tumor, but metastasize with similar incidence and localization. Hypomelanotic variant melanoma cells, even those in grossly nonnecrotic parts of the transplants, show signs of low viability like swelling of the cytoplasm or cellular condensation, and disintegration. Autophagic vacuoles are numerous. They appear to be formed by enclosure of a portion of cytoplasm by cisternae of smooth endoplasmic reticulum or trans-Golgi network. These limiting cisternae contain tyrosinase as evidenced by deposition of electron dense reaction product on incubation with tyrosine or DOPA. Other sites of ultrastructural tyrosinase reaction are melanosomes and the smooth-surfaced cisternae and vesicles of the trans-Golgi network. We postulate the low cell viability, associated with autophagosome formation, is the cause for the growth retardation of the MI variant, and that the lower melanin content of these tyrosinase-rich cells is due to sequestration of a substantial portion of newly synthesized enzyme into autophagic vacuoles before it has the chance of being incorporated into melanosomes.
J Invest Dermatol 1987 Nov
PMID:Pathology and ultrastructural characteristics of a hypomelanotic variant of transplantable hamster melanoma with elevated tyrosinase activity. 311 4

Chemotactic migration, production of superoxide anion (O2-), and the release of beta-glucuronidase from azurophilic granules were determined in polymorphonuclear leukocytes (PMN) from 135 patients with infectious (e.g., pyoderma, acne conglobata, erysipelas) as well as noninfectious (psoriasis) skin diseases. Purified C5a and the formylated tripeptide FMLP were used as stimuli. In addition, longitudinal profiles of PMN activities were performed at daily intervals in several patients. There was a complete absence of PMN responses (chemotaxis, O2--production, and enzyme release) specifically induced by C5a in 25 patients suffering from various inflammatory diseases of the skin. In these patients PMN responsiveness for the tripeptide FMLP was either normal or increased. The C5a-dependent defect of PMN was transient and correlated with disease activity. When normal PMN were incubated with sera from C5a-defective patients, no inherent stimulatory or inhibitory activities compared to control sera were seen. Pretreatment of normal PMN in vitro with various concentrations of C5a failed to completely deactivate PMN without affecting FMLP dependent functions. These observations demonstrate the presence of a functional defect in circulating PMN during acute cutaneous inflammation. The in vitro experiments suggest transient blocking of C5a-dependent PMN functions by a cell-bound factor which seems not to be C5a or C5adesarg.
J Invest Dermatol 1985 Sep
PMID:Transient absence of C5a-specific neutrophil function in inflammatory disorders of the skin. 316 55

The activities of several lysosomal hydrolases (beta-galactosidase, beta-hexosaminidase, alpha-mannosidase, beta-glucuronidase and acid phosphatase) were determined in serum and blood lymphocytes from patients affected with scleroderma. Statistical comparisons between means of patient and control groups (Student's t test) showed a significant difference in serum beta-galactosidase and acid phosphatase between patients and controls (serum beta-galactosidase: 36.5 +/- 22 nmol/h/ml in the scleroderma group versus 24 +/- 13 nmol/h/ml in the control group; serum acid phosphatase 853 +/- 345 nmol/h/ml in the scleroderma group versus 634 +/- 295 nmol/h/ml in the control group). These differences were significant (p less than 0.01). Both enzyme activities were also significantly increased in the group with systemic scleroderma, but the difference was less in the group with localized scleroderma (this is discussed in terms of statistics and pathophysiology). The other enzyme activities determined were not significantly modified. The validity of these results is discussed, together with their diagnostic value and with the pathophysiological hypotheses put forward to explain the high levels found.
Ann Dermatol Venereol 1986
PMID:[Serum lysosomal hydrolases in various forms of scleroderma]. 381 96


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