Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

DEODAN is a lysozyme lysate from Lactobacillus bulgaricus for oral administration which has shown antitumor activity in mice and humans. The effects of this preparation on some functions of monocytes/macrophages and on host resistance to experimental infections were examined. The oral administration to mice of DEODAN-150 mg/kg daily (the recommended dose in humans) caused an increase of the spreading ability and phagocytic activity of peritoneal macrophages, which showed morphological signs of cell activation. The level of Interleukin-1 (IL-1) secreted in the culture supernatant of peritoneal macrophages of DEODAN-treated mice was found to be slightly increased only when the mice were treated with 150 mg/kg DEODAN for 10 days. However, the in vitro incubation of human blood monocytes with DEODAN resulted in induction of membrane-bound and cytoplasmic IL-1 and Tumor Necrosis Factor (TNF)-alpha. The oral treatment of mice with DEODAN also caused a decrease in mortality after experimental infections with Klebsiella pneumoniae and Listeria monocytogenes. These results indicate that DEODAN activates the phagocytic and secretory functions of mononuclear cells and increases host resistance to bacterial infections.
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PMID:Stimulating effect of DEODAN (an oral preparation from Lactobacillus bulgaricus "LB51") on monocytes/macrophages and host resistance to experimental infections. 843 22

In most bacteriophages of gram-negative bacteria, the phage endolysin is released to its murein substrate through a lesion in the inner membrane. The lesion is brought about by a second phage-encoded lysis function. For the first time, we present evidence that the same strategy is elaborated by a phage of a gram-positive bacterium. Thus, there appears to be an evolutionarily conserved lysis pathway for most phages whether their host bacterium is gram negative or gram positive. Phage phi 29 gene 14, the product of which is required for efficient lysis of Bacillus subtilis, was cloned in Escherichia coli. Production of protein 14 in E. coli resulted in cell death, whereas production of protein 14 concomitantly with the phi 29 lysozyme or unrelated murein-degrading enzymes led to lysis, suggesting that membrane-bound protein 14 induces a nonspecific lesion in the cytoplasmic membrane.
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PMID:The missing link in phage lysis of gram-positive bacteria: gene 14 of Bacillus subtilis phage phi 29 encodes the functional homolog of lambda S protein. 843 97

Four temperature-sensitive mutations in the divIB gene of Bacillus subtilis have been localized to the region corresponding to the C-terminal half of the 263-residue DivIB protein. Antiserum was raised to the 80% C-terminal portion lying on one side of a putative transmembrane (hydrophobic) segment, and used to examine aspects of the nature and localization of the DivIB protein in the cell. A single DivIB species of a size equal to the full-length protein encoded by the divIB gene was detected in wild-type cells. Cell fractionation studies established that DivIB is associated preferentially with the cell envelope (membrane plus cell wall), with approximately 50% being released into solution upon treatment of cells with lysozyme under conditions that yield protoplasts. Of the remaining 50%, approximately half remained firmly associated with the membrane fraction. On the basis of the 'positive-inside rule' of von Heijne (1986) it is suggested that the topology of membrane-bound DivIB is such that the long C-terminal portion is directed to the outside and the smaller N-terminal portion to the inside of the cell. DivIB in protoplasts was rapidly degraded by proteinase K under conditions where there was no general proteolysis of the cytoplasmic proteins. This is consistent with its absence from the cytoplasm, and with the predicted membrane topology. Septum positioning in a divIB null mutant, which grows as filaments at temperatures of 30 degrees C and below, was found to be normal. It appears that DivIB is needed for achieving the appropriate rate of initiation of septum formation at normal division sites. It is proposed that the C-terminal portion of DivIB, localized on the exterior surface of the membrane and in juxtaposition to the peptidoglycan, normally interacts with another protein (or proteins) to initiate septum formation.
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PMID:Characterization of mutations in divIB of Bacillus subtilis and cellular localization of the DivIB protein. 845 77

We report the first characterization of plasma-membrane-bound tyrosine phosphatase activity in the haemoprotozoan. Trypanosoma brucei. Several enzymic properties of the membrane fraction were identical to other protein tyrosine phosphatases (PTPases), such as (a) insensitivity to inhibitors of other protein phosphatases, including tetramisole, sodium tartrate and okadaic acid, (b) inhibition by sodium vanadate, and (c) activation by spermidine. Additionally, T. brucei PTPase activity presented two novel features, an acidic pH optimum at pH 4.0-5.0 and a very low Km value (2.5 nM) for the specific synthetic substrate, Tyr(P)Raytide. Higher Km values of 170 nM for Tyr(P)-RCML (RCML, reduced, carboxamidomethylated and maleylated lysozyme) and of 3 mM for the non-specific inorganic substrate p-nitrophenyl phosphate, suggested that the PTPase activity of T. brucei was substrate specific. Reconstitution experiments on bloodstream-stage membrane proteins revealed that three polypeptides of 148, 115 and 72 kDa contained vanadate-inhibitable PTPase activity. Modulator assays revealed that the 72-kDa protein was responsible for the observed spermidine stimulation, but indicated that the modulator profile of the 148-kDa protein was most similar to the whole membrane fraction. Furthermore, the PTPase activity of T. brucei was life-cycle-stage regulated. Neither the whole membrane fraction nor the reconstituted proteins of the procyclic insect stage dephosphorylated tyrosine residues.
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PMID:Characterization of a life-cycle-stage-regulated membrane protein tyrosine phosphatase in Trypanosoma brucei. 857 47

Self-reactive B cells from tolerant double-transgenic (Dbl-Tg) mice coexpressing hen egg lysozyme (HEL) and rearranged anti-HEL immunoglobulin genes have a relatively short life span when compared to normal B cells, irrespective of whether they are exposed to antigen in multivalent membrane-bound form (mHEL-Dbl-Tg mice) or soluble form (sHEL-Dbl-Tg mice). The factors responsible for determining the fate of these B cells after encounter with self-antigen were investigated using a cell-tracking technique in which anti-HEL Ig-Tg spleen cells were labeled with the intracellular dye 5-carboxyfluorescein diacetate-succinimidyl ester (CFSE) and injected either into non-Tg recipients or a variety of HEL-Tg hosts. In non-Tg recipients, HEL-binding B cells persisted in the circulation and could be detected in the follicles of the spleen for at least 5 d. On transfer into either mHEL-Tg or sHEL-Tg hosts, they underwent activation and then rapidly disappeared from the blood and spleen over the next 3 d, consistent with the short life span reported previously. Immunohistology of spleens from sHEL-Tg recipients indicated that the transferred B cells had migrated to the outer margins of the periarteriolar lymphoid sheath (PALS), where they were detectable for 24 h before being lost. The positioning of B cells in the outer PALS depended on a critical threshold of Ig receptor binding corresponding to a serum HEL concentration between 0.5 and 15 ng/ml, but was not restricted to endogenously expressed HEL in that the same migratory pattern was observed after transfer into non-Tg recipients given exogenous (foreign) HEL. Moreover, bone marrow-derived immature Ig-Tg B cells homed to the outer PALS of sHEL-Tg mice and then disappeared at the same rate as mature B cells, indicating that the stage of maturation did not influence the fate of self-reactive B cells in a tolerant environment. On the other hand, HEL-binding B cells transferred into sHEL-Dbl-Tg recipients persisted over the 3-d period of study, apparently due to insufficient availability of antigen, as indicated by the fact that the degree of Ig receptor downregulation on the transferred B cells was much less than in sHEL-Tg recipients. If T cell help was provided to Ig-Tg B cells at the time of transfer into sHEL-Tg recipients in the form of preactivated CD4+ T cells specific for major histocompatibility complex-peptide complexes on the B cell surface, HEL-binding B cells migrated through the outer PALS of the spleen to the follicle, where they formed germinal centers, or to adjacent red pulp, where they formed proliferative foci and secreted significant amounts of anti-HEL antibody. Taken together, these results indicated that the outcome of the interaction between self-antigen and B cells is largely determined by a combination of the degree of receptor engagement and availability of T cell help.
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PMID:The fate of self-reactive B cells depends primarily on the degree of antigen receptor engagement and availability of T cell help. 864 4

The light microscopic and ultrastructural appearances of unusual filamentous aggregates in a right parietal meningioma in a 14-year-old boy are described. The tumor showed prominent meningothelial as well as fibroblastic components and was graded as an atypical meningioma. By light microscopy, eosinophilic, PAS-positive, granular, irregularly shaped Rosenthal fiber-like structures were widespread within the tumor, in both an intra- and an extracellular location. By immunohistochemical staining, similar location of positivity was obtained for vimentin, laminin, and collagen type IV. The inclusions were nonreactive for keratin, lysozyme, alpha-1-antitrypsin, and ubiquitin. Ultrastructurally, these aggregates were composed of an irregular tangle of filaments with electron dense condensations, sometimes with a lattice pattern. The intracellular aggregates were membrane-bound, and some were found within dilated rough endoplasmic reticulum, while extracellularly, they filled up spaces between adjacent tumor cells. Less prominently, flocculent osmiophilic nonfilamentous material was also seen within the inclusions. These observations suggest that these novel inclusions in a meningioma are composed of intermediate filaments (vimentin) and extracellular matrix proteins, with active synthesis in the rough endoplasmic reticulum and subsequent extrusion from the tumor cells into the extracellular spaces.
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PMID:Filamentous aggregates in a meningioma. 894 Jul 65

N-Acetyl-D-glucosaminylpyrophosphorylundecaprenol (GlcNAc-P-P-Und), an intermediate in the biosynthesis of the enterobacterial common antigen in E.coli and some O-antigen chains in gram-negative bacteria, is formed by the transfer of GlcNAc 1-P from UDP-GlcNAc to Und-P, analogous to the reaction forming GlcNAc-P-P-dolichol (GlcNAc-P-P-Dol) in mammalian cells. Since the microsomal enzyme from animal cells exhibits a strong preference for Dol-P, which contains a saturated alpha-isoprene unit, the polyisoprenyl phosphate specificity of the homologous bacterial enzyme was characterized. The enzyme remained bound to the membrane fraction when spheroplasts, formed by lysozyme-EDTA treatment, were lysed in hypotonic buffer. GlcNAc-P-P-Und synthase (GPT) activity was elevated in a strain of E.coli bearing the rfe gene, which encodes GPT on a multicopy plasmid, and virtually absent from rfe null mutants. GPT actively utilized fully unsaturated polyprenyl phosphate (Poly-P) substrates with maximal activity seen with (C55) Und-P, but was unable to utilize (C55)Dol-P. This substrate specificity contrasts with the microsomal GPT from pig brain, which actively utilized (C55)Dol-P, but not Und-P, as substrate. GPT activity bound to particulate fractions from three strains of bacilli also exhibited a strict preference for fully unsaturated Poly-P substrates. Unexpectedly, E.coli GPT activity cofractionated with the cytosolic marker enzyme, beta-galactosidase, and not the membrane-bound enzyme, D-lactate dehydrogenase, in cells disrupted in a French pressure cell. The properties and polyisoprenyl phosphate specificity of the soluble form of GPT were identical to the activity associated with the membrane preparations obtained from spheroplasts. The evolutionary and functional significance of the use of polyisoprenyl glycosyl carrier lipids with saturated alpha-isoprene units in eukaryotes remains uncertain.
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PMID:Polyisoprenyl phosphate specificity of UDP-GlcNAc:undecaprenyl phosphate N-acetylglucosaminyl 1-P transferase from E.coli. 913 38

Graves' Disease results from the production of autoantibodies against receptors for thyroid stimulating hormone (TSH) on thyroid epithelial cells, and represents the prototype for numerous autoimmune diseases caused by autoantibodies that bind to organ-specific cell membrane antigens. To study how humoral tolerance is normally maintained to organ-specific membrane antigens, transgenic mice were generated selectively expressing membrane-bound hen egg lysozyme (mHEL) on the thyroid epithelium. In contrast to the deletion of autoreactive B cells triggered by systemic mHEL (Hartley, S.B., J. Crosbie, R. Brink, A.B. Kantor, A. Basten, and C.C. Goodnow. 1991. Nature. 353:765-769), selective expression of mHEL autoantigen on thyroid cells did not trigger elimination or inactivation of circulating HEL-reactive B cells. These results provide evidence that tolerance is not actively acquired to organ-specific antigens in the preimmune B cell repertoire, underscoring the importance of maintaining tolerance to such antigens by other mechanisms. The role of an intact endothelial barrier in sequestering organ-specific antigens from circulating preimmune B cells is discussed.
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PMID:Self-reactive B cells are not eliminated or inactivated by autoantigen expressed on thyroid epithelial cells. 939 69

Self-reactive B cells Tg for both a bcl-xL death inhibitory gene and an Ig receptor recognizing hen egg lysozyme (HEL-Ig) efficiently escaped developmental arrest and deletion in mice expressing membrane-bound self-antigen (mHEL). In response to the same antigen, Tg HEL-Ig B cells not expressing bcl-xL were deleted, while cells expressing bcl-2 were arrested at the immature B stage. Bcl-xL Tg B cells escaping negative selection were anergic in both in vitro and in vivo assays and showed some evidence for receptor editing. These studies suggest that Bcl-x may have a distinct role in controlling survival at the immature stage of B cell development and demonstrate that tolerance is preserved when self-reactive B cells escape central deletion.
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PMID:Self-reactive B lymphocytes overexpressing Bcl-xL escape negative selection and are tolerized by clonal anergy and receptor editing. 969 34

We have previously demonstrated that antigen-specific T cell help can rescue mature Ig transgenic (Tg) hen egg lysozyme (HEL)-specific B cells from tolerance induction upon transfer into soluble HEL-expressing Tg hosts. Here we extend these findings by showing that T cell help could also rescue both immature and mature self-reactive B cells from rapid deletion in response to high-avidity membrane-bound HEL. Moreover, although short-lived anergic peripheral B cells that had matured in the presence of soluble self antigen could not be rescued by provision of T cell help, a proportion of immature anergic IgM+ IgD- CD23- B cells from the bone marrow of the same donors survived and proliferated when given help following transfer to a soluble or membrane HEL-expressing host. In other words, T cell help must be available relatively soon after the antigen signal to prevent induction of tolerance. Consistent with this interpretation, the stronger stimulus provided by membrane-bound antigen, which deletes immature B cells before they leave the bone marrow, did not afford an opportunity for T cell help to rescue tolerant immature bone marrow-derived B cells upon transfer in vivo. Nevertheless, these B cells were capable of responding to T cell help in vitro, which speaks against an immutable susceptibility of immature B cells to tolerance induction. Taken together, these data indicate that the strength of the antigen signal and availability of T cell help are the primary determinants of the fate of both immature and mature B cells, consistent with the model proposed by Bretscher and Cohn more than 25 years ago.
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PMID:Rescue of self-reactive B cells by provision of T cell help in vivo. 971 Feb 32


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