Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
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The wing discs and fat body of Manduca sexta larvae contain enzymes (i.e. carboxylesterase and epoxide hydratase) that can convert the C18 juvenile hormone (JH) to the acid, diol and acid diol. No evidence of oxidative degradation was noted. In vitro studies suggest that JH can be compartmentalized within the cells of the fat body where it is less accessible to degradative mechanisms. Experiments utilizing a hemolymph-binding protein fraction (BPF) in vitro with fat body and imaginal discs indicate that the BPF retards the uptake of JH by tissues and its subsequent degradation by tissue enzymes. BPF also appears to protect JH from degradation by enzymes released into the medium. By these mechanisms the insect can maintain elevated JH titers for relatively long periods. Binding protein may also keep JH in solution in the hemolymph allowing its rapid distribution throughout the insect. The data suggest that the binding protein plays a key role in maintaining juvenile hormone titers.
Mol Cell Endocrinol 1975 Sep
PMID:The influence of hemolymph-binding protein on juvenile hormone stability and distribution in Manduca sexta fat body and imaginal discs in vitro. 17 Nov 83

All of several hundred erythromycin resistant single site mutants of Bacillus subtilis W168 are temperature senstive for sporulation. The mutants and wild type cells grow vegetatively at essentially the same rates at both permissive (30 degrees C) and nonpermissive (47 degrees C) temperatures. In addition cellular protein synthesis, cell mass increases and cell viabilities are similar in mutant and wild type strains for several hours after the end of vegetative growth (47 degrees C). in the mutants examined, the temperature sensitive periods begin when the sporulation process is approximately 40% completed, and end when the process is 90% completed. At nonpermissive temperatures, the mutants produce serine and metal proteases at 50% of the wild type rate, accumulate serine esterase at 16% of the wild type rate, and do not demonstrate a sporulation related increase in alkaline phosphatase activity. The eryR and spots phenotypes cotransform 100%, and cotransduce 100% using phage PBS1. Revertants selected for ability to sporulate normally at 47 degrees C (spot), simultaneously regain parental sensitivity to erthromycin. No second site revertants are found. Ribosomes from eryR spots strains bind erythromycin at less than 1% of the wild type rate. A single 50S protein (L17) from mutant ribosomes shows an altered electrophoretic mobility. Ribosomes from spo+ revertants bind erythromycin like parental ribosomes and their proteins are electrophoretically identical to wild type. These data indicate that the L17 protein of the 50S ribosomal subunit from Bacillus subtilis may participate specifically in the sporulation process.
Mol Gen Genet 1977 Jan 18
PMID:Erythromycin resistant mutations in Bacillus subtilis cause temperature sensitive sporulation. 40 47

An in vitro method has been developed for the quantitative estimation of juvenile hormone (JH) esterase activity in the hemolymph of the Colorado beetle Leptinotarsa decemlineata Say. The apparent Km value for JH-esterase was determined. JH-esterase and general carboxyesterase activities were estimated throughout the life cycle and under different photoperiodic conditions. High activities were observed in fourth instar larvae and in beetles just before diapause. Lower activities were found in third instar larvae, long-day, diapause and post-diapause beetles. Similar variations were found in general carboxyesterase activity but not in protein concentration. A possible role for the esterase in the regulation of the JH titer is discussed.
Mol Cell Endocrinol
PMID:Age-dependent changes in juvenile hormone esterase and general carboxyesterase activity in the hemolymph of the colorado potato beetle, Leptinotarsa decemlineata. 123

Dibasic esters (DBE) solvent has been demonstrated to induce a mild degeneration of the olfactory, but not the respiratory epithelium of the rat nasal cavity following a 90-day inhalation exposure. Previous work has demonstrated that acid phosphatase release is a reliable index of DBE-induced cytotoxicity in an in vitro system of rat nasal explants. In the present study, rat nasal explants were examined microscopically and ultrastructurally following incubation in varying concentrations of a representative DBE, dimethyl adipate (DMA). DMA-induced microscopic and ultrastructural changes in rat nasal explants correlated well with biochemical perturbations associated with DBE exposure in a previous study. In both studies, olfactory epithelium was more susceptible to DMA-induced toxicity than respiratory epithelium and DMA-induced nasal toxicity was attenuated by pretreatment with a carboxylesterase inhibitor. The results of this study support the hypothesis that DBE and potentially other inhaled organic esters induce nasal toxicity via a common mechanism, carboxylesterase-mediated production of toxic acid metabolites. It was established that carboxylesterase-rich sustentacular cells are the primary target cells for DBE toxicity in rat nasal explants. It was proposed that degeneration of nasal olfactory sensory cells observed in rats following 90-day inhalation exposure to DBE may be secondary to necrosis and loss of sustentacular cells.
Exp Mol Pathol 1992 Jun
PMID:A microscopic and ultrastructural evaluation of dibasic esters (DBE) toxicity in rat nasal explants. 163 80

Cytotoxic T lymphocytes (CTL) contain a potent cytolytic pore-forming protein (PFP, perforin or cytolysin) localized in their cytoplasmic granules. In the presence of calcium, perforin lyses a variety of target cells (TC) non-specifically. CTL, however, are generally resistant to the lytic effect of perforin. In this work, cytoplasts from CTL and susceptible TC were made by centrifuging cells on a Ficoll density gradient in the presence of cytochalasin B. Characterization by electron microscopy and a serine esterase assay established that both CTL and TC cytoplasts were completely devoid of nuclei and CTL cytoplasts contained essentially no granules. CTL cytoplasts are just as resistant to perforin-mediated lysis as the intact CTL, and both TC and their corresponding cytoplasts are very sensitive to lysis. Furthermore, CTL cytoplasts are less effective than TC cytoplasts in inhibiting hemolysis, a property shared by the respective intact cells. These results indicate that soluble granular components do not confer resistance on CTL, and suggest that the protective agent(s) acts by impeding perforin binding to the CTL membrane.
Mol Immunol 1991 Sep
PMID:Cytoplasts from cytotoxic T lymphocytes are resistant to perforin-mediated lysis. 192 7

The mutant c-fgr protein (p58c-fgr/F523) containing Phe-523 instead of Tyr-523 exhibited transforming activity in NIH 3T3 cells like other protein-tyrosine kinases of the src family, but normal p58c-fgr (p58c-fgr/wt) did not. The mutant protein showed tyrosine kinase activity threefold higher than that of the normal protein in vitro. Surprisingly, transfection of the normal c-fgr gene into NIH 3T3 cells resulted in induction of sodium fluoride (NaF)-sensitive alpha-naphthyl butyrate esterase (alpha-NBE), a marker enzyme of cells of monocytic origin, which was not induced in v-src-, v-fgr-, or lyn-transfected NIH 3T3 cells. The NaF-sensitive alpha-NBE induced in c-fgr transfectants was shown by isoelectric focusing to have a pI of 5.2 to 5.4, a range which was the same as those for thioglycolate-induced murine peritoneal macrophages and 1 alpha,25-dihydroxyvitamin D3-treated WEHI-3B cells. Immunoblotting studies with antiphosphotyrosine antibodies revealed that 58-, 62-, 75-, 120-, 200-, and 230-kDa proteins were commonly phosphorylated at tyrosine residues in NIH 3T3 cells transfected with normal and mutated c-fgr, while 95-kDa protein was significantly phosphorylated at tyrosine residues in cells transfected with the mutated c-fgr. These findings suggest that tyrosine phosphorylation of specific cellular substrate proteins is important in induction of NaF-sensitive alpha-NBE and cell transformation by p58c-fgr.
Mol Cell Biol 1991 Dec
PMID:Human c-fgr induces a monocyte-specific enzyme in NIH 3T3 cells. 194 88

Serotonin (5-hydroxytryptamine) functions as a neurotransmitter and a hormone. Its diverse actions are mediated by at least seven distinct cell surface receptor subtypes. The serotonin receptor subtype 2 (gene symbol HTR2) is a G-protein-coupled receptor, expressed primarily in the cerebral cortex, where upon stimulation it stimulates the hydrolysis of inositol phospholipids. We have mapped the HTR2 locus to human chromosome 13 and to mouse chromosome 14 by somatic cell hybrid analysis. Linkage studies in CEPH families, using a PvuII RFLP detected with the HTR2 probe, revealed tight linkage between HTR2 and ESD, the locus for esterase D. The most likely position for HTR2 is between ESD and RB1, the retinoblastoma-1 gene. The homologous loci in mouse, Rb-1 and Esd(Es-10) are on mouse chromosome 14, close to ag, agitans, a recessive neurological mutation. Having mapped Htr-2 to mouse chromosome 14, we predict that it falls into this known conserved gene cluster.
Somat Cell Mol Genet 1990 Nov
PMID:The serotonin receptor subtype 2 locus HTR2 is on human chromosome 13 near genes for esterase D and retinoblastoma-1 and on mouse chromosome 14. 198 30

Treatment of monocytes or K562 cells with proteolytic enzymes like pronase or trypsin, increases both the affinity of the type II Fc receptor for IgG and the signaling via this receptor. In the present study we evaluated whether other proteases could similarly enhance Fc gamma RII affinity. We furthermore assessed whether all cell types expressing Fc gamma RII display this effect. Therefore, proteins from the coagulation system and PMN-derived enzymes were tested for effects on Fc gamma RII-mediated ligand binding. Enzymes of the coagulation system were tested both in fibrinogen-depleted plasma, as well as in purified form. No effects were found on Fc gamma RII-mediated rosette formation for both situations. In contrast, supernatant of stimulated granulocytes as well as leucocyte elastase were observed to be active in augmenting EA-hIgG rosette formation of thrombocytes and myeloid cell lines K562 and U937. The B cell lines Raji and Daudi, did not show enhanced rosette formation after enzyme treatment. The active component from granulocyte supernatant was partially characterized as a serine esterase with an apparent Mw of 30 kD. We tested whether the isotype specificity of Fc gamma RII on K562 cells changes upon enzyme treatment. It was found that all three tested murine subclasses gamma 1, gamma 2a, gamma 2b, bound equally well to this receptor, and interaction with all isotypes was enhanced to the same extent.
Mol Immunol 1990 Dec
PMID:PMN-derived proteases enhance the affinity of Fc gamma receptor II on myeloid cells, but not on B cells. 214 7

fms genes encoding either wild-type or constitutively activated colony-stimulating factor 1 receptors (CSF-1R) were introduced by retroviral infection into long-term mouse lymphoid cultures. Four early pre-B-cell lines transformed by the feline v-fms oncogene underwent spontaneous and irreversible differentiation to macrophages when transferred from RPMI 1640 to Iscove modified Dulbecco medium. Expression of wild-type human CSF-1R in early pre-B cells conferred no proliferative advantage unless human CSF-1 was added to the culture medium. A clonal, factor-dependent early pre-B-cell line (D1F9), selected for continuous growth on NIH 3T3 cell feeder layers producing human CSF-1, could be maintained in RPMI 1640 medium containing interleukin-7 (IL-7) but also differentiated to macrophages when grown in Iscove modified Dulbecco medium containing human CSF-1. The macrophages retained parental immunoglobulin gene rearrangements and proviral insertions, lost B-cell antigens, expressed butyrate esterase and MAC-1, were actively phagocytic, and no longer survived in IL-7. Unlike factor-independent v-fms transformants, the irreversible commitment of D1F9 cells to differentiate in the macrophage lineage could be suppressed by IL-7, depended on human (but not mouse) CSF-1, and was inhibited by an antibody to human CSF-1R. Signals mediated by transduced CSF-1R can therefore play a deterministic role in cell differentiation.
Mol Cell Biol 1990 Jun
PMID:Macrophage lineage switching of murine early pre-B lymphoid cells expressing transduced fms genes. 216 May 84

A human cDNA probe was used to screen a panel of mouse-Chinese hamster somatic cell hybrids to determine the chromosomal location of the retinoblastoma susceptibility gene (Rb-1) in mouse. The Rb-1 gene mapped to mouse chromosome 14. Thus, the retinoblastoma susceptibility gene is syntenic with esterase 10 (the mouse homolog of human esterase D). The chromosomal assignment of the mouse Rb-1 gene was further confirmed by using the same probe to study mouse-rat microcell hybrids. Since the human retinoblastoma susceptibility gene (RB1) along with the gene for esterase D is on chromosome 13q14, these data indicate this linkage group is conserved in man and mouse.
Somat Cell Mol Genet 1989 Sep
PMID:Assignment of retinoblastoma susceptibility gene to mouse chromosome 14. 278 16


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