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Yeast Spheroplasts Formed by Cell Wall-Degrading Enzymes from Oerskovia sp 总被引:3,自引:2,他引:1
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Oerskovia sp. produces inducible extracellular enzymes which degrade the walls of various yeasts. Yeast spheroplasts are formed from both log- and stationary-phase cells. 相似文献
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The lurcher (Lc) mutant mouse strain exhibits postnatal degeneration of cerebellar Purkinje cells. We have typed progeny from an intersubspecific, phenotypic backcross at seven loci to develop a genetic linkage map which spans approximately 35 cM surrounding and including the Lc locus on mouse chromosome 6. [(Mus musculus castaneus x B6CBA-Aw-J/A-Lc)F1 x B6CBA-Aw-J/A]N2 progeny were scored visually for the lurcher phenotype and molecularly, through restriction fragment length polymorphism analysis, for six cloned markers. Two candidate genes, Npy and Pcp-1, which map to mouse chromosome 6 and which are expressed in the cerebellum, are demonstrated to be distinct from Lc. Three genes are shown to be closely linked to the Lc locus, and the map order cen-Cpa-Npy-Cbl-1-Lc-Igk, Fabpl-Pcp-1 is determined. The molecular genetic linkage map presented here represents progress toward isolating a clone of the Lc gene. 相似文献
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T D Nguyen G G Heintz L M Kaiser C A Staley I L Taylor 《The Journal of biological chemistry》1990,265(11):6416-6422
Neuropeptide Y (NPY), a neurotransmitter contained within intrinsic nerves of the small intestine, inhibits secretion when added to the serosal side of intestinal mucosa mounted in Ussing chambers. Using NPY radiolabeled with IODO-GEN, lactoperoxidase, or the Bolton-Hunter reagent, we have localized high affinity NPY receptors to the serosal laterobasal membranes of the rat intestinal epithelial cell, isolated according to a recently described protocol that minimizes contamination with endoplasmic reticulum, Golgi, and brush-border membranes. In addition, certain species of radiolabeled NPY, including those labeled with IODO-GEN at the tyrosine residue 36, also demonstrated an ability to bind to brush-border membranes. These receptors were specific for NPY since the homologous peptides, pancreatic polypeptide and peptide YY, were less efficient than NPY in inhibiting the membrane binding of radiolabeled NPY. By cross-linking NPY to its receptor with either disuccinimidyl suberate or dithiobis(succinimidyl propionate) and analyzing the resulting complexes on sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by radioautography, we identified two NPY receptor species with molecular sizes of 52-59 kDa and 37-39 kDa. The 37-39-kDa species further possesses a disulfide bond which may attach it to a separate approximately 5-kDa subunit, as evidenced by retarded migration in the absence of the reducing agent dithiothreitol. The intestinal NPY receptor is slightly smaller than the rat brain receptor previously characterized using similar techniques. The localization of NPY receptors on laterobasal membranes is consistent with previous anatomic and physiologic findings, and their identification by cross-linking techniques will constitute the basis for detailed characterization. 相似文献
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Aamir Ahmad Shadan Ali Alia Ahmed Azfur S. Ali Avraham Raz Wael A. Sakr KM Wahidur Rahman 《PloS one》2013,8(1)
Herceptin failure is a major clinical problem in breast cancer. A subset of breast cancer patients with high HER-2/neu levels eventually experience metastatic disease progression when treated with Herceptin as a single agent. Mechanistic details of development of this aggressive disease are not clear. Therefore, there is a dire need to better understand the mechanisms by which drug resistance develops and to design new combined treatments that benefit patients with aggressive breast cancer and have minimal toxicity. We hypothesized that 3, 3′-diindolylmethane (DIM), a non-toxic agent can be combined with Herceptin to treat breast cancers with high levels of HER-2/neu. Here, we evaluated the effects of Herceptin alone and in combination with DIM on cell viability, apoptosis and clonogenic assays in SKBR3 (HER-2/neu-expressing) and MDA-MB-468 (HER-2/neu negative) breast cancer cells. We found that DIM could enhance the effectiveness of Herceptin by significantly reducing cell viability, which was associated with apoptosis-induction and significant inhibition of colony formation, compared with single agent treatment. These results were consistent with the down-regulation of Akt and NF-kB p65. Mechanistic investigations revealed a significant upregulation of miR-200 and reduction of FoxM1 expression in DIM and Herceptin-treated breast cancer cells. We, therefore, transfected cells with pre-miR-200 or silenced FoxM1 in these cells for understanding the molecular mechanism involved. These results provide experimental evidence, for the first time, that DIM plus Herceptin therapy could be translated to the clinic as a therapeutic modality to improve treatment outcome of patients with breast cancer, particularly for the patients whose tumors express high levels of HER-2/neu. 相似文献
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