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“A novel actinobacterium, strain S-1412(T), was isolated from a deep sediment sample, collected from the southern Black Sea coast of Turkey, and was examined using a polyphasic approach. The organism had chemical and morphological
features typical of the genus Streptomyces. The cell wall of the novel strain contained LL-diaminopimelic acid. Whole-ell hydrolysates contained galactose, glucose and traces of xylose. The polar lipid profile of S1412(T) consisted of the predominant compound diphosphatidylglycerol, moderate amounts of phosphatidylethanolamine and phosphatidylinositol, and minor amounts of phosphatidylglycerol. Strain S1412(T) exhibited an unusual quinone system, with the predominant compounds MK-10(H-8), MK-9(H-8) and MK-10(H-6) and small amounts of MK-9(H-6) and MK-10(H-4). Major fatty acids were iso-C-16:0, iso-C-16:1 H and anteiso-C-17:0.
The 16S rRNA gene sequence similarities for strain Histone Methyltransf inhibitor S1412(T) with respect to the most closely related type strains of species of the PP2 nmr genus Streptomyces were less than 97.0%. Phenotypic data clearly distinguished the isolate from its closest relatives, Streptomyces specialis GW 41-1564(T), Streptomyces mayteni YIM 60475(T), Streptomyces hainanensis YIM 47672(T), Streptomyces avicenniae MCCC1A01535(T) and Streptomyces sedi YIM 65188(T). Based on chemotaxonomic, phenotypic and genotypic characteristics, strain S1412T is considered to represent a novel species of the genus Streptomyces, for which the name Streptomyces hoynatensis sp. nov. is proposed. The type strain is S1412(T) Selleckchem Duvelisib (=KCTC 29097(T)=DSM 42069(T)).”
“In the present study, we investigated whether celecoxib could induce the expression of NKG2D ligands in clonogenic colon cancer cells, and increase their susceptibility to NK cell-mediated cell death. Celecoxib and its non-coxib analog, 2,5-dimethyl celecoxib, induced ULBP-1 and DR5 in both COX-2 negative HCT-15 cells and COX-2 positive HT-29 cells. Celecoxib increased their susceptibility to NK92 cells in both DELFIA assay and soft agar colony forming assay.
The inducibility of ULBP-1 and DR5 by celecoxib was not different between CD44- and CD44+ HCT-15 cells, and CD133- and CD133+ HT-29 cells. Celecoxib increased the susceptibility of highly clonogenic CD44+ HCT-15 and CD133+ HT-29 cells to NK92 cells, at least comparable to less clonogenic CD44- HCT-15 and CD133- HT-29 cells, respectively. In addition, celecoxib induced CHOP, and thapsigargin, an inducer of ER (endoplasmic reticulum) stress, induced DR5 but not ULBP1 in HCT-15. Taken together, these findings suggest that celecoxib induces the expression of ULBP-1 as well as DR5 in clonogenic colon cancer cells via COX-2 and ER stress-independent pathways, and increases their susceptibility to NK cells. (C) 2014 Elsevier Inc. All rights reserved.