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Friend erythroleukemia

Included among other differentiating cell lines which have been established in culture, is the human promyelocytic cell line HL-60, which differentiates into more mature myeloid cells upon treatment with retinoic acid and prostaglandin E] (PGEi). Friend erythroleukemia cells differentiate into hemoglobin-producing cells when treated with either dimethyl sulfoxide, or hexamethylene bis-acetamide. [Pg.467]

Riggs, M.G., Whittaker, R.G., Neumann, J.R. and Ingram, V.M. (1977) Butyrate causes histone modification in HeLa and Friend erythroleukemia cells. Nature, 268, 462-464. [Pg.217]

Sklar MD, Prochownik EV (1991) Modulation of cisplatinum resistance in friend erythroleukemia cells by c-myc. Cancer Res 51 2118-2123... [Pg.90]

Ginsberg BH, Chatterjee P, Yorek MA. Insulin sensitivity is increased in Friend erythroleukemia cells enriched in polyunsaturated fatty acid. Receptor 1991 1 155-166. [Pg.870]

Friend et al. [1] made the striking observation that dimethyl sulfoxide (DMSO)-treated Friend erythroleukemia cells (FEE) differentiate in vitro. Subsequently, a number of other chemicals, including butyric acid,hypoxanthine andhexamethylene bis-acetamide were shown to induce Friend cells [2], These inducers appear to remove a block in the differentiation process but the mechanisms involved are unknown. The finding that benzamide and nicotinamide induced Friend cells [3, 4] suggested that since both compounds were inhibitors of poly(ADP-ribose) polymerase, poly(ADP-ribosylation) may have a role in the differentiation process. Furthermore, since poly(ADP-ribose) polymerase requires DNA strand breaks for activity [5], these observations implicated DNA strand breaks in FEE differentiation. [Pg.446]

Pulito VL, Miller DL, Sassa S, Yamane T (1983) DNA fragments in Friend erythroleukemia cells induced by dimethyl sulfoxide. Proc Natl Acad Sci USA 80 5912-5915... [Pg.451]

NISHIOKA, Y. and SILVERSTEIN, S. Alterations in the protein synthetic apparatus of Friend erythroleukemia cells infected with vesicular stomatitis virus or Herpes simplex virus. [Pg.98]

Niacin Analogs That Induce Differentiation of Friend Erythroleukemia Cells are Able to Cause DNA Hypomethylation... [Pg.339]

Friend erythroleukemia cells (FELCs) are retroviras-transformed murine leukemia cells of the erythroid lineage, blocked in a relatively early stage of differentiation (1). These cells can be induced to differentiate into erythroid-like cells able to synthesize hemoglobin mRNA, heme, and hemoglobin (Hb) (2, 3). Nicotinamide (NAm), a potent inhibitor of poly(ADP-ribose) synthetase, has been shown to be a moderate inducer of FELCs differentiation (4). Other inhibitors of poly(ADP-ribose) synthetase were also found to be capable of inducing differentiation (5). These investigations hypothesized that the inhibition of poly(ADP-ribose) turnover was the primary biochemical mechanism leading to differentiation of FELCs by NAm and related compounds. [Pg.339]

The A -bromo-, chloro-, and fluoro-acetyl derivatives of 2-amino-2-deoxy-D-glucose and -o-galactose have been prepared and tested for cytotoxic activity the per-O-acetylated A -bromoacetyl derivatives in either the glucose or galactose series were most effective against Friend erythroleukemia cells. A -nictotinoyl derivatives of 2-amino-2-deoxy-D-glucose and its ethyl a- and j8-pyranoside have been prepared. ... [Pg.77]

The etiology of microcytic hypochromic anemias as a class can be ascribed to decreased hemoglobin synthesis. Al has been shown to inhibit hemoglobin synthesis in Friend erythroleukemia cells (Abreo et al. 1990) and in bone marrow cells (Zamen et al. 1992), where it also accumulates. In vitro studies evaluating incorporation of Fe " into heme have identified heme, rather than globin, synthesis as the inhibited pathway in uremia (Moriyama et al. 1975). The most common cause of a fault in heme synthesis leading to microcytic anemia is iron deficiency or lack of availability. Although Al-related anemia is refractory to Fe, the anemia could be caused by an interaction between Al and Fe metabolism. [Pg.148]

A report by Garg and Brown (1983) shows that retinoids can also promote differentiation of certain cell lines of Friend erythroleukemia cells, inducing cells to synthesize hemoglobin and to increase acetylcholinesterase activity analogous to the response of the cells to the classic inducer dimethyl sulfoxide. Not all Friend leukemic cell lines respond to retinoic acid (Breitman et al., 1980b Garg... [Pg.226]

Hill, T. M., Sinden, R. R., and Sadler, J. R., 1983, Herpes simplex virus types 1 and 2 induce shutoff of host protein synthesis by different mechanisms in Friend erythroleukemia cells, J. Virol. 45 241. [Pg.387]

Nishioka, Y., and Silverstein, S., 1978, Requirement of protein synthesis for the degradation of host mRNA in Friend erythroleukemia cells infected with HSV-1, J. Virol. 27 619. [Pg.388]

Dell Aquila, M.L., H.T. Nguyen, C.L. Herald, G.R. Pettit, and P.M. Blumberg Inhibition by Bryostatin 1 of the Phorbol Ester-induced Blockage of Differentiation in Hexamethylene Bisacetamide-treated Friend Erythroleukemia Cells. Cancer Res. 47, 6006 (1987). [Pg.193]


See other pages where Friend erythroleukemia is mentioned: [Pg.45]    [Pg.372]    [Pg.178]    [Pg.178]    [Pg.221]    [Pg.226]    [Pg.462]    [Pg.417]    [Pg.344]    [Pg.147]    [Pg.156]    [Pg.246]    [Pg.266]    [Pg.240]   
See also in sourсe #XX -- [ Pg.246 ]




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