Topic
Friend leukemia
About: Friend leukemia is a research topic. Over the lifetime, 319 publications have been published within this topic receiving 7463 citations.
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TL;DR: The findings support the concept that cellular division and, thereby the production of new cellular types are not required for gene activation and the expression of an erythroid phenotype and suggest plasma membrane-cytoskeleton involvement in the initiation of the erystroid maturation process in this system.
Abstract: Friend erythroleukemia cells grown in culture and induced to differentiate along the erythroid developmental pathway by dimethyl sulfoxide (DMSO) were used as a model system to investigate the requirement for cellular replication to express a differentiated erythroid phenotype. That cytokinesis is not essential for DMSO-induced erythroid differentiation as measured by the synthesis and accumulation of hemoglobin was shown by experiments using cytochalasin B. In these studies, hemoglobin was found to accumulate in Friend cells treated simultaneously with DMSO and cytochalasin B; such treatment caused cells to become enlarged and multinucleated due to inhibition of cytokinesis by cytochalasin B. In contrast, exposure of cells to cytochalasin B for at least 48 hr prior to DMSO caused significant inhibition of erythroid differentiation. The findings support the concept that cellular division and, thereby the production of new cellular types are not required for gene activation and the expression of an erythroid phenotype. These effects of cytochalasin B on DMSO-induced differentiation of Friend leukemia cells also suggest plasma membrane-cytoskeleton involvement in the initiation of the erythroid maturation process in this system.
13 citations
TL;DR: Observations support the theory that the concentrations of specific transfer RNA's are regulated by a mechanism that is sensitive to the extent of their aminoacylation.
Abstract: Friend leukemia cells incubated with sublethal concentrations of histidinol for 5 to 6 days show up to twofold increases in their relative concentrations of histidine transfer RNA and no change in the relative concentrations of leucine transfer RNA. A similar effect is seen when cells are grown to stationary phase in the presence of 0.2 times the amount of histidine in Eagle's minimum essential medium. These observations support the theory that the concentrations of specific transfer RNA's are regulated by a mechanism that is sensitive to the extent of their aminoacylation.
12 citations
TL;DR: Results demonstrated that at early stages of TNF‐induced inhibition of tumor growth (a) phospholipid catabolism was significantly enhanced; (b) morphological changes were apparently correlated with alterations in the levels of phosphatidylcholine and its catabolic products.
12 citations
TL;DR: It is found that Friend leukemia cells treated with histidinol show no significant changes in GTP or ATP pool sizes, although this treatment does produce the expected inhibition of rRNA and tRNA synthesis.
Abstract: Histidinol is known to cause deacylation of histidyl-tRNA in cultured mammalian cells, thereby producing a functional deprivation of histidine. Such deprivation of an essential amino acid is known to produce various effects, including inhibition of tRNA synthesis and of nucleolar RNA synthesis and processing. It has been proposed [Grummt, F. & Grummt, I. (1976) Eur. J. Biochem. 64, 307-312] that this response to amino acid deprivation is mediated by decreases in GTP and ATP pool sizes caused by a deacylated-tRNA-dependent hydrolysis of GTP. In contrast, we find that Friend leukemia cells treated with histidinol show no significant changes in GTP or ATP pool sizes, although this treatment does produce the expected inhibition of rRNA and tRNA synthesis.
12 citations
01 Jan 2016
TL;DR: In this article, the authors studied SFFV production in somatic cell hybrids made between Friend leukemia cells (FLC) and cells expressing various differ-entiation programs, and found that all FLC lines except those that do not incorporate BrdUrd are unchanged in hybrids that maintain the expression of erythroid differentiation.
Abstract: All Friend cells-except thymidine kinase (ATP:thymidine 5'-phosphotransferase, EC 2.7.1.21)-deficient mutants-are highly inducible for the release of biologically active spleen focus-forming virus (SFFV) after exposure to BrdUrd. We studied SFFV production in somatic cell hybrids made between Friend leukemia cells (FLC) and cells expressing various differ- entiation programs. High inducibility of SFFV and release of.con- stitutive Friend virus (FV) and SFFV are eliminated in all hybrids in which the potential for erythroid differentiation is suppressed. FV release and its induction by BrdUrd are unchanged in hybrids that maintain the expression of erythroid differentiation. Friend virus (FV)-transformed Friend leukemia cells (FLC) grow in culture and differentiate to cells that synthesize hemo- globin on exposure to dimethyl sulfoxide (Me2SO) (1, 2). Some but not all of these cell lines, release type C virus (3, 4). How- ever, all FLC lines except those that do not incorporate BrdUrd (3), whether derived through transformation with the polycy- themia-producing strain of FV (FVP) (3) or the anemia-produc- ing strain of FV (FVA) (this paper), are highly inducible for spleen focus-forming virus (SFFV) release. The inducibility is several orders of magnitude above that observed for endoge- nous virus induction in normal murine fibroblastic cell lines (5). The property of superinduction could be related to a general property such as the transformed state of a cell or could be as- sociated specifically with a particular type of differentiated cell. To distinguish between these alternatives, we tested cell hy- brids between FLC and cells of hematopoietic and nonhema- topoietic origin (6-9).
12 citations