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mezerein/leukemia

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Biological response modifiers released by a mezerein-treated human monocytic leukemia cell line, THP-1.

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After mezerein treatment of suspension cultures of the acute monocytic human leukemia cell line THP-1, cells became adherent to plastic culture surfaces, lost division potential, acquired Fc receptors, displayed phagocytic activity, and expressed increased nonspecific esterase staining. Serum-free

Secretion of interleukin-1 beta by a leukemia cell line in response to lipopolysaccharide and mezerein.

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The acute monocytic leukemia cell line, THP-1, is frequently used as a model to study the mechanism of cell-mediated immune response. The model is justified, in part, because THP-1 cells can be induced to express features of activated peripheral blood monocytes or tissue macrophages. The current

Stimulation of diploid fibroblast growth with serum-free medium conditioned by mezerein-treated monocytic leukemia cells.

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Medium conditioned by mezerein-treated human acute monocytic leukemia cells (THP-1) stimulated human fibroblast replication. Maximum mitogenic activity was elaborated by THP-1 cells with a 24-hr incubation in 10(-7) M mezerein (activator phase) followed by a 36-hr incubation in insulin-supplemented

Differential effects of various protein kinase C activators on protein phosphorylation in human acute myeloblastic leukemia cell line KG-1 and its phorbol ester-resistant subline KG-1a.

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Human myeloid leukemia KG-1 cells are induced to differentiate to macrophage-like cells by tumor-promoting phorbol esters, such as 12-O-tetradecanoylphorbol-13-acetate (TPA). Cells from the cloned subline, KG-1a, unlike the parental line, are resistant to the differentiating effect of TPA. In the

Modulation of protein kinase C activity and calcium-sensitive isoform expression in human myeloid leukemia cells by bryostatin 1: relationship to differentiation and ara-C-induced apoptosis.

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Previous studies have shown that pretreatment of human myeloid leukemia cells (HL-60) with the protein kinase C (PKC) activator bryostatin 1 potentiates ara-C-induced apoptosis. To test the hypothesis that this capacity stems from down-regulation of PKC activity and/or Ca2+-dependent (group-I; cPKC)

Characterization of inhibitory activities secreted by THP-1 leukemia cells and regulation by interferon-gamma.

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Cells of the monocytic leukemia line, THP-1, mimic several of the functional characteristics of activated monocytes and macrophages following incubation in the tumor promoting agent, mezerein. The current paper explores the nature of the factors in medium conditioned by THP-1 cells which inhibit

The production of interleukin 1 by a differentiating rat myelomonocytic leukemia line.

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We have succeeded in isolating a rat myelomonocytic leukemia cell line (c-WRT-7) that is capable of producing a factor with biological and biochemical properties similar to those ascribed to interleukin 1 (IL-1). Lipopolysaccharides (LPS), phorbol myristate acetate (PMA) and mezerein were found to

Synergistic induction of apoptosis in human leukemia cells (U937) exposed to bryostatin 1 and the proteasome inhibitor lactacystin involves dysregulation of the PKC/MAPK cascade.

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Cotreatment with a minimally toxic concentration of the protein kinase C (PKC) activator (and down-regulator) bryostatin 1 (BRY) induced a marked increase in mitochondrial dysfunction and apoptosis in U937 monocytic leukemia cells exposed to the proteasome inhibitor lactacystin (LC). This effect was

Differential effects of diacylglycerols and 12-O-tetradecanoylphorbol-13-acetate on protein phosphorylation and cell proliferation of tumor promoter-dependent leukemia cell line A65T.

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The growth of A65T cells, a mouse thymic leukemia cell line, was strictly dependent on the presence of tumor promoters, such as 12-O-tetradecanoylphorbol-13-acetate (TPA), teleocidin and mezerein. In the presence of the tumor promoters, A65T cells proliferated rapidly in a concentration-dependent

Effects of bryostatin 1 and other pharmacological activators of protein kinase C on 1-[beta-D-arabinofuranosyl]cytosine-induced apoptosis in HL-60 human promyelocytic leukemia cells.

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We have demonstrated previously that bryostatin 1, a macrocylic lactone with putative protein kinase C (PKC)-activating properties, synergistically augments the antileukemic actions of the deoxycytidine analog 1-[beta-D-arabinofuranosyl]cytosine (ara-C) in HL-60 human promyelocytic leukemia cells

Modulation of the expression of Bcl-2 and related proteins in human leukemia cells by protein kinase C activators: relationship to effects on 1-[beta-D-arabinofuranosyl]cytosine-induced apoptosis.

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We have previously reported that pretreatment of HL-60 human promyelocytic leukemia cells with the non-tumor-promoting protein kinase C (PKC) activator bryostatin 1 potentiates induction of apoptosis by the antimetabolite 1-[beta-D-arabinofuranosyl]cytosine (ara-C) (Biochem Pharmacol 47:839,1994).

Induction of differentiation in human promyelocytic HL-60 leukemia cells activates p21, WAF1/CIP1, expression in the absence of p53.

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The melanoma differentiation associated gene, mda-6, which is identical to the P53-inducible gene WAF1/CIP1, encodes an M(r) 21,000 protein (p21) that can directly inhibit cell growth by repressing cyclin dependent kinases. mda-6 was identified using subtraction hybridization by virtue of its

Specific induction of RGS16 (regulator of G-protein signalling 16) mRNA by protein kinase C in CEM leukaemia cells is mediated via tumour necrosis factor alpha in a calcium-sensitive manner.

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The RGS (regulator of G-protein signalling) proteins are GTPase-activating proteins for activated Galpha subunits. We investigated the effects of protein kinase C (PKC) on RGS proteins in various T cell lines by treating them with PMA. mRNA levels of both RGS16 and tumour necrosis factor alpha

In vitro effects of bryostatin 1 on the metabolism and cytotoxicity of 1-beta-D-arabinofuranosylcytosine in human leukemia cells.

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Bryostatin 1 is a macrocyclic lactone protein kinase C (PK-C) activator which has demonstrated promising antileukemic activity in preclinical studies. We have examined the effect of this agent on the metabolism and cytotoxicity of 1-beta-D-arabinofuranosylcytosine (ara-C) in both log phase and

Regulation by interferon gamma of function in the acute monocytic leukemia cell line, THP-1.

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THP-1 is an acute monocytic leukemia cell line which acquires phenotypic and functional monocytoid-like features following incubation with mezerein. The current study concerned the modulation of these features by rIFN gamma. rIFN gamma induces the time-dependent enhancement of HLA-DR expression in
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