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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three distinct Fc receptors for IgG, Fc gamma RI, Fc gamma RII and Fc gamma RIII are known to be associated with human myeloid cells. Using mAb specific for these receptors, and the hydridoma cells lines that produce these mAb, we have examined the ability of each of these receptors on different myeloid cells and cell lines to mediate killing of tumor and red cell targets. Hybridoma cells (HC) expressing anti-Fc gamma RI, Fc gamma RII or Fc gamma RIII upon their surface were used as model self-directed tumor targets. Chicken erythrocytes (CE) were used as another type of target cell and in this case effector cell cytotoxicity was mediated by heteroantibodies (HA) composed of Fab fragments of anti-Fc gamma R mAb covalently linked to Fab fragments of rabbit anti-CE antibodies. Monocytes, lymphocytes, polymorphonuclear cells (PMNs) and the myeloid cell lines U937, HL-60 and THP-1 were used as effector cells either in their native state or after activation with rIFN-gamma. Direct comparison of cytotoxicity by the same effector cell population against both tumor and erythroid targets has permitted definitive evaluation of the ability of the different Fc gamma R to promote cytolysis under two different conditions. Monocytes were able to utilize Fc gamma RI, Fc gamma RII and Fc gamma RIII in killing both CE and HC targets, and incubation with rIFN-gamma augmented their ability to kill CE, particularly through Fc gamma RI. Fc gamma RII and Fc gamma RIII mediated killing of CE by untreated neutrophils. rIFN-gamma induced PMNs to express Fc gamma RI and to mediate killing of CE through this receptor. Moreover, HC targets were not lyzed by untreated neutrophils, but rIFN-gamma activated neutrophils killed HC bearing surface anti-Fc gamma RI and anti-Fc gamma RII, but not anti-Fc gamma RIII. Myeloid cell lines HL-60 and U937 were unable to perform cytotoxicity without prior culture with rIFN-gamma, following which they killed CE through Fc gamma RI and Fc gamma RII, but were still incapable of HC lysis. THP-1, another myeloid cell line, was cytotoxic to CE through Fc gamma RI and Fc gamma RII without activation. Following rIFN-gamma treatment, cytotoxicity through these two Fc gamma R increased and was also mediated by Fc gamma RIII but these cells were still unable to kill HC.(ABSTRACT TRUNCATED AT 400 WORDS)
Mol Immunol 1989 Oct
PMID:The functional properties of Fc gamma RI, II and III on myeloid cells: a comparative study of killing of erythrocytes and tumor cells mediated through the different Fc receptors. 253 42

Transcription of the low-density lipoprotein receptor (LDL-R) gene in the human monocytic leukemic cell line THP-1 and in the human hepatocarcinoma cell line Hep-G2 is regulated by second messengers of the diacylglycerol-protein kinase C (DAG-PKC), inositol 1,4,5-triphosphate-Ca2+, and cyclic AMP pathways. Exogenous phospholipase C (which releases DAG and inositol 1,4,5-triphosphate), PKC activators (phorbol esters and DAG), Ca2+ ionophores, and a cyclic AMP analog all transiently induced accumulation of LDL-R mRNA. The effects of these three signal-transducing pathways were to a large extent additive. Furthermore, PKC stimulation effected an increase in LDL binding, which suggested that the increase in LDL-R mRNA resulted in an increase in functional cell surface receptor activity. These results suggest that uptake of cholesterol by these cells is under control of both intracellular cholesterol levels and external signals.
Mol Cell Biol 1989 Jun
PMID:Involvement of second messengers in regulation of the low-density lipoprotein receptor gene. 254 77

Exposure to carbon monoxide (CO) during the fetal and neonatal period was used to evaluate cardiac ventricular regional weight and myocyte growth response to an increased hemodynamic load. Date-mated Sprague-Dawley rats inhaled 200 ppm CO from day 7 of pregnancy until parturition; another group of pregnant rats inhaled room air. At birth, pups from these two groups were subdivided into four groups: (1) control group (AIR/AIR), that was maintained in room air in utero and post-partum; (2) AIR/CO group, which received CO only after birth; (3) CO/CO group, which received CO exposure in utero and post-partum; and (4) CO/AIR group, which received CO exposure in utero but was maintained in room air post-partum. Rats were removed from litters at selected intervals from birth to 28 days of age and used to determine regional ventricular weights and ventricular dry weights, and to obtain isolated myocyte preparations for measurement of cell size characteristics and allow calculation of cell numbers. Compared with AIR raised control animals, right ventricular weight was increased in animals exposed to CO during the fetal period. Post-natal CO exposure caused an increase in left ventricular weight. Heart weight to body weight ratio of animals exposed to CO post-natally only (AIR/CO) gradually increased to reach that of the CO/CO group by 12 days of age, while animals exposed to AIR post-natally following fetal CO exposure gradually decreased their heart weight to body weight ratio toward that of the control animals by 28 days of age. Binucleated cells first appeared at 4 days of age in all groups. Myocyte volume was similar in both groups at birth and increased from six through 28 days of age. Left ventricle plus septum and right ventricle cell volumes of the CO/CO group were smaller than the controls at 28 days of age in spite of heavier wet and dry weights in the CO-exposed rats. At birth, the CO-exposed animals had more myocytes in the RV compared to AIR-exposed controls. Carbon monoxide exposure after birth resulted in left ventricular myocyte hyperplasia. The results of this study indicate that increased hemodynamic load due to CO exposure during the fetal period results in cardiomegaly because of increased myocyte hyperplasia. This cellular response is sustained through the early neonatal period in animals exposed to CO both in utero and post-partum.
J Mol Cell Cardiol 1986 May
PMID:Cardiomegaly due to myocyte hyperplasia in perinatal rats exposed to 200 ppm carbon monoxide. 294 90

The ret transforming gene was activated by recombination between two unlinked segments of human DNA, most likely during transfection of NIH 3T3 cells. To further define this transforming gene, we isolated and sequenced ret cDNA clones. The nucleotide sequence indicates that the active ret transforming gene encodes a fusion protein with a carboxy-terminal domain which is 40 to 50% homologous to members of the tyrosine kinase gene family. This tyrosine kinase domain is preceded by a hydrophobic sequence characteristic of a transmembrane domain. Transcription of the ret tyrosine kinase sequence was detected in the SK-N-SH neuroblastoma, HL-60 promyelocytic leukemia, and THP-1 monocytic leukemia cell lines, but not in 25 other human tumor cell lines surveyed. The ret tyrosine kinase may thus represent a cell surface receptor which is expressed in a restricted range of human cells.
Mol Cell Biol 1987 Apr
PMID:ret transforming gene encodes a fusion protein homologous to tyrosine kinases. 303 15

The possibility of genetic identification of mutations in asporogenic yeast by the technique of intrageneric fusion of yeast protoplasts of Candida tropicals and Saccharomyces cerevisiae has been demonstrated for Candida tropicals strains G5-9 (Ade- Leu-) and G32-4 (Leu-). The mutations to auxotrophy ade- in the strain G5-9 and leu- in G32-4 of Candida tropicals are allelic to ade2 and leu1 mutations in the genes of Saccharomyces cerevisiae yeast. The allelic character of adenine auxotrophy mutation in Candida tropicals and ade2 mutation in Saccharomyces cerevisiae is confirmed by the absence of AIR-carboxylase activity in cellular extract from the strain G5-9.
Mol Gen Mikrobiol Virusol 1988 Jan
PMID:[Identification of mutations in the asporogenic yeast Candida tropicalis using intrageneric fusion of protoplasts]. 328 58

We have adapted a human monocytic leukemia cell line [THP-1c12(+)] so that it can proliferate in a completely protein-free chemically defined medium of an equal mixture of Dulbecco's modified Eagle's minimum essential medium and Ham's F12. This cell line was designated as THP-1c12(-). When a sufficient number of THP-1c12(-) cells was seeded in culture, the maximum cell density after 6 days of culture was 1 X 10(6)/ml with a doubling time of 30 hr. Transferrin showed a slight stimulative effect on the growth of THP-1c12(-) cells, but insulin did not. The surface profile of THP-1c12(-) was the same as that of THP-1c12(+), which possessed Mol. Mo5, LeuM3, My9 and Ia-like antigens as well as a large number of Fc receptors. Phagocytic ability with respect to IgG-coated sheep red blood cells was evident in both THP-1c12(+) and THP-1c12(-) cells. A small percentage of THP-1c12(-) cells retained the ability to reduce nitroblue tetrazolium when stimulated with 12-tetradecanoyl-phorbol-13-acetate. Culture supernatant from THP-1c12(-) stimulated the incorporation of 3H-thymidine into its own cells, suggesting an autocrine mechanism by which the growth of THP-1c12(-) cells is induced in a protein-free medium.
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PMID:Adaptation of a human monocytic leukemia cell line (THP-1) in a protein-free chemically defined medium. 355 Nov 91

A novel cultured cell line, P31/Fujioka, of monocytoid nature was established from leukemic cells in the peripheral blood of a seven-year-old boy with acute monoblastic leukemia. The P31/Fujioka cells have abundant cytoplasm, an indented nucleus of monocytoid appearance, pseudopods detectable by electron microscopy and alpha-naphthyl butyrate esterase activity which is completely inhibited by NaF, but they have no peroxidase activity. Immunologically, the P31/Fujioka cells possess Fc gamma-receptor and phagocytic activity towards sensitized erythrocytes (oxEAIgG), and are reactive with various monoclonal antibodies such as OKM1, anti-Mol, FMC10, FMC12 and OKI1. Chromosome analysis revealed the presence of marker chromosome 11q--due to Nos. 7; 11 translocation and No. 9 pericentric inversion. These findings indicate that the P31/Fujioka cells are derived from the patient's monoblastic leukemia cells and show a more distinct monocyte antigen than other known monocytoid cultured cell lines, U-937 and THP-1. The absence of Epstein-Barr virus nuclear antigen of this line was confirmed.
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PMID:A novel monocytoid cultured cell line, P31/Fujioka, derived from acute monoblastic leukemia. 696 83

Aromatase cytochrome P450 mRNA and activity was strongly expressed in THP 1 myeloid leukaemia cells after treatment with phorbol-myristate-acetate (PMA) and dexamethasone, low level expression was caused by calcitriol. mRNA species of 4.0, 3.0, 2.4 and 1.1 kb size were differentially stimulated. After calcitriol-mediated differentiation (72 h, measured by CD 14 expression) mRNA expression was further enhanced by PMA (45-fold), dexamethasone (15-fold), oestradiol (3.7-fold), testosterone (2.5-fold) and androstenedione (3.5-fold). Forskolin, cAMP and follicle stimulating hormone had no stimulatory effect. Oestradiol formation from testosterone (oestradiol radioimmunoassay in culture supernatants) increased to > 2000 pg/ml/10(6) cells/24 h after PMA-stimulation, mirrored mRNA expression and was suppressed below 10% of original values in the presence of 4-OH-androstenedione. Exons I.2 and I.4 were expressed in PMA-stimulated cells only, exon I.3 in both PMA- and dexamethasone-stimulated cells. A new splicing variant was expressed after calcitriol-stimulation, which did not hybridize to an exon II-derived oligonucleotide but to an exon III-derived one. Local aromatisation of androgens into oestradiol may be important in the concerted crosstalk of cells of the monocyte/macrophage lineage with their respective tissues in inflammation and bone metabolism.
Mol Cell Endocrinol 1995 Apr 28
PMID:Expression and regulation of aromatase cytochrome P450 in THP 1 human myeloid leukaemia cells. 754 22

Glutathione (GSH) depletion in mitogen-stimulated T lymphocytes has been shown to markedly inhibit their proliferative response. This block in proliferation is associated with a significant reduction in total RNA and DNA synthesis; however, the specific mechanism involved in this inhibition of proliferation is unknown. Miller et al. have reported that lowering intracellular GSH levels by greater than 30%, in murine and human tumor cell lines of non-hematopoietic origin, leads to down-regulation of HA-, Ki- and N-ras oncogene expression [Miller. A.C., Gafner, J., Clark, E.P. and Samid, D. (1993) Mol. Cell Biol., 13, 4416-4422]. The reduction in ras transcript levels correlated with the extent of GSH depletion and was independent of the specific mode of oncogene activation. Since the activity of p21(ras) is thought to be involved in pathways of T cell activation, we set out to determine whether down-regulation of ras expression in T cells could be the mechanism by which T cell proliferation was inhibited in GSH-depleted T lymphocytes. Despite reducing the GSH level of concanavalin A-activated human peripheral blood mononuclear cells by 66%, no effect on ras mRNA expression was observed. Similarly, no reduction of ras transcript levels were detected in a human T cell line (Jurkat) or in a human monocytic cell line (THP-1) depleted of glutathione. Our results demonstrate that the mechanism by which GSH depletion inhibits T cell proliferation does not appear to involve a decrease in ras mRNA expression. In addition, our results suggest that differences in the regulation of ras mRNA expression may exist between lymphoid/monocytic cells of non-hematopoietic origin.
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PMID:N-ras mRNA expression is unaffected in glutathione-depleted cells of hematopoietic origin. 765 16

The cytokines interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF-alpha) are released by mononuclear phagocytes in vitro after stimulation with mycobacteria and are considered to mediate pathophysiologic events, including granuloma formation and systemic symptoms. We demonstrated that the Mycobacterium tuberculosis cell wall component lipoarabinomannan (LAM) is a very potent inducer of IL-1 beta gene expression in human monocytes and investigated the mechanism of this effect. We localized the LAM-, lipopolysaccharide (LPS)-, and TNF-alpha-inducible promoter activity to a -131/+15 (positions -131 to +15) DNA fragment of the IL-1 beta gene by deletion analysis and chloramphenicol acetyltransferase assay. Within this DNA fragment, there were two novel 9-bp motifs (-90/-82 and -40/-32) with high homology to the nuclear factor-IL6 (NF-IL6) binding site. Site-directed mutagenesis demonstrated that the two NF-IL-6 motifs could be independently activated by LAM, LPS, or TNF-alpha and that they acted in an orientation-independent manner. DNA mobility shift assay revealed specific binding of nuclear protein(s) from LAM-, LPS-, or TNF-alpha-stimulated THP-1 cells to the NF-IL6 motifs. We conclude that the two NF-IL6 sites mediate induction of IL-1 beta in response to the stimuli LAM, LPS, and TNF-alpha.
Mol Cell Biol 1993 Jun
PMID:Regulation of the interleukin-1 beta (IL-1 beta) gene by mycobacterial components and lipopolysaccharide is mediated by two nuclear factor-IL6 motifs. 768 3


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