Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Based on homology with the mouse interleukin 4 (IL-4) cDNA that expresses B cell, T cell, and mast cell stimulating activities (Lee, F. et al., (1986) Proc. Natl. Acad. Sci. USA 83, 2061), we have isolated from a Balb/c mouse liver DNA library the mouse chromosomal gene and analyzed its overall structure. The gene occurs as a single copy in the haploid genome and contains four exons and three introns. The exon sequences almost completely match the cloned cDNA sequence. Interestingly, there is a fairly high degree of homology between mouse IL-4 and mouse IL-2 genes extending more than 200 bp upstream of a "TATA" like sequence located 20 bp upstream of the transcription initiation site. These sequences may play an important role in the regulated expression of this gene in concanavalin A or antigen-stimulated T lymphocytes. The supernatant of COS7 cells transfected with plasmid DNA containing the entire gene exhibited both T cell growth factor and mast cell growth factor activities.
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PMID:Structural analysis of the mouse chromosomal gene encoding interleukin 4 which expresses B cell, T cell and mast cell stimulating activities. 302 76

The human epidermal growth factor-receptor (EGF-R) was introduced into primary mouse bone marrow cells (BMC), utilizing retrovirus mediated gene transfer. Cultivation of infected BMC in the presence of interleukin-3 (IL-3) led to the outgrowth of IL-3 dependent myeloid cells, which efficiently expressed functional EGF-R, exhibiting its two characteristic affinity states. EGF acts on these cells synergistically with IL-3 in stimulating DNA synthesis and cell proliferation even under IL-3 saturation conditions. However, EGF was not sufficient to replace the requirement for IL-3. In contrast, EGF was able to maintain proliferation of a factor-dependent hemopoietic cell line (FDC-P1) infected with the EGF-R retrovirus in the absence of IL-3, but these cells did not respond to EGF in the presence of IL-3. No influence of EGF on IL-3 induced mast cell differentiation of BMC expressing the EGF-R could be observed by histological criteria. These data show that the expression of EGF-R alone is not sufficient to induce or maintain cell proliferation in IL-3 dependent bone marrow derived cells, although it can do so in established hemopoietic cell lines.
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PMID:Expression of functional human EGF receptor on murine bone marrow cells. 305 64

A cDNA sequence coding for a unique mouse interleukin that expresses B-cell-, T-cell, and mast-cell-stimulating activities has been isolated from a mouse helper T-cell cDNA library. The library, constructed in the pcD expression vector, was screened by transfecting COS monkey cells with DNA pools to express the products encoded by full-length cDNA inserts. By assaying the transfected cell supernatants, we identified clones encoding a factor that stimulates T-cell and mast cell lines. This factor also induces Ia expression on resting B cells and enhances IgG1 and IgE production by B cells, two properties of B-cell-stimulatory factor 1. The DNA sequence codes for a polypeptide of 140 amino acid residues including a putative signal peptide. These results demonstrate that a single cDNA clone distinct from interleukin 2 and interleukin 3 encodes a polypeptide with multiple biological activities.
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PMID:Isolation and characterization of a mouse interleukin cDNA clone that expresses B-cell stimulatory factor 1 activities and T-cell- and mast-cell-stimulating activities. 308 12

Interleukin 3 (IL-3) is a regulatory glycoprotein required for the proliferation and differentiation of cells from many if not all hemopoietic lineages. With the emergence of the competence-progression model of cell proliferation, which predicts that growth factors function at specific stages of the cell cycle, we examined the possibility that IL-3 functions at a specific stage of the cell cycle. C-63 cells were developed as a cell line from normal murine bone marrow. They have a mast cell phenotype and require pokeweed-stimulated spleen cell-conditioned medium (CM), a rich source of IL-3, for their continued growth. Exponentially growing cells were transferred from growth medium, which contains CM, to medium lacking CM or IL-3. After 24 hours, cell viability had decreased 40-50%. The remaining viable cells did not incorporate 3H-thymidine, and displayed a single peak at G1 in a DNA histogram. Restimulation of these cells with CM or IL-3 resulted in a dramatic rise in 3H-thymidine uptake 20-24 hours after restimulation. DNA histograms of restimulated cultures indicated that the cells were progressing in a wave-like fashion throughout the remainder of the cell cycle. The length of time necessary for cells to be in contact with CM or IL-3 before they could progress into the remainder of the cell cycle was also examined. Cells incubated with CM or IL-3 for less than 16 hours could not progress into S phase, whereas cells incubated for 16 hours or longer could progress into S phase and through the remainder of the cell cycle. These data suggest that IL-3 exerts its function at a specific stage of the cell cycle.
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PMID:Interleukin 3 and cell cycle progression. 308 27

B-cell stimulatory factor-1 (BSF-1) is a T-cell product of relative molecular mass 20,000 (Mr, 20K) initially described as a cofactor required for DNA synthesis by resting mouse B cells stimulated with low concentrations of anti-IgM antibodies. It acts on resting B cells to enhance the expression of class II major histocompatibility complex (MHC) molecules, to prepare these cells to respond more promptly to subsequent stimuli, such as anti-IgM antibodies, and causes the secretion of IgG1 and IgE by B cells stimulated with lipopolysaccharide (LPS). BSF-1 has been shown to stimulate T cell lines, resting T cells and some mast cell lines. Recently, the designation interleukin-4 (IL-4) has been suggested for BSF-1. We report here the existence of high-affinity cell-surface receptors specific for BSF-1 on both B and T lymphocytes, and on cells of several other haematopoietic lineages, including mast cell, macrophage and undifferentiated haematopoietic cell lines. Resting B and T lymphocytes express receptors, which increase in number upon activation of B cells with LPS or anti-IgM, and of T cells with concanavalin A. Cross-linking of 125I-labelled-BSF-1 to its receptors creates a complex of Mr approximately 80,000.
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PMID:Receptors for B-cell stimulatory factor-1 expressed on cells of haematopoietic lineage. 310 Sep 61

The effects of polymethylmethacrylate (PMMA) exposure upon macrophage viability and function were studied in an attempt to determine what role these cells play in the loosening of cemented arthroplasties. P388D1 murine macrophage cell line was exposed to PMMA and polystyrene particles of similar size and concentration. DNA synthesis following exposure to PMMA or polystyrene was studied by [3H]thymidine incorporation. Macrophage function was studied by analyzing the ability of activated macrophages to kill mast cell targets following particle exposure. Our results demonstrate that exposure of macrophages to PMMA particles in vitro inhibits DNA synthesis and impairs their cytotoxic ability. Histologic examination revealed that macrophages phagocytose both PMMA and styrene particles, but the former eventually lyse these cells. Our studies suggest that the histologic appearance of macrophages and foreign body giant cells at the bone-cement interface may be secondary to a repetitive cycle of PMMA particle phagocytosis and cell death, similar to that found in a foreign body granulomatous response.
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PMID:Effects of polymethylmethacrylate exposure upon macrophages. 317 62

The effect of cultured bone marrow cell supernatant (BMS) was studied on the proliferative response of cells of the transformed murine epidermal cell line Pam 212. Elevated DNA synthesis was found in Pam 212 cells cultured with BMS from bone marrow cells grown in spleen cell conditioned medium with concanavalin A (ConA). Pam cell proliferative activity was related to the histamine content in the culture supernatant. Neither spleen cell conditioned medium with IL1, IL2, or IL3 activity, nor ConA alone, showed any effect on Pam cell growth. A soluble mediator from the cultured bone marrow cells with mast cell characteristics was thought to be responsible for the stimulation of Pam cell growth, and Con A appeared to be a prerequisite for generation of this factor by the bone marrow cells.
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PMID:Lymphokine mediated production of an epidermal cell proliferation factor by cultured murine bone marrow cells. 350 9

We have isolated, cloned, and characterized cDNA and genomic DNA corresponding to the mRNA and gene for the rat mast cell protease, RMCP II. The amino acid sequence deduced from the cDNA provides evidence that this protease is synthesized as a precursor, with a signal peptide and additional residues at the N and C termini. RNA homologous to the cDNA is expressed only in mast cells. Analysis of RNA from the two subclasses of mast cell, mucosal and serosal, indicates subclass specific expression of the different proteases found in each of these two subclasses. S1 protection analysis and the sequence of the genomic clone indicate that the serosal mast cell protease, RMCP I, is likely to be coded for by a separate, highly homologous gene. A comparison of the exon/intron structure of the RMCP II gene with genes of related serine proteases further indicates that RMCP II is a member of a family of proteases distinct from those found in the pancreas. We have also isolated a third gene, highly homologous to RMCP II but different from it and from the gene for RMCP I. Analysis of the 5' transcriptional control region of both genes showed striking homology to the TATA box and enhancer regions of the pancreatic proteases.
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PMID:Cloning of the mast cell protease, RMCP II. Evidence for cell-specific expression and a multi-gene family. 354 19

A single intraperitoneal injection of Compound 48/80 in rats causes mast cell activation which is followed by a proliferation in fibroblasts and mesothelial cells in the mesentery. The same is true of organ-cultured rat mesentery, but in cultured guinea-pig mesentery Compound 48/80 has no morphological effects on mast cells and does not induce proliferation. The relationship between mast-cell secretion and cell proliferation in surrounding cells was studied further in the investigation now presented. Proliferation was estimated (a) by cytophotometric Feulgen DNA measurements in individual fibroblast and mesothelial cell nuclei; (b) by measurements of incorporation of 3H-TdR into DNA; (c) and by estimation of mitotic frequency. Mast-cell secretion was studied morphologically and by biochemical quantitation of histamine release. Compound 48/80 is a potent mast cell activator in the rat, stimulating mast cells to secretion. The results of this study suggest that Polymyxin B, another powerful mast-cell activator, apparently chemically unrelated to Compound 48/80, also stimulates the mesenterial cells to proliferation in the rat. In the guinea-pig Compound 48/80 does not induce mast-cell secretion or proliferation in fibroblasts and mesothelial cells in the mesentery. The results give further evidence that the cell proliferation induced by Compound 48/80 and Polymyxin B in rat mesentery is causally related to mast-cell secretion.
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PMID:Further studies on the relationship between drug-induced mast-cell secretion and local cell proliferation. 616 43

The proliferation of rat peritoneal mast cells was examined under normal conditions in vivo. DNA content of individual mast cells was measured by cytofluorometry after staining with the bibenzimidazole dye Hoechst 33258. Diploid non mast cells from each rat were used as a biological standard, which resulted in small long-term variations in the method. The proportion of mast cells in the S + G2 region of the DNA distribution was about 4% for young rats (24 days old, body-weights about 60 g). It decreased in relation to body-weight, and was less than 1% for 105-day-old rats weighing 400 g. During the same growth period the total number of mast cells in the peritoneal cavity increased about 8-fold. The total number of proliferating cells, about 30,000, remained constant throughout the observation period. No evidence of polyploidization or accumulation in G2 of mast cell nuclei was found. It is concluded that peritoneal mast cells increase in number by mitotic proliferation of differentiated cells.
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PMID:DNA distribution of mast cell populations in growing rats. 616 37


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