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Results: 941 to 948 of 948

Publication Record


Mechanisms of oncogene cooperation: activation and inactivation of a growth antagonist.
Ragozzino MM, Kuo A, DeGregori J, Kohl N, Ruley HE
(1991) Environ Health Perspect 93: 97-103
MeSH Terms: Adenovirus Early Proteins, Animals, Antigens, Polyomavirus Transforming, Cell Line, Cell Line, Transformed, Cell Transformation, Neoplastic, Cricetinae, Epistasis, Genetic, Fibroblasts, Gene Expression Regulation, Neoplastic, Genes, Retinoblastoma, Genes, ras, Genetic Complementation Test, Hybrid Cells, Mesocricetus, Mice, Mice, Nude, Neoplasms, Experimental, Oncogene Proteins, Viral, Oncogenes, Phenotype, Platelet-Derived Growth Factor, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-sis, Proto-Oncogene Proteins p21(ras), Rats
Show Abstract · Added May 29, 2014
Gene transfer experiments have defined limitations with regard to the ability of individual oncogenes to transform cultured cells to a tumorigenic state. The stable transformation of REF52 cells by either the ras or sis oncogenes requires the continuous expression of a second collaborating oncogene, such as adenovirus-5 E1A or SV40 large T-antigen. Our studies suggest that the function of the nuclear collaborators is to antagonize dominant growth controls which limit the ability of REF52 cells to proliferate in response to mitogenic stimuli.
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26 MeSH Terms
Natural killer cells activated by interleukin 2 treatment in vivo respond to interleukin 2 primarily through the p75 receptor and maintain the p55 (TAC) negative phenotype.
Weil-Hillman G, Voss SD, Fisch P, Schell K, Hank JA, Sosman JA, Sugamura K, Sondel PM
(1990) Cancer Res 50: 2683-91
MeSH Terms: Antibodies, Monoclonal, Antigens, Differentiation, T-Lymphocyte, CD3 Complex, CD56 Antigen, Dose-Response Relationship, Drug, Humans, Interleukin-2, Killer Cells, Lymphokine-Activated, Lymphocyte Activation, Phenotype, Receptors, Antigen, T-Cell, Receptors, Interleukin-2
Show Abstract · Added March 5, 2014
Interleukin 2 (IL-2) induced activation of unstimulated resting natural killer (NK) cells or resting T-cells initially occurs following binding of IL-2 through the p75 receptor that is expressed primarily by these cells. However, this IL-2/p75 interaction induces TAC chain synthesis and formation of high affinity IL-2 receptor required for the proliferation of resting peripheral blood lymphocytes. In this study, we present data indicating that NK cells activated by in vivo IL-2 treatment, in contrast to resting NK cells, respond and proliferate to further IL-2 in vitro using primarily the p75 receptor with only a minor component of cells responding through the high affinity receptor. These in vivo activated NK cells minimally expressed the TAC chain and maintained this TAC negative phenotype while proliferating in response to IL-2. The primary involvement of the p75 receptor in the proliferative response of these cells to IL-2 was demonstrated by the need for concentrations of IL-2 higher than 44 pM to obtain a significant response and by the dramatic inhibition of this response by anti-p75 monoclonal antibody. Anti-TAC monoclonal antibody inhibited only the poor proliferation obtained at low doses of IL-2 suggesting a minor role for TAC and high affinity IL-2 receptors. This was in contrast to the partial inhibition of proliferation by anti-p75 or anti-TAC observed in unstimulated pretherapy peripheral blood lymphocytes suggesting that these cells respond to IL-2 through both high affinity receptors and intermediate affinity p75 receptors. The T-cells isolated from in vivo activated peripheral blood lymphocytes, despite expressing TAC, were not responsive to IL-2, suggesting that these cells express predominantly nonfunctional low affinity TAC receptors. NK cells activated by IL-2 in vivo represent a unique model system of IL-2 dependent cells that respond and proliferate to IL-2 essentially through the p75 IL-2 receptor.
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12 MeSH Terms
Type 1 fimbriation and fimE mutants of Escherichia coli K-12.
Blomfield IC, McClain MS, Princ JA, Calie PJ, Eisenstein BI
(1991) J Bacteriol 173: 5298-307
MeSH Terms: Alleles, Blotting, Southern, DNA, Bacterial, Enzyme-Linked Immunosorbent Assay, Escherichia coli, Fimbriae, Bacterial, Genotype, Mutation, Phenotype, Plasmids, Restriction Mapping
Show Abstract · Added May 20, 2014
We reexamined the influence of fimE, also referred to as hyp, on type 1 fimbriation in Escherichia coli K-12. We found that one strain used previously and extensively in the analysis of type 1 fimbriation, strain CSH50, is in fact a fimE mutant; the fimE gene of CSH50 contains a copy of the insertion sequence IS1. Using a recently described allelic exchange procedure, we transferred the fimE::IS1 allele from CSH50 to our present wild-type strain, MG1655. Characterization of this IS1-containing strain (AAEC137), together with another fimE mutant of MG1655 (AAEC143), led to two conclusions about the role of fimE. First, the formation of phase variant colony types, reported widely in strains of E. coli, depends on mutation of fimE, at least in K-12 strain MG1655. Here we showed that this phenomenon reflects the ability of fimE to stimulate the rapid inversion of the fim invertible element from on to off when the bacteria are grown on agar. Second, our analysis of fimE mutants, which is limited to chromosomal constructs, provided no evidence that they are hyperfimbriate. We believe that these results, which are at odds with a previous study using fim-containing multicopy plasmids, reflect differences in gene copy number.
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11 MeSH Terms
Immunologic evaluation of hematopoietic chimeric rhesus monkeys.
Duncan BW, Harrison MR, Zanjani ED, Tarantal AF, Adzick NS, Bradley SM, Longaker MT, Jennings RW, Roberts LJ, Bigler ME
(1991) Transplant Proc 23: 841-3
MeSH Terms: Animals, Blood Cell Count, Chimera, Female, Fetal Tissue Transplantation, Fetus, Hematopoietic Stem Cell Transplantation, Immunoglobulins, Liver, Lymphocyte Activation, Macaca mulatta, Phenotype, Pregnancy
Added December 10, 2013
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13 MeSH Terms
Molecular cloning and transformation of cyclodiene resistance in Drosophila: an invertebrate gamma-aminobutyric acid subtype A receptor locus.
Ffrench-Constant RH, Mortlock DP, Shaffer CD, MacIntyre RJ, Roush RT
(1991) Proc Natl Acad Sci U S A 88: 7209-13
MeSH Terms: Amino Acid Sequence, Animals, Cattle, Chromosome Walking, Cloning, Molecular, Cosmids, Crosses, Genetic, DNA, DNA Transposable Elements, Dieldrin, Drosophila, Drug Resistance, Female, Gene Rearrangement, Insecticides, Macromolecular Substances, Male, Molecular Sequence Data, Phenotype, Protein Conformation, Rats, Receptors, GABA-A, Restriction Mapping, Sequence Homology, Nucleic Acid, Transformation, Genetic
Show Abstract · Added June 9, 2010
Cyclodiene resistance represents 60% of the reported cases of insecticide resistance and is also present in vertebrates. Resistance is due to insensitivity of the cyclodiene/picrotoxinin binding site on the gamma-aminobutyric acid subtype A (GABAA) receptor-chloride ionophore complex. Following isolation of cyclodiene-resistant Drosophila mutants, we report the cloning of the locus conferring resistance via a "chromosomal walk" and rescue of the susceptible phenotype by P-element-mediated germ-line transformation. Amino acid sequence analysis of a cDNA from the locus reveals homology with vertebrate GABAA subunits. To our knowledge, this represents the first cloning of an invertebrate GABA receptor and also allows us to manipulate the resistance status of an insect via germ-line transformation. This gene may be useful as a selectable marker in other insect systems.
1 Communities
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25 MeSH Terms
Buschke-Ollendorff syndrome associated with elevated elastin production by affected skin fibroblasts in culture.
Giro MG, Duvic M, Smith LT, Kennedy R, Rapini R, Arnett FC, Davidson JM
(1992) J Invest Dermatol 99: 129-37
MeSH Terms: Blotting, Southern, Cells, Cultured, Connective Tissue Diseases, Elastin, Female, Fibroblast Growth Factor 2, Fibroblasts, Humans, Male, Microscopy, Electron, Middle Aged, Nevus, Osteopoikilosis, Pedigree, Phenotype, RNA, Messenger, Skin, Skin Neoplasms, Syndrome, Transforming Growth Factor beta
Show Abstract · Added December 10, 2013
Buschke-Ollendorff syndrome (BOS; McKusick 16670) is an autosomal dominant connective-tissue disorder characterized by uneven osseous formation in bone (osteopoikilosis) and fibrous skin papules (dermatofibrosis lenticularis disseminata). We describe two patients in whom BOS occurred in an autosomal dominant inheritance pattern. The connective tissue of the skin lesions showed both collagen and elastin abnormalities by electron microscopy. Cultured fibroblasts from both patients produced 2-8 times more tropoelastin than normal skin fibroblasts in the presence of 10% calf serum. Involved skin fibroblasts of one patient produced up to eight times normal levels, whereas apparently uninvolved skin was also elevated more than threefold. In a second patient, whose involvement was nearly complete, elastin production was high in involved areas and less so in completely involved skin. Transforming growth factor-beta 1 (TGF beta 1), a powerful stimulus for elastin production, brought about similar relative increases in normal and BOS strains. Basic fibroblast growth factor, an antagonist of TGF beta 1-stimulated elastin production, was able to reduce elastin production in basal and TGF beta 1 stimulated BOS strains. Elastin mRNA levels were elevated in all patient strains, suggesting that Buschke-Ollendorff syndrome may result, at least in part, from abnormal regulation of extracellular matrix metabolism that leads to increased steady-state levels of elastin mRNA and elastin accumulation in the dermis.
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20 MeSH Terms
Phenotypic alterations in fibroblasts and fibrosarcoma cells that overexpress latent transforming growth factor-beta 1.
Beauchamp RD, Sheng HM, Bascom CC, Miller DA, Lyons RM, Torre-Amione G, Moses HL
(1992) Endocrinology 130: 2476-86
MeSH Terms: Animals, Blotting, Northern, Cell Line, Embryo, Mammalian, Fibroblasts, Fibrosarcoma, Gene Expression, Kinetics, Mice, Mice, Inbred C3H, Phenotype, Plasmids, Poly A, RNA, RNA, Messenger, Receptors, Cell Surface, Receptors, Transforming Growth Factor beta, Sarcoma, Experimental, Suramin, Transfection, Transforming Growth Factor beta
Show Abstract · Added May 3, 2013
Mouse embryo-derived AKR-2B fibroblasts and murine fibrosarcoma cells (the 1591 cell line) were transfected with a murine transforming growth factor-beta 1 (TGF beta 1) cDNA under the transcriptional control of either the simian virus-40 early promoter or the cytomegalovirus promoter/enhancer. Selected clones secreted 2- to 4-fold more TGF beta-competing activity into their media than the parental cell line or neomycin-transfected controls. The TGF beta 1 released into the cell-conditioned medium was latent. Despite the latency of the overexpressed TGF beta 1, TGF beta 1-transfected cells exhibited phenotypic features of TGF beta 1-treated cells. When confluent, the TGF beta 1-transfected cells had the morphological characteristics of the parental cells that have been treated with active TGF beta 1. AKR-2B cells that expressed higher levels of TGF beta 1 also expressed high levels of c-sis and c-myc mRNAs and decreased TGF beta 2 and TGF beta 3 mRNAs in the same manner as parental AKR-2B cells that had been treated with active TGF beta 1. The transfected 1591 cells that overexpressed TGF beta 1 bound less [125I]TGF beta 1 than did parental 1591 cells, but after a mild acid wash demonstrated an increase in [125I]TGF beta 1 binding. Our results suggest that these TGF beta 1-transfected fibroblast and fibrosarcoma cells have the capacity to activate TGF beta; however, as very little activated TGF beta is detected in the medium, it is hypothesized that these cells activate latent TGF beta 1 and bind the activated TGF beta 1, thus acquiring a phenotype consistent with TGF beta 1-treated cells.
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21 MeSH Terms
Genes involved in androgen biosynthesis and the male phenotype.
Waterman MR, Keeney DS
(1992) Horm Res 38: 217-21
MeSH Terms: Aldehyde-Lyases, Androgens, Cholesterol Side-Chain Cleavage Enzyme, Cytochrome P-450 Enzyme System, Female, Humans, Male, Mutation, Phenotype, Sex Differentiation, Steroid 17-alpha-Hydroxylase
Show Abstract · Added February 12, 2015
A series of enzymatic steps in the testis lead to the conversion of cholesterol to the male sex steroid hormones, testosterone and 5 alpha-dihydrotestosterone. Mutations in any one of these steps are presumed to alter or block the development of the male phenotype. Most of the genes encoding the enzymes involved in this pathway have now been cloned, and mutations within the coding regions of these genes do, in fact, block development of the male phenotype.
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11 MeSH Terms