Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P13232 (Interleukin-7)
 580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cloned cell strains with adverse patterns of differentiation obtained from 7,12-dimethylbenz(a)anthracene-induced rat mammary tumor tissue were used to study the effects of glucocorticoid hormones on morphology and proliferation. HH-16 clone 2/1 cells apparently reflecting mesenchymal cells of the stromal part of the mammary gland grow as elongated, mostly bipolar fibroblasts in criss-cross patterns. When cultured in the presence of glucocorticoids, the cells flattened, lost bipolarity, extended in size, and showed arrest of growth at confluence, possibly due to contact inhibition. Immunocytochemical examination of dexamethasone-treated cells revealed actin cables which were absent in untreated cells. The hormone-treated cells expressed Mr 50,000-67,000 cytokeratins, and the extracellular matrix proteins fibronectin and laminin were increased. The in vitro effects on morphology and growth were reversible 3-4 days after withdrawal of the glucocorticoids. In dexamethasone-treated animals the growth of fibrosarcomas produced by inoculation of newborn rats with HH-16 clone 2/1 cells was reduced, and the survival time of the tumor-bearing animals was extended. Apparently, morphology and growth of HH-16 clone 2/1 fibrosarcoma cells can be controlled by glucocorticoids. In comparison, epithelioid HH-16 clone 4 cells established simultaneously from 7,12-dimethylbenz(a)anthracene-induced rat mammary tumor were unresponsive to glucocorticoids.
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PMID:Glucocorticoid-induced alterations of morphology and growth of fibrosarcoma cells derived from 7,12-dimethylbenz(a)anthracene rat mammary tumor. 314 85

Clone 4 MDCK cells, which generate a transepithelial electrical resistance (TER) of greater than 2,000 omega.cm2, were used to examine the role of membrane lipids in the barrier function of tight junctions. Phospholipid acyl groups were modified by supplementing cells grown in serum-free medium with 18:1(n-9), 18:3(n-3), or 18:3(n-6) complexed to albumin. Although both of these polyunsaturated fatty acids depress the melting point of membrane phospholipids, only 18:3(n-6) contributes significantly to eicosanoid production. Saturation indices of the phospholipids of cells supplemented with albumin alone, 18:1(n-9), 18:3(n-3), or 18:3(n-6) were 0.77, 0.78, 1.81, and 1.65, respectively. After trypsinization or removal of Ca2+, cells supplemented with 18:3(n-6) required longer periods of time to reestablish TER than did nonsupplemented cells or those incubated with 18:3(n-3) or 18:1(n-9). In contrast to MDCK strains I and II, clone 4 MDCK cells required continuous protein synthesis not only to reseal preexisting junctions after the addition of Ca2+ to Ca2+-depleted monolayers, but also to maintain steady-state TER. The rate of decay of TER in the presence of 1 microgram/ml of cycloheximide was 1.5 times greater in cells supplemented with either of the two 18:3 isomers than it was in nonsupplemented controls or in cells supplemented with 18:1(n-9). No significant difference was observed in the steady-state TER or selectivity of the tight junctions after fatty acid supplementation. These results suggest that there is a change in the dynamics of junction formation, rather than an alteration in their intrinsic properties.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of tight junction formation in clone 4 MDCK cells by fatty acid supplementation. 316 53

Lectin-binding characteristics of a previously described highly metastatic variant (clone 4), derived in vivo from a poorly metastatic rat mammary adenocarcinoma (DMBA-8), have been investigated. of the lectins studied clone 4 cells, unlike the parent cells, bound Ulex europaeus agglutinin (UEA-1; specificity alpha-L-fucose) and peanut agglutinin (PNA; specificity D-galactose). These differences may be related to the greatly enhanced ability of clone 4 cells to form lung foci after intravenous injection. After neuraminidase treatment the differential binding of PNA, as shown by flow cytofluorography, was abrogated whereas that of UEA was unchanged. After separation by SDS-PAGE, four proteins in total cell extracts of clone 4 cells bound 125I-UEA applied to the gels. These had subunit molecular weights greater than 100,000 daltons and were also found in cellular extracts of another highly metastatic rat mammary adenocarcinoma (MAT 13762-B), but were missing from DMBA-8 cell extracts. In clone 4 and MAT 13762-B cells exogenous 3H-fucose was mainly incorporated into four fucoproteins of similar molecular weights to those which bound 125I-UEA. DMBA-8 cells, which incorporated slightly less exogenous fucose, showed a different pattern of fucoprotein labelling, which would seem to explain why DMBA-8 cells failed to bind UEA. Differences in cell surface protein iodination patterns were also noted between DMBA-8 and clone 4 cells.
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PMID:Lectin-binding characteristics of related high- and low-metastatic rat mammary adenocarcinoma cell lines. 367 43

Cloned lines of Adriamycin (ADR)-sensitive and -resistant P388 leukemia have been established from single cell cultures. A marker chromosome M1 was found in all cells in the heterogeneous resistant P388/ADR parental line as well as in the cloned resistant lines P388/ADR/3 and P388/ADR/7; a different marker chromosome M2 was present in the heterogeneous sensitive P388 parental line as well as the cloned sensitive line P388/4. Dose-survival studies showed that D0, the dose of Adriamycin reducing survival to 1/e (i.e., 37% of the initial population), was 33 +/- 5 (SE) nM for sensitive P388/4 cells, 169 +/- 17 nM for resistant P388/ADR/3 cells, and 336 +/- 28 nM for the more resistant P388/ADR/7 cells. Drug uptake in sensitive P388/4 cells was 1.6-fold greater than in resistant P388/ADR/3 cells and 2.1-fold greater than in resistant P388/ADR/7 cells. The number of DNA single-strand breaks produced per microM Adriamycin was 131 +/- 9 rad equivalents in sensitive clone 4 cells, 41 +/- 8 rad equivalents in resistant clone 3 cells, and 33 +/- 11 rad equivalents in resistant clone 7 cells. The number of DNA double-strand breaks per microM Adriamycin was 1721 +/- 126 rad equivalents in sensitive cells, 117 +/- 36 rad equivalents in resistant P388/ADR/3 cells, and 194 +/- 16 rad equivalents in resistant P388/ADR/7 cells. Differences in drug uptake were insufficient to explain the higher incidence of DNA single- and double-strand breaks in sensitive cells. These findings strongly support the concept that resistance to Adriamycin in P388 leukemia cells is multifactorial; however, this study did not resolve whether these changes arise from a single pleiotropic mutation or from multiple mutations. In sensitive P388/4 cells the number of DNA single-strand breaks formed could all be attributed to double-strand breaks. However, in both resistant cell lines the level of induction of single-strand breaks was in excess of that due to double-strand breaks, and this excess of single-strand breaks appeared to vary directly with the degree of resistance, being greater in the more resistant clone 7 cells than in the less resistant clone 3 cells. In both sensitive and resistant cell lines the ratio of true single- to double-strand breaks varied inversely with the concentration of Adriamycin. Finally, the cytotoxic activity of Adriamycin appeared to correlate more closely with formation of DNA double-strand breaks than with single-strand lesions.
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PMID:Resistance to adriamycin: relationship of cytotoxicity to drug uptake and DNA single- and double-strand breakage in cloned cell lines of adriamycin-sensitive and -resistant P388 leukemia. 369 20

The extent to which exogenous 18:3(n-3) and 18:3(n-6) were desaturated and elongated and the degree to which they and their derivatives altered the unsaturation index of cell glycerolipids were compared using clone 4 MDCK cells grown in lipid- and serum-free medium. Despite differences in the degree of unsaturation of the individual polyunsaturated fatty acids produced from 18:3(n-3) or 18:3(n-6), the unsaturation index of phospholipids increased similarly from 0.7 in control cells grown in serum- and lipid-free medium to ca. 1.6 in those supplemented with fatty acid. The added fatty acids had little effect on cell growth. The conversion of 18:3(n-6) to 20:3(n-6) and 20:4(n-6) was more rapid than that of 18:3(n-3) to 20:4(n-3) and 20:5(n-3). No significant quantities of 20:3(n-3) or 18:4(n-3) were noted. When both 18:3 isomers were supplied simultaneously, marked differences in the amounts of some species of n-3 and n-6 polyunsaturated fatty acids were observed. The presence of 18:3(n-6) and/or its derivatives suppressed levels of 20:4(n-3) and 20:5(n-3), perhaps through inhibition of the delta 6 and delta 5 desaturases responsible for their synthesis from 18:3(n-3). Similarly 18:3(n-3), and/or its longer more unsaturated derivatives, diminished the formation of 20:4(n-6) from 18:3(n-6). No marked effect on the products derived from elongation alone were observed.
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PMID:Metabolism and incorporation into glycerolipids of exogenous 18:3(n-3) and 18:3(n-6) by MDCK cells. 374 38

Data presented in this study describes the isolation and characterization of two anti-fluorescein (F1) hybridoma proteins 3-24 and 12-40, both IgG1, kappa with a Ka = 2.8 and 3.4 X 10(6) M-1, respectively, at 37 degrees C. These clones inhibited (6.8 +/- 2.8 -20.8 +/- 0.6% at 1 microgram/well) the idiotype-anti-idiotype interactions (IAII) of anti-F1 clones 3-13 and 3-17, which define a previously described low affinity idiotype family. Antibodies 3-24 and 12-40 also inhibited (45.0 +/- 3.0 and 61.3 +/- 5.6%, respectively, at 1 microgram/well) an IAII defined by a high affinity (Ka = 5.2 +/- 1.5 X 10(9) M-1 at 37 degrees C) anti-F1 clone, 4-4. Hybridoma proteins 3-13 and 3-17 possess similar affinities for F1 (Ka = 3.8 +/- 5.1 and 5.9 +/- 4.0 X 10(4) M-1) and are known to be idiotypically unrelated to clone 4-4. While 3-24 and 12-40 appeared very similar, non-identity of their active sites was established by heterologous idiotypic inhibitions, fine specificity of binding and spectral measurements (Qmax and lambda max) of bound F1. All IAII (3-13, 3-17, 9-40 and 4-4) were inhibited greater than 80% by the presence of 10(-4) M F1 or F1-BSA. In addition, four intermediate affinity (6.0 X 10(6) less than or equal to Ka less than or equal to 5.3 X 10(8) M-1) anti-F1 clones, comprising a second previously described idiotype family (designated the 9-40 family) were further analyzed. Inhibition of the 9-40 IAII by all heterologous proteins in the 9-40 family (except clone 5-27), and clones 3-24, 12-40 and 4-4 ranged from 87.7 +/- 1.3 to 95.4 +/- 1.0% at 1 microgram/well. Titration of the 9-40 IAII inhibition by antibodies 9-40, 3-24, 12-40 or 4-4 generated essentially superimposable profiles. In reciprocal inhibition experiments, using the 4-4 IAII, clones 3-24, 12-40, 9-40 and 4-4 gave distinct idiotypic titration patterns. Thus, members of the 9-40 family, 3-24 and 12-40 were more closely related to intermediate affinity clone 9-40 than high affinity clone 4-4.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Linkage of low and high affinity anti-fluorescein idiotype families. 382 41

Three monoclonal antibodies (1G3, 2H11, and 3G12) specific for a syngeneic Ek-specific T-cell clone, clone 4, have been established. The antibodies specifically blocked not only the activation of the clone in response to the specific antigen Ek but also the activation by IL-2. Kinetic studies of the blocking activity revealed that the antibodies blocked activation not only through steric hindrance of the antigen-binding site of the receptor but also via inhibition of DNA synthesis. The antibodies induced unresponsiveness of the clone to the specific antigen Ek, but not to nonspecific activation by IL-2. The state of unresponsiveness induced by 1G3 continued for 14 days, the longest time so far examined. The recovery from the unresponsiveness (tolerance) was not observed unless the clone cells proliferated vigorously in response to IL-2. The idiotope recognised by 1G3 was different from that by 2H11 and/or 3G12. This might explain some functional differences elicited by the antibodies.
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PMID:T-cell receptor expressed on an autoreactive T-cell clone, clone 4. I. Induction of various T-receptor functions by anti-T idiotypic antibodies. 387 21

The nucleotide sequence of a full-length (8.8-kilobase) endogenous C-type human retroviral DNA (clone 4-1) is presented and compared with that of Moloney murine leukemia virus (MoMuLV) DNA. Colinearity of deduced amino acids of clone 4-1 with MoMuLV in the gag and pol regions was clearly evident, and overall amino acid homology in these regions was about 40%. Identification of the putative N terminus of gag and p30, the gag-pol junction, and the C terminus of pol could be established on the basis of sequence homology with MoMuLV. Unique characteristics of the endogenous human retroviral DNA included a tRNA Glu primer binding site separated from the 5' long terminal repeat by a pentanucleotide and a putative env sequence which does not appear to overlap the C terminus of pol and has virtually no homology with the env gene of known infectious retroviruses. Clone 4-1 represents a defective prototype of a human C-type retrovirus which integrated into the germ line some time in the distant past.
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PMID:Nucleotide sequence of a full-length human endogenous retroviral segment. 399 94

Three related human prostate carcinoma cell lines, PC-3, 1-LN-PC-3-1A (1-LN), and 1-LN-PC-3-1A clone 4 (clone 4) were compared in terms of relative metastatic capacity in adult and young male nude mice. Only 1-LN produced lung metastases after intravenous injection into both 6- to 8-week-old and 4-week-old nude mice, as well as in mice injected intraperitoneally. The extent of the phenotypic diversity exhibited by these human prostate tumor lines was influenced by inherent dissemination ability, age of the host, and route of injection. These lines provide a useful system for the analysis of the biology of human tumor metastasis in nude mice.
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PMID:Factors influencing phenotypic diversity of human prostate carcinoma cells metastasizing in athymic nude mice. 400 33

The regulation of ppp(A2'p)nA-(2-5A)-dependent RNase (RNase L or RNase F) was investigated in NIH 3T3, clone 1 cells using 2-5A-binding and nuclease activity assays. Minimal levels of 2-5A-dependent RNase were detected in actively dividing clone 1 cells; these levels were independently induced by growth arrest or interferon treatment. Accordingly, levels of the RNase were enhanced during growth arrest by confluency regardless of the presence or absence of interferon or antibody to interferon in the media. Measurement of 2-5A-dependent RNase was unaffected by the addition of any of six different proteinase inhibitors to the cells prior to extraction. The expression of 2-5A-dependent RNase in growth-arrested, interferon-treated cells was still relatively low (about one-third to one-half of that found in similarly treated murine Ehrlich ascites tumor cells). Although this amount of 2-5A-dependent RNase could not be detected by 2-5A-mediated ribosomal RNA cleavage, the activity was identified using a more sensitive novel assay for 2-5A-dependent RNase. In addition, introduction of 2-5A or poly(I) X poly(C) into growth-arrested, interferon-treated cells resulted in some inhibition of protein synthesis. The results indicated that the expression of 2-5A-dependent RNase in NIH 3T3, clone 1 cells is regulated under different physiological conditions and that low levels of 2-5A-dependent RNase were insufficient to significantly inhibit encephalomyocarditis virus replication.
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PMID:Independent regulation of ppp(A2'p)nA-dependent RNase in NIH 3T3, clone 1 cells by growth arrest and interferon treatment. 401 82


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