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排序方式: 共有1094条查询结果,搜索用时 31 毫秒
1.
Transformation of NIH 3T3 cells by overexpression of the normal coding sequence of the rat neu gene. 总被引:8,自引:2,他引:6
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While the normal human erbB-2 gene is potently transforming when overexpressed in NIH 3T3 cells, its rat homolog, the neu gene, seems to acquire transforming properties only upon alteration of its coding sequence. In this study, we compared the effects of different levels of expression of normal erbB-2 and neu in NIH 3T3 cells. Our results revealed that the normal rat neu gene acts as a potent oncogene when sufficiently overexpressed in NIH 3T3 cells. 相似文献
2.
R Meschini M T Quaranta M Fiore C Polcaro E Possagno F Palitti 《Mutation research》1988,204(4):645-648
The induction of sister-chromatid exchanges (SCE) and chromosomal aberrations (Ch.Ab.) by the herbicide maleic hydrazide (MH) has been investigated in Chinese hamster ovary (CHO) cells grown in vitro and in bone marrow cells of mice treated in vivo. MH induces SCE and Ch.Ab. in CHO cells without metabolic activation; however, no induction of SCE was found in the in vivo experiments. 相似文献
3.
4.
Transcriptional activation of jun and actin genes by estrogen during mitogenic stimulation of rat uterine cells. 总被引:4,自引:0,他引:4
5.
A mos oncogene-containing retrovirus, myeloproliferative sarcoma virus, transforms rat thyroid epithelial cells and irreversibly blocks their differentiation pattern. 总被引:8,自引:1,他引:7
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![点击此处可从《Journal of virology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
A Fusco G Portella P P Di Fiore M T Berlingieri R Di Lauro A B Schneider G Vecchio 《Journal of virology》1985,56(1):284-292
6.
G. Clementi F. Nicoletti F. Patacchioli A. Prato F. Patti C.E. Fiore † M. Matera U. Scapagnini 《Journal of neurochemistry》1983,40(3):885-886
Abstract: The effects of calcitonin on neurochemical parameters related to the tuberoinfundibular dopaminergic system have been investigated in an attempt to elucidate how calcitonin decreases serum prolactin levels. Intracerebroventricular human or salmon calcitonin injection decreases serum prolactin, medial basal hypothalamic dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) and hypophysial DA and increases hypophysial DOPAC. Results suggest that calcitonin may decrease prolactin secretion via the tuberoinfundibular dopaminergic system. 相似文献
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8.
Mechanisms by which EGF receptor and TGF alpha contribute to malignant transformation 总被引:2,自引:0,他引:2
E Di Marco J H Pierce S A Aaronson P P Di Fiore 《Natural immunity and cell growth regulation》1990,9(3):209-221
Alterations affecting the epidermal growth factor/transforming growth factor alpha-responsive mitogenic pathway are frequently detected in malignancies. In particular, the epidermal growth factor receptor has been found overexpressed in a number of human tumors. Production and secretion of transforming growth factor type alpha has also been shown in several tumor cells but not in their normal counterparts. In this review we describe the establishment of in vitro model systems to study the transforming potential of these molecules and summarize our current understanding of the mechanisms involved in transformation by genes encoding a growth factor and a growth factor receptor. 相似文献
9.
Leukocyte inhibitory factor activates human neutrophils and macrophages to release leukotriene B4 and thromboxanes 总被引:1,自引:0,他引:1
P Conti M Reale R C Barbacane M Bongrazio M R Panara S Fiore R Dempsey L Borish 《Cytokine》1990,2(2):142-148
Recent evidence has proved that cytokines can stimulate the production of 5-lipoxygenase products. Leukotriene B4 (LTB4) is a major mediator of leukocyte activation in acute inflammatory reactions, which produce chemotaxis, lysosomal enzyme release, and cell aggregation. Leukocyte inhibitory factor (LIF) also causes biological responses related to inflammation, i.e., LIF directly induces specific granule secretion by polymorphonuclears (PMNs) and potentiates many formyl-methionyl-leucyl-phenylalanine (FMLPs) mediated responses. Since arachidonic acid products are important mediators of inflammation, we have studied the effects of LIF on the arachidonic acid cascade products LTB4 and thromboxane A2 (TxA2). Resuspended at a final concentration of greater than 95% polymorphonuclear PMNs were isolated and tested with some cytokines on the release of LTB4 and TxA2. Peripheral blood mononuclear cells were isolated and seeded in Petri dishes and incubated for 60 min. Adherent macrophages were used for the cytokine stimulation study. Both types of leukocytes were treated with LIF, interleukin 6 (IL 6), and granulocyte-monocyte colony stimulating factor (GM-CSF) at different concentrations, and test agents A23187 and FMLP. Radioimmunoassay for LTB4 and TxB2 was determined by the resulting supernatants. Treatment of PMNs and macrophages with LIF at different concentrations proved to generate significant increases in LTB4 and TxA2 production. This was compared with IL 6 and GM-CSF, which had no effects. In these experiments, TxA2 generations could not be attributed to platelet contamination of PMN suspensions. The quantity of platelet contamination was not sufficient to influence how much TxB2 was produced. The similarities of LIF to other arachidonate stimulating cytokines suggest a similar mode of action in producing hematologic changes typical of tissue injury.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
10.
Marco G. Baroni Juan C. Alcolado Claudia Gragnoli Anna M. Franciosi M. Gisella Cavallo Vincenzo Fiore Paolo Pozzilli David J. Galton 《Human genetics》1994,93(6):675-680
Despite the strong evidence for a major role played by genetic factors in the aetiology of non-insulin-dependent diabetes mellitus (NIDDM), the genes involved are still unknown. Association studies of candidate genes for the inheritance of NIDDM have so far yielded inconclusive results. Some evidence exists for an association between NIDDM and the glucose transporter gene GLUT1, involved in basal glucose transport, although this has not been confirmed. In the present study we have tested the hypothesis of linkage between NIDDM and the GLUT1 gene, using affected sib-pairs. With this method the concordance observed for a given gene marker is compared with that expected under the assumption of no linkage between that marker and the disease. Fifty-four pedigrees (22 Italians and 32 British), for a total of 82 sibpairs were studied by the affected sib-pair method proposed by Weeks and Lange, using two restriction fragment length polymorphisms (RFLPs) at the GLUT1 locus, the MspI RFLP, at an estimated 0.171 recombination frequency from the GLUT1 gene, and the XbaI RFLP, located within the GLUT1 gene and previously shown to be associated with the disease. Results showed that the MspI marker and NIDDM segregate independently; for the XbaI RFLP, linkage could be shown only if the results were weighted by the allele frequency [f(p) = 1/p], and only in the Italian and the combined (Italian and British) sib-pair groups. Multilocus analysis with both markers was also negative. We conclude that the GLUT1 gene is very unlikely to play a major role in the aetiology of NIDDM, although an accessory role cannot be excluded, and studies of the gene sequence should help to clarify this question. 相似文献