排序方式： 共有10条查询结果，搜索用时 62 毫秒
1
1.
Fungal morphogenesis: cell wall construction in Mucor rouxii 总被引：17，自引：0，他引：17
An autoradiographic study revealed two different patterns of cell wall constructioni associated with two types of morphogenesis in Mucor rouxii. In hyphae, the cell wall was preferentially synthesized in the apical region; these cylindrical walls seemed to be generated by a sharply descending gradient of wall synthesis radiating from the apex. In spherical cells (germinating spores, yeast cells), wall formation occurred largely, if not entirely, in uniformly dispersed fashion over the entire cell periphery. 相似文献
2.
Direct interaction of a ligand for the erbB2 oncogene product with the EGF receptor and p185erbB2 总被引：23，自引：0，他引：23
R Lupu R Colomer G Zugmaier J Sarup M Shepard D Slamon M E Lippman 《Science (New York, N.Y.)》1990,249(4976):1552-1555
The erbB2 oncogene encodes a 185-kilodalton transmembrane protein whose sequence is similar to the epidermal growth factor receptor (EGFR). A 30-kilodalton factor (gp30) secreted from MDA-MB-231 human breast cancer cells was shown to be a ligand for p185erbB2. An antibody to EGFR abolished the tyrosine phosphorylation induced by EGF and transforming growth factor-alpha (TGF-alpha) but only partially blocked that produced by gp30 in SK-BR-3 breast cancer cells. In two cell lines that overexpress erbB2 but do not expresss EGFR (MDA-MB-453 breast cancer cells and a Chinese hamster ovary cell line that had been transfected with erbB2), phosphorylation of p185erbB2 was induced only by gp30. The gp30 specifically inhibited the growth of cells that overexpressed p185erbB2. An antibody to EGFR had no effect on the inhibition of SK-BR-3 cell colony formation obtained with gp30. Thus, it appeared that gp30 interacted directly with the EGFR and erbB2. Direct binding of gp30 to p185erbB2 was confirmed by binding competition experiments, where gp30 was found to displace the p185erbB2 binding of a specific antibody to p185erbB2. The evidence described here suggests that gp30 is a ligand for p185erbB2. 相似文献
3.
Nuclear estrogen receptor from MCF-7 cells undergoes a time-dependent, hormone-inducible transformation to a form that is less extractable from nuclei and less exchangeable with ligand. This receptor-modifying, intranuclear event is independent of receptor loss (processing) and appears associated with hormone responsiveness (progesterone-receptor induction) in these cells. The magnitude of receptor loss, however, is variable and apparently not a prerequisite for hormone action to induce progesterone receptor. 相似文献
4.
Gendrel AV Lippman Z Yordan C Colot V Martienssen RA 《Science (New York, N.Y.)》2002,297(5588):1871-1873
The Arabidopsis gene DDM1 is required to maintain DNA methylation levels and is responsible for transposon and transgene silencing. However, rather than encoding a DNA methyltransferase, DDM1 has similarity to the SWI/SNF family of adenosine triphosphate-dependent chromatin remodeling genes, suggesting an indirect role in DNA methylation. Here we show that DDM1 is also required to maintain histone H3 methylation patterns. In wild-type heterochromatin, transposons and silent genes are associated with histone H3 methylated at lysine 9, whereas known genes are preferentially associated with methylated lysine 4. In ddm1 heterochromatin, DNA methylation is lost, and methylation of lysine 9 is largely replaced by methylation of lysine 4. Because DNA methylation has recently been shown to depend on histone H3 lysine 9 methylation, our results suggest that transposon methylation may be guided by histone H3 methylation in plant genomes. This would account for the epigenetic inheritance of hypomethylated DNA once histone H3 methylation patterns are altered. 相似文献
5.
Transfection of v-rasH DNA into MCF-7 human breast cancer cells bypasses dependence on estrogen for tumorigenicity 总被引：12，自引：0，他引：12
A Kasid M E Lippman A G Papageorge D R Lowy E P Gelmann 《Science (New York, N.Y.)》1985,228(4700):725-728
The natural history of estrogen-responsive breast cancers often involves a phenotypic change to an estrogen-unresponsive, more aggressive tumor. The human breast cancer cell line, MCF-7, which requires estradiol for tumor formation in vivo and shows growth stimulation in response to estradiol in vitro, is a model for hormone-responsive tumors. The v-rasH onc gene was transfected into MCF-7 cells. The cloned MCF-7ras transfectants, which expressed the v-rasH messenger RNA and v-rasH p21 protein (21,000 daltons), were characterized. In contrast to the parental cell line, MCF-7ras cells no longer responded to exogenous estrogen in culture and their growth was minimally inhibited by exogenous antiestrogens. When tested in the nude mouse, the MCF-7ras cells were fully tumorigenic in the absence of estrogen supplementation. Thus, cells acquiring an activated onc gene can bypass the hormonal regulatory signals that trigger the neoplastic growth of a human breast cancer cell line. 相似文献
6.
Shenstone Esperanza Lippman Zach Van Eck Joyce 《Plant foods for human nutrition (Dordrecht, Netherlands)》2020,75(3):316-325
Plant Foods for Human Nutrition - The Physalis genus of the Solanaceae family is home to many edible food crops including tomatillo, goldenberry, and groundcherry. These Physalis members have... 相似文献
7.
8.
Estrogen-induced factors of breast cancer cells partially replace estrogen to promote tumor growth 总被引：12，自引：0，他引：12
The hormone 17 beta-estradiol acts through its receptor system to induce MCF-7 human breast cancer cells to form tumors in athymic mice. In vitro studies have identified the production of estrogen-induced growth factors from MCF-7 cells that may have a role in growth control. These induced growth factors were sufficient to stimulate MCF-7 tumor growth in ovariectomized athymic mice, thus partially replacing estradiol. Growth factors may act as estrogen-induced "second messengers" in estrogen-responsive growth of human breast cancer. 相似文献
9.
10.
Lippman A Newman SA Testa G Harris J 《Science (New York, N.Y.)》2005,307(5709):515-7; author reply 515-7
1