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251.
Gertrude Mungyer Wim N. P. Willemsen Rune Rolland Hans M. Vemer Francs C. S. Ramaekers Paul H. K. Jap Lambert G. Poels 《In vitro cellular & developmental biology. Plant》1987,23(2):111-117
Summary Cellular elements from the mucous membrane of the uterus and oviducts and from peritoneal washings were cultured. The in vitro
behavior of these cells was compared to elucidate the histogenesis of endometriosis and the role of various diagnostic procedures.
In 65% of the cultured matrial obtained by uterine-tubal flushing, proliferating cells of the uterine-tubal mucous membrane
were present. Their morphology and behavior corresponded to those of cultured cells obtained by separate washing of the uterine
cavity and the tubes, respectively, curetted material, and biopsies of endometriosis lesions.
Epithelial and stromal cells were identified using phase contrast microscopy, electron microscopy, and immunohistochemical
methods. These cell types did not occur in peritoneal washings before the flushing of uterus and tubes. It was therefore assumed
that they were detached and transported to the pelvic cavity during the above-mentioned procedures. In view of their intensive
proliferation they may form the basis in the development of nodules of endometriosis. This would support the implantation
theory concerning the pathogenesis of endometriosis. Interactions between epithelial and mesothelial cells point to the possible
role of the latter in encapsulating the endometrial elements. 相似文献
252.
Emil Pilipcinec Tako T. Huisman Peter T.J. Willemsen Ben J. Appelmelk Frits K. de Graaf Bauke Oudega 《FEMS microbiology letters》1994,123(1-2):202-206
Abstract Tn 10 transposon mutagenesis of Escherichia coli producing K99 fimbriae was carried out to identify host factors involved in regulation or biosynthesis of fimbriae. Two chromosomal mutants were obtained that showed a strongly reduced cell surface expression of K99 fimbriae upon colony blotting and ELISA. Analysis by inversed PCR and nucleotide sequencing showed that one mutant (EP14) contained the Tn 10 transposon in rfaQ , affecting theexpression of the rfaQGP gene cluster, whereas the other mutant (EP35) was affected in a, to date, unknown region of the genome. Immunoblotting analysis confirmed a Rd1 type of LPS of mutant strain EP14. These findings for the first time indicated an effect of LPS core biosynthesis on the biogenesis of fimbriae at the cell surface. Preliminary experiments indicated that K99 major subunits, in contrast to K88 subunits, strongly bind LPS molecules. 相似文献
253.
J. Willemsen 《Aquatic Ecology》1979,13(2-3):94-95
254.
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256.
EDC3 phosphorylation regulates growth and invasion through controlling P‐body formation and dynamics
Jeremiah J Bearss Sathish KR Padi Neha Singh Marina CardoVila Jin H Song Ghassan Mouneimne Nikita Fernandes Yang Li Matthew R Harter Jaime MC Gard Anne E Cress Wolfgang Peti Andrew DL Nelson J Ross Buchan Andrew S Kraft Koichi Okumura 《EMBO reports》2021,22(4)
Regulation of mRNA stability and translation plays a critical role in determining protein abundance within cells. Processing bodies (P‐bodies) are critical regulators of these processes. Here, we report that the Pim1 and 3 protein kinases bind to the P‐body protein enhancer of mRNA decapping 3 (EDC3) and phosphorylate EDC3 on serine (S)161, thereby modifying P‐body assembly. EDC3 phosphorylation is highly elevated in many tumor types, is reduced upon treatment of cells with kinase inhibitors, and blocks the localization of EDC3 to P‐bodies. Prostate cancer cells harboring an EDC3 S161A mutation show markedly decreased growth, migration, and invasion in tissue culture and in xenograft models. Consistent with these phenotypic changes, the expression of integrin β1 and α6 mRNA and protein is reduced in these mutated cells. These results demonstrate that EDC3 phosphorylation regulates multiple cancer‐relevant functions and suggest that modulation of P‐body activity may represent a new paradigm for cancer treatment. 相似文献
257.
Sublocalization of an invasion-inducing locus and other genes on human chromosome 7. 总被引:3,自引:0,他引:3
G G Habets R A van der Kammen V Willemsen M Balemans J Wiegant J G Collard 《Cytogenetics and cell genetics》1992,60(3-4):200-205
By somatic cell fusion studies between noninvasive mouse T-lymphoma cells and invasive human activated normal T-cells we have previously shown that the genetic information responsible for the induction of invasive and metastatic potential in interspecies T-cell hybrids is located on human chromosome 7. Apparently, genes derived from normal activated T-cells are dominantly expressed in the hybrids and control the invasive and, as a consequence, metastatic potential of these T-lymphoma cells. To sublocalize the invasion-inducing locus on chromosome 7 we have generated hybrids that harbor only specific regions of human chromosome 7 with or without a small fragment of human chromosome 21. Analysis of these hybrids revealed that the invasion-inducing locus maps to 7p12----cen. The human DNA complement of the hybrids was confirmed by Southern blot analysis using a large panel of chromosome 7-specific DNA probes. Several of these genes could be further sublocalized. These included: ARAF2 to 7p12----cen, D7S21 to 7pter----p12, ACTB to 7p15----p12, EGFR to 7p12, MDH2 to 7cen----q22, and PDGFA to 7pter----p15. 相似文献