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María Lorena Falcone Ferreyra Jordane Biarc Alma L Burlingame Paula Casati 《Plant signaling & behavior》2010,5(10):1222-1225
Ribosomal protein L10 (RPL10) is a ubiquitous protein that participates in joining the 40S and 60S ribosomal subunits into a functional 80S ribosome; however, increasing evidence indicates that RPL10 from various organisms has multiple extra-ribosomal functions, besides being a constituent of ribosome and its role in translation. Arabidopsis thaliana contains in its genome three genes encoding RPL10, named RPL10A, RPL10B and RPL10C. Previously, we found that in maize and in A. thaliana, UV-B induces a reduction in protein biosynthesis, probably as a consequence of ribosomal damage; however, cellular recovery occurs in the absence of UV-B. Here, we show that RPL10s are differentially regulated by UV-B in a dosage and time dependent manner: RPL10C is induced, RPL10B is downregulated at high UV-B intensity and RPL10A is not UV-B regulated. In addition, by co-immunoprecipitation studies using RPL10 antibodies and proteins from control and UV-B irradiated Arabidopsis plants, we demonstrate that RPL10 associates with different proteins under the two different conditions, including nuclear proteins, suggesting that at least one isoform may have extra-ribosomal roles.Key words: UV-B exposure, translation, ribosomal protein, co-immunoprecipitation 相似文献
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Barna Dudok Peter M. Klein Ernie Hwaun Brian R. Lee Zizhen Yao Olivia Fong John C. Bowler Satoshi Terada Fraser T. Sparks Gergely G. Szabo Jordan S. Farrell Jim Berg Tanya L. Daigle Bosiljka Tasic Jordane Dimidschstein Gord Fishell Attila Losonczy Hongkui Zeng Ivan Soltesz 《Neuron》2021,109(6):997-1012.e9
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Dilara Akcora Duy Huynh Sally Lightowler Markus Germann Sylvie Robine Jan R. de May Jeffrey W. Pollard E. Richard Stanley Jordane Malaterre Robert G. Ramsay 《Stem cell research》2013,10(2):203-212
Gastrointestinal (GI) homeostasis requires the action of multiple pathways. There is some controversy regarding whether small intestine (SI) Paneth cells (PCs) play a central role in orchestrating crypt architecture and their relationship with Lgr5 + ve stem cells. Nevertheless, we previously showed that germline CSF-1 receptor (Csf1r) knock out (KO) or Csf1 mutation is associated with an absence of mature PC, reduced crypt proliferation and lowered stem cell gene, Lgr5 expression. Here we show the additional loss of CD24, Bmi1 and Olfm4 expression in the KO crypts and a high resolution 3D localization of CSF-1R mainly to PC. The induction of GI-specific Csf1r deletion in young adult mice also led to PC loss over a period of weeks, in accord with the anticipated long life span of PC, changed distribution of proliferating cells and this was with a commensurate loss of Lgr5 and other stem cell marker gene expression. By culturing SI organoids, we further show that the Csf1r?/? defect in PC production is intrinsic to epithelial cells as well as definitively affecting stem cell activity. These results show that CSF-1R directly supports PC maturation and that in turn PCs fashion the intestinal stem cell niche. 相似文献
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Veronique van den Berghe Elke Stappers Bram Vandesande Jordane Dimidschstein Roel Kroes Annick Francis Andrea Conidi Flore Lesage Ruben Dries Silvia Cazzola Geert Berx Nicoletta Kessaris Pierre Vanderhaeghen Wilfred van IJcken Frank G. Grosveld Steven Goossens Jody J. Haigh Gord Fishell Eve Seuntjens 《Neuron》2013,77(1):70-82