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1 r MSCI-mediated transcriptional silencing of Rpl10.
2 rearrangements controlling the insertion of Rpl10.
3 elix 95 region being adjacent to the protein Rpl10.
4 nexpected and may suggest a nuclear role for Rpl10.
5 tically, rs26802900 is a significant eQTL of RPL10.
6 ty with the gene for human ribosomal protein RPL10.
7 chemoproteomics, we validate that 1 engages RPL10.
10 Here, we show that cysteines in Rps26 and Rpl10 are readily oxidized, rendering the proteins non-f
15 ion of RPL10L prevents the death of cultured RPL10-deficient somatic cells, and Rpl10l-promoter-drive
16 ression quantitative locus (eQTL) regulating RPL10 expression in the putamen and other brain tissues
17 ated that Arabidopsis (Arabidopsis thaliana) RPL10 genes are involved in development and translation
19 10l-promoter-driven transgenic expression of Rpl10 in spermatocytes restores spermatogenesis and fert
20 ating intersubunit rotation originating from rpL10 in the core of the large subunit (LSU) through bot
25 es transcription of a ribosomal protein L10 (Rpl10)-like gene and the cell cycle inhibitor p27, and i
27 tural and biochemical effects, suppressed an rpL10 mutant, re-establishing rotational equilibrium.
29 Moreover, the characterization of double rpl10 mutants indicates that the three AtRPL10s differen
30 ing that the block in 60S export in lsg1 and rpl10 mutants results indirectly from failing to recycle
31 and the block in 60S export in both lsg1 and rpl10 mutants was also suppressed by mutant Nmd3 protein
33 the dominant LSG1 mutant also traps a mutant Rpl10 protein that does not normally bind stably to the
36 (PDS) or a ribosomal protein-encoding gene, RPL10 (QM), in Nicotiana benthamiana We analyzed the exp
37 Here, this paradox is explored using the rpL10-R98S (uL16-R98S) mutant yeast model of the most co
39 ion of NOTCH1 eliminated these phenotypes in RPL10-R98S cells, in part via downregulation of PKC-thet
40 roliferation defect is eventually rescued by RPL10-R98S mouse lymphoid cells that acquire 5-fold more
41 ous cancer types, for example, the recurrent RPL10-R98S mutation in T-cell acute lymphoblastic leukem
45 ried out an extensive mutational analysis of Rpl10 to identify mutations that would allow us to map a
46 nd translocation of the downstream component RPL10 to the nucleus, where it interacts with a newly id
48 pl10l expression compensates for the lack of Rpl10, which exhibits a broad expression pattern but is
49 y of Rpl10l, a murine autosomal retrogene of Rpl10 with testis-specific expression, disturbs ribosome
50 p is not necessary for stable interaction of Rpl10 with the ribosome, suggesting that it plays a dyna