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PICT-1 is a major nucleolar sensor of the DNA damage repair response and an important upstream regulator of p53 via the RPL11-MDM2-p53 pathway.
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A novel pathogenic mutation in RPL11 identified in a patient diagnosed with diamond Blackfan anemia as a young adult.
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RPL splicing variant is associated with Diamond-Blackfan anemia.
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Simulation of HEY1 Ser-68 phosphorylation prevents its interaction with p53, RPL11 and MDM2 and abolishes HEY1 migration to nucleolar caps upon ribosomal stress. Our findings uncover a novel mechanism for cross-talk between Notch signalling and nucleolar stress
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Data suggest 5S ribosomal RNA is a direct target of miR-150 and miR-383 in esophageal squamous cell carcinoma (ESCC); overexpression of miR-150 and miR-383 inhibits ESCC cell proliferation in vitro and in vivo and intensifies RPL11/c-Myc interaction.
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Ribosomal proteins L11 and L5 activate TAp73 by overcoming MDM2 inhibition.
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Data indicate that ribosomal protein (L11) promotes the recruitment of microRNA-130a (miR-130a) to oncoprotein c-Myc in response to UV irradiation treatment.
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Data indicate that ribosomal protein L11 (RPL11)-expressing cells proliferated more rapidly than the ribosomal protein L11 (RPL11)-expressing cells.
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Findings uncover a mechanism by which RPL5 and RPL11 can co-operatively suppress c-Myc expression, allowing a tightly controlled ribosome biogenesis in cells.
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levels of branched-chain aminotransferase-1 (BCAT1) transcripts are significantly decreased on the polysomes of both RPS19 and RPL11 cells and that translation of BCAT1 protein is especially impaired in cells with small RP gene mutations
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Findings suggest that PICT1 has a crucial role in gastric cancer progression by regulating the MDM2-TP53 pathway through RPL11.
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Unlike other tumor suppressors, RPL5 and RPL11 play essential roles in normal cell proliferation.
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disrupted nucleoli may provide a platform for L5- and L11-dependent p53 activation, implying a role for the nucleolus in p53 activation by ribosomal biogenesis stress
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RPL11 mutations led to a dramatic decrease in progenitor cell proliferation and a delayed erythroid differentiation with a marked increase in apoptosis and G0/1 cell cycle arrest with activation of p53.
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The studies provide insights on how nucleolar stress through L11 and NEDD8 can activate the transcriptional activity of p53.
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ARF activates p53, at least partly by induction of ribosomal stress, which results in L11 suppression of MDM2
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Hydrophilic residues are crucial for ribosomal protein L11 (RPL11) interaction with zinc finger domain of MDM2 and p53 protein activation
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Results identify a novel regulatory paradigm wherein L11 plays a critical role in controlling c-myc mRNA turnover via recruiting miR-24/miRISC in response to ribosomal stress.
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Data report that depletion of L37 leads to cell cycle arrest in a MDM2/L11- and p53-dependent manner.
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Knockdown of L29 or L30 enhanced the interaction of MDM2 with L11 and L5 and markedly inhibited MDM2-mediated p53 ubiquitination, suggesting that direct perturbation of 60 S ribosomal biogenesis activates p53 via L11- and L5-mediated MDM2 suppression.
