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1 ncluding fibrillarin (FIB-1/FBL) and RPL-11 (RPL11).
2 RPL11 are crucial for the stable binding and RPL11 suppression of MDM2 activity toward p53.
3 rexpression of ribosomal proteins (RP)L5 and RPL11, which bind and inhibit HDM2, stabilizing p53.
4                      Interestingly, RPL5 and RPL11 co-resided on c-Myc mRNA and suppressed c-Myc expr
5 rt hairpin RNA knockdown of RPS19, RPL5, and RPL11 expression in normal human CD34(+) cells.
6 by several ribosomal proteins (RPs), such as RPL11 and RPL5, which inhibit MDM2 and activate p53.
7          Several ribosomal proteins, such as RPL11, RPL5, RPL23, RPL26 or RPS7, have been shown to ha
8 vidence for the specific interaction between RPL11 and the zinc finger of MDM2 via hydrophilic residu
9               Here, we generated conditional RPL11-deletion mice to investigate in vivo effects of im
10 bearing MDM2(C305F) mutation, which disrupts RPL11- and RPL5-MDM2 binding, with Apc(min/+) mice, whic
11 well as CD34+ progenitors with downregulated RPL11 exhibit a markedly decreased hypusination in eryth
12 L23, like depletion of other RPs, except for RPL11 and RPL5, induces a p53 response and that the effe
13                    Mechanistically, we found RPL11 haploinsufficiency activates p53 in hematopoietic
14 n of the small (e.g., RPS19) or large (e.g., RPL11) ribosomal subunit are found in more than half of
15  of the zinc finger domain of MDM2 and human RPL11.
16 ly present in patients carrying mutations in RPL11.
17                            Basic residues in RPL11 are crucial for the stable binding and RPL11 suppr
18 diated depletion of TAK1 or RELA resulted in RPL11-dependent activation of p53 signaling.
19                       Ribosomal protein L11 (RPL11) has been shown to activate p53 by binding to MDM2
20 iation of PRAS40 with ribosomal protein L11 (RPL11).
21 r knockdown of the ribosomal stress mediator RPL11.
22 , APC loss leads to overexpression of c-MYC, RPL11 and RPL5 in mouse colonic tumor cells irrespective
23 1, which can be counteracted by depletion of RPL11.
24 paired by further knocking down the level of RPL11 or RPL5.
25 he effects of RAP-011 in zebrafish models of RPL11 ribosome deficiency.
26 ns such as RPS23, leading to upregulation of RPL11 and stabilization of p53.
27 upregulation of p53 in a manner dependent on RPL11.
28                  However, we found that only RPL11 or RPL5, in a mutually dependent manner, elicit th
29 ssion, which are all features of the RPL5 or RPL11 DBA phenotype.
30  was more pronounced in cells of the RPL5 or RPL11 phenotype.
31 s to either ribosomal protein L7a (RPL7a) or RPL11, the latter an essential component of the IRBC.
32 effect is observed upon depletion of RPS6 or RPL11.
33 nic effect of PRAS40 and identify the PRAS40-RPL11 complex as a promising target for p53-restorative
34 cing an RP-binding mutation in MDM2 prevents RPL11 haploinsufficiency-caused p53 activation and rescu
35 o the discovery that the previously proposed RPL11-dependent mechanism of p53 induction, thought to b
36  prevented by depletion of ribosomal protein RPL11.
37 lymphoma, both p19ARF and ribosomal proteins RPL11 and RPL5 respond to c-MYC activation to induce p53
38 53 dosage by deleting one p53 allele rescues RPL11 haploinsufficiency-induced inhibition of erythropo
39 cent discovery of the ribosomal protein (RP) RPL11 interacting with and inhibiting the E3 ubiquitin l
40  biogenesis checkpoint (IRBC) complex, RPL5, RPL11, and 5S rRNA, are reduced following MYC silencing.
41 enic mutations in three more RP genes, RPL5, RPL11, and RPS7.
42  We also demonstrate that mutations of RPL5, RPL11, or RPS7 in DBA cells is associated with diverse d
43 P) genes, RPS19, RPS24, RPS17, RPL35A, RPL5, RPL11, and RPS7, in about 43% of patients.
44 set of ribosomal proteins (RPs): RPS7, RPL5, RPL11, and RPL23.
45 nexpectedly, there is no change in free RPL5/RPL11 levels, but there is a striking increase in IRBC c
46 ome biogenesis leads the consumption of RPL5/RPL11 into nascent ribosomes, reducing p53 levels and en
47                       Our study reveals that RPL11 forms a stable complex with MDM2 in vitro through
48         Consequently, INZ induces RS and the RPL11/RPL5-MDM2 interaction, activating p53.
49  rescued by wild-type PRAS40, but not by the RPL11-binding-null PRAS40T246A mutant.
50 e found that PRAS40 negatively regulates the RPL11-HDM2-p53 nucleolar stress response pathway and sup
51 ivates the p53 tumour suppressor through the RPL11/RPL5-Mdm2 pathway, with characteristics of nucleol
52 o synchronize the nuclear import of RPs uL5 (RPL11) and uL18 (RPL5), which are both critical for prod
53 also validated the phenotypic impacts of uL5/RPL11 and eL15/RPL15 deficiency on retina development an
54 olecular foundation for better understanding RPL11 inhibition of MDM2 function.
55 al protein, it still remains elusive whether RPL11 inactivates MDM2 via direct action on this zinc fi
56  of the MDM2 zinc finger in association with RPL11, we conducted hydrogen-deuterium exchange mass spe
57  to drastically impair MDM2 interaction with RPL11 and thus escapes the inhibition by this ribosomal
58 Here, we show that RPL5, co-operatively with RPL11, guides the RNA-induced silencing complex (RISC) t
59                      Moreover, patients with RPL11-haploinsufficient Diamond-Blackfan anemia as well