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1 RPL11 are crucial for the stable binding and RPL11 suppression of MDM2 activity toward p53.
2                      Interestingly, RPL5 and RPL11 co-resided on c-Myc mRNA and suppressed c-Myc expr
3 by several ribosomal proteins (RPs), such as RPL11 and RPL5, which inhibit MDM2 and activate p53.
4          Several ribosomal proteins, such as RPL11, RPL5, RPL23, RPL26 or RPS7, have been shown to ha
5 vidence for the specific interaction between RPL11 and the zinc finger of MDM2 via hydrophilic residu
6 bearing MDM2(C305F) mutation, which disrupts RPL11- and RPL5-MDM2 binding, with Apc(min/+) mice, whic
7 L23, like depletion of other RPs, except for RPL11 and RPL5, induces a p53 response and that the effe
8 n of the small (e.g., RPS19) or large (e.g., RPL11) ribosomal subunit are found in more than half of
9  of the zinc finger domain of MDM2 and human RPL11.
10 ly present in patients carrying mutations in RPL11.
11                            Basic residues in RPL11 are crucial for the stable binding and RPL11 suppr
12                       Ribosomal protein L11 (RPL11) has been shown to activate p53 by binding to MDM2
13 iation of PRAS40 with ribosomal protein L11 (RPL11).
14 r knockdown of the ribosomal stress mediator RPL11.
15 , APC loss leads to overexpression of c-MYC, RPL11 and RPL5 in mouse colonic tumor cells irrespective
16 1, which can be counteracted by depletion of RPL11.
17 paired by further knocking down the level of RPL11 or RPL5.
18 he effects of RAP-011 in zebrafish models of RPL11 ribosome deficiency.
19 ns such as RPS23, leading to upregulation of RPL11 and stabilization of p53.
20 upregulation of p53 in a manner dependent on RPL11.
21                  However, we found that only RPL11 or RPL5, in a mutually dependent manner, elicit th
22 effect is observed upon depletion of RPS6 or RPL11.
23 nic effect of PRAS40 and identify the PRAS40-RPL11 complex as a promising target for p53-restorative
24 o the discovery that the previously proposed RPL11-dependent mechanism of p53 induction, thought to b
25 lymphoma, both p19ARF and ribosomal proteins RPL11 and RPL5 respond to c-MYC activation to induce p53
26 enic mutations in three more RP genes, RPL5, RPL11, and RPS7.
27  We also demonstrate that mutations of RPL5, RPL11, or RPS7 in DBA cells is associated with diverse d
28 P) genes, RPS19, RPS24, RPS17, RPL35A, RPL5, RPL11, and RPS7, in about 43% of patients.
29 set of ribosomal proteins (RPs): RPS7, RPL5, RPL11, and RPL23.
30                       Our study reveals that RPL11 forms a stable complex with MDM2 in vitro through
31         Consequently, INZ induces RS and the RPL11/RPL5-MDM2 interaction, activating p53.
32  rescued by wild-type PRAS40, but not by the RPL11-binding-null PRAS40T246A mutant.
33 e found that PRAS40 negatively regulates the RPL11-HDM2-p53 nucleolar stress response pathway and sup
34 ivates the p53 tumour suppressor through the RPL11/RPL5-Mdm2 pathway, with characteristics of nucleol
35 olecular foundation for better understanding RPL11 inhibition of MDM2 function.
36 al protein, it still remains elusive whether RPL11 inactivates MDM2 via direct action on this zinc fi
37  of the MDM2 zinc finger in association with RPL11, we conducted hydrogen-deuterium exchange mass spe
38  to drastically impair MDM2 interaction with RPL11 and thus escapes the inhibition by this ribosomal
39 Here, we show that RPL5, co-operatively with RPL11, guides the RNA-induced silencing complex (RISC) t

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