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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
15 , APC loss leads to overexpression of c-MYC, RPL11 and RPL5 in mouse colonic tumor cells irrespective
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
27 We also demonstrate that mutations of RPL5, RPL11, or RPS7 in DBA cells is associated with diverse d
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
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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