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RPL26 — TP53
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Takagi et al., Cell 2005
(Cell Transformation, Neoplastic) :
These findings demonstrate the importance of increased translation of p53 in DNA-damage responses and suggest critical
roles for
RPL26 and nucleolin in affecting
p53 induction
Ofir-Rosenfeld et al., Mol Cell 2008
:
We now report that Mdm2
regulates p53 levels also by targeting
ribosomal protein L26
Lindström et al., PloS one 2010
(Brain Neoplasms...) :
In these settings,
RPL11 was critical for maintaining p53 protein stability but was not strictly
required for
p53 protein synthesis
Sun et al., J Biol Chem 2010
:
Perturbation of
60 S ribosomal biogenesis
results in ribosomal protein L5- and L11 dependent
p53 activation
Chen et al., Genes Dev 2010
:
Optimal induction of
p53 protein after DNA damage
requires RPL26 mediated increases in p53 mRNA translation
Chen et al., J Biol Chem 2012
:
Excessive RPL26 disrupts NCL dimerization, and point mutations in the NCL interacting region of RPL26 reduce NCL-RPL26 interactions and attenuate both
RPL26 binding to human p53 mRNA and
p53 induction by RPL26 ... These observations suggest a model in which the base pairings in the p53 UTR interaction regions are critical for both translational
repression and stress induction of
p53 by NCL and
RPL26 , respectively, and that disruption of a NCL-NCL homodimer by RPL26 may be the switch between translational repression and activation after stress