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TP53 — USO1
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Li et al., Oncogene 2006
:
Consistent with this observation, we demonstrate that loss of
p53 leads to the stabilization of
TA-p63-gamma that is reversible by ectopic p53
Jacobs et al., Neuron 2005
:
While both TAp63 and p53 induce similar apoptotic signaling proteins and require BAX expression and function for their effects,
TAp63 induces neuronal death in the absence of p53, but
p53 requires coincident p63 expression for its proapoptotic actions
Malaguarnera et al., Mol Cancer Res 2008
(Thyroid Neoplasms) :
Second, a
TAp73alpha mutant ( G264W ), which is devoid of DNA binding capability, is still able to
increase p53 protein levels by competing with p53 for Mdm2 protein binding ... Taken together, these results indicate that in thyroid cancer cells,
TAp73alpha is able to
increase p53 protein level and function by interfering with Mdm2 mediated p53 degradation
Zhang et al., PloS one 2012
(Ovarian Neoplasms) :
Like
p53 , the transcriptionally active
TAp73 can
mediate cellular response to chemotherapeutic agents in human cancer cells by up-regulating the expressions of its pro-apoptotic target genes such as PUMA, Bax, NOXA