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STAT1 — 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
Baran-Marszak et al., Blood 2004
:
Our results show that imbalance between the antiproliferative/proapoptotic isoform STAT1alpha and the proliferative isoform
STAT1beta is likely to play a crucial role in the regulation of proliferation and apoptosis and that STAT1alpha may
regulate p53 activity and sensitize B cells to fludarabine induced apoptosis
Townsend et al., J Cell Sci 2005
(Cell Transformation, Neoplastic) :
We also show that
STAT-1 is
required for ATM dependent phosphorylation of NBS1 and
p53 but not for BRCA1 or H2AX phosphorylation following DNA damage
Youlyouz-Marfak et al., Cell Death Differ 2008
:
STAT1 activation was obtained in the presence of both the secretion inhibitor brefeldine A and the inhibitor of RNA synthesis, actinomycin D.
p53 dependent
STAT1 activation was reversed by overexpression of MDM2 and siRNAs against p53 ... Genetic analysis of p53 showed that expression of transcriptionally inactive
p53 punctual mutants markedly
increased Y701-STAT1 phosphorylation, and suggests that the p53 DNA binding domain was alternatively involved in STAT1 activation or p53 multimerization
Najjar et al., J Leukoc Biol 2008
:
STAT1alpha , expressed alone, enhanced cell death, potentiated the fludarabine induced apoptosis, and
enhanced the nuclear location, the phosphorylation, and the transcriptional activity of
p53
Chen et al., Oncol Rep 2013
(Carcinoma, Hepatocellular...) :
The
effect of
STAT1 overexpression or silencing on the levels of
p53 and cyclin E expression was determined by quantitative PCR and western blot assays