◀ Back to CDKN1A
CDKN1A — POU4F1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Direct p53 effectors:
POU4F1 (POU4F1)
→
p21CIP1 (CDKN1A)
(transcription, activates)
Le Cam et al., Cell 2006, Harms et al., Cancer Res 2007, Shi et al., Mol Cell 2007, Das et al., Cell 2007, Xu et al., J Biol Chem 2007, Gamper et al., Mol Cell Biol 2008, el-Deiry et al., Cancer Res 1995
Evidence: mutant phenotype, reporter gene, physical interaction
-
NCI Pathway Database Direct p53 effectors:
POU4F1 (POU4F1)
→
p21CIP1 (CDKN1A)
(transcription, activates)
Harms et al., Cancer Res 2007, Shi et al., Mol Cell 2007, Das et al., Cell 2007, Xu et al., J Biol Chem 2007, Gamper et al., Mol Cell Biol 2008, Tang et al., Cell 2008, el-Deiry et al., Cancer Res 1995
Evidence: mutant phenotype, reporter gene, physical interaction
-
NCI Pathway Database Direct p53 effectors:
POU4F1 (POU4F1)
→
p21CIP1 (CDKN1A)
(transcription, activates)
Harms et al., Cancer Res 2007, Shi et al., Mol Cell 2007, Das et al., Cell 2007, Xu et al., J Biol Chem 2007, Gamper et al., Mol Cell Biol 2008, Jansson et al., Nat Cell Biol 2008, el-Deiry et al., Cancer Res 1995
Evidence: mutant phenotype, reporter gene, physical interaction
Text-mined interactions from Literome
Perez-Sanchez et al., Nucleic Acids Res 2002
:
Distinct promoter elements mediate the co-operative
effect of
Brn-3a and p53 on the
p21 promoter and their antagonism on the Bax promoter ... Thus,
Brn-3a inhibits activation of the Bax promoter by p53 but
enhances the ability of p53 to activate the
p21 promoter ... In contrast, a minimal
p21 promoter is
activated by
Brn-3a and such activation can not be abolished without abolishing basal promoter activity
Gascoyne et al., Oncogene 2004
:
Furthermore, overexpression of EWS/Fli-1 but not EWS or Fli-1 inhibits Brn-3a associated growth arrest and neurite outgrowth in neuronal cells, and specifically inhibits
Brn-3a dependent
activation of
p21 and SNAP-25 transcription