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CDKN1A — CEBPA
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Timchenko et al., Nucleic Acids Res 1999
:
We have previously found that loss of
C/EBPalpha in hepatocytes of newborn livers
leads to increased proliferation, to a reduction in
p21 protein levels and to an induction of S phase-specific E2F/p107 complexes
Wu et al., J Virol 2003
:
CCAAT/enhancer binding protein alpha interacts with ZTA and
mediates ZTA induced
p21 ( CIP-1 ) accumulation and G ( 1 ) cell cycle arrest during the Epstein-Barr virus lytic cycle
Tan et al., Cancer Res 2005
(Genetic Predisposition to Disease...) :
Interestingly, only C/EBPalpha positive nodules were positive for nuclear p21, suggesting that
C/EBPalpha may be
required to direct
p21 to the cell nucleus to inhibit growth
Chen et al., J Urol 2013
(Carcinoma, Transitional Cell...) :
RGD-MAP8 was used to determine its effect on signaling pathway
activation ( nuclear factor-?B, NRF2 and
CEBP ), gene expression (
p21 , interleukin-6 and 8, CXCL1, CXCL2 and CCL20 ) and cytotoxicity ( trypan blue exclusion and HMGB1 release ) in human urothelial carcinoma cells
Timchenko et al., Genes Dev 1996
:
Our studies demonstrate that
C/EBPalpha activates
p21/SDI-1 by increasing p21/SDI-1 gene expression and by post-translational stabilization of p21/SDI-1 protein
Cram et al., J Biol Chem 1998
(Liver Neoplasms, Experimental) :
The stimulation of
p21 protein levels and promoter activity, as well as inhibition of CDK2 mediated retinoblastoma protein phosphorylation, by the synthetic glucocorticoid, dexamethasone,
required the expression of
C/EBP alpha
Fussenegger et al., Nat Biotechnol 1998
:
By tetracycline regulated coexpression of p21 and the differentiation factor
CCAAT/enhancer binding protein alpha ( which both stabilizes and
induces p21 ), we have achieved effective cell-cycle arrest