Detail information of PPI "HPI103715"

Interactionp53  <==>  p21
Role & StateRS:0000077,regulator; RS:0000002,activity; RS:0000068,activator;
Interaction TypeIT:0000068,transcription; IT:0000079,suppression; IT:0000271,express; IT:0000078,regulation; IT:0000275,mediate; IT:0000176,suppress; IT:0000114,activation;
Biological ProcessBP:0040007,growth; BP:0007050,cell cycle arrest; BP:0006917,induction of apoptosis; BP:0006915,apoptosis; BP:0007049,cell cycle; BP:0051318,G1 phase;
Biological FunctionBF:0010843,promoter activity;
Subcelluar Location        ---
Detection Method        ---
Reference10874474_4, The activity of cdk2 was inhibited in response to ceramide during this process. p21 protein and mRNA were remarkably induced, while the protein level of p53, known as a transcriptional activator of p21, was not elevated at the same condition. p21 induction was also observed in the Hep3B cells lacking a functional p53 after exposure to ceramide.
Reference12175703_3, In Hep G2 cells, aloe-emodin induced p53 expression and was accompanied by induction of p21 expression that was associated with a cell cycle arrest in G1 phase.
Reference14522900_9, Both ING1 and p53 were able to suppress AFP transcription and cause p21 induction; hSIR2, a negative regulator of the p53 protein, showed the opposite effects on the AFP promoter and, like HDAC1, repressed p21 promoter activity.
Reference16288208_7, Interestingly, expression of AP2 in the absence of radiation repressed p53-mediated induction of p21 and this effect was explained by a reduction in p53 stability induced by AP2alpha overexpression.
Reference16628636_7, Adenoviral vector encoding siRNA against PTTG1 (Ad.PTTG1-siRNA) depleted PTTG1 specifically and efficiently in SH-J1 hepatoma cells, which resulted in activation of p53 that led to increased p21 expression and induction of apoptosis.
Reference19655806_7, The results of luciferase reporter assay indicated that TMT-induced apoptosis seemed to adopt a transcription-dependent route, by activating p53 target genes such as PUMA and p21.
Reference19662644_10, In p53 positive Hep G2 cells, EGCG blocked the progression of cell cycle at G1 phase by inducing p53 expression and further up-regulating p21 expression.
Reference20948430_10, However, p53 is not the only regulator in the stimulation of NCPMF-60 on p21 transcriptional level and posttranscriptional level.
Reference9224400_7, Looking at the whole liver samples, 100% of the HCV-positive patients expressed NOS-2 vs 12.5% in the normal samples. p53 was not detected in either group but there was upregulation of p21 over baseline expression in a number of the HCV-positive patients.
Reference9719464_3, In SK-HEP-1 cells, the addition of C6-ceramide resulted in a dose- and time-dependent growth suppression and DNA fragmentation characteristics of apoptosis. p21 protein was induced during that process, while the protein level of p53, known as a transcriptional activator of p21, was not elevated under the same condition.