anti-P53-Regulated Apoptosis-Inducing Protein 1 (TP53AIP1) Antibodies

Human P53-Regulated Apoptosis-Inducing Protein 1 (TP53AIP1) interaction partners

1. Bioinformatic analysis identified TP53AIP1 as a direct target for miR-505.

2. results show that constitutional truncating TP53AIP1 mutations predispose to CMM in the French population

3. Data indicate that p53-regulated apoptosis-inducing protein 1 (p53AIP1) inhibits the proliferation of PC-3M cells, arrests cell cycle at S/G2-M phase, decreases the abilities of invasion and migration and promotes cell apoptosis.

4. These studies indicate the critical role of p53AIP1 under DNA damaging stresses for cell fate determination in rheumatoid arthritis-fibroblast-like synovioctes containing the p53R248Q mutation.

5. Apak competes with p53 for binding to inhibit p53AIP1 expression.

6. large sample size of the combined cohort rejects a high-risk effect greater than 2.2 and indicates a limited role of TP53AIP1 in prostate cancer predisposition

7. p53AIP1 regulates the mitochondrial apoptotic pathway.

8. The expression of Ki67 and p53 in various forms of leukoplakia point to the increasing instability of the genome in parallel with the severity of leukoplakia.

9. expression of the p53 mutant, R248Q, in liver cancer cells may enhance their drug resistance and upregulation of P-glycoprotein activity may contribute to this protective effect.

10. Roscovitine induced up-regulation of p53AIP1 protein and the depolarization of mitochondrial potential.

11. p53AIP1 gene is important for non-small cell lung cancer progression and may be a possible prognostic marker

12. Insufficient expression of p53AIP1 may play a role in gastric carcinogenesis in patients infected with H. pylori infection.

13. Insufficient expression of p53AIP1 may play a role in gastric carcinogenesis in patients infected with H. pylori infection.

14. Data suggest that the combination of p53AIP1 and survivin gene expression may be a powerful tool to stratify subgroups with better or worse prognosis from the variable non-small cell lung cancer population.