anti-Tumor Protein P53 Binding Protein 2 (TP53BP2) Antibodies

Human Tumor Protein P53 Binding Protein 2 (TP53BP2) interaction partners

1. p53 activation and XIAP suppression were two independent ways that ASPP2 enhance the sensitivity of chemotherapy.

2. Our data demonstrates that ASPP2kappa plays a distinctive role as an antiapoptotic regulator of the TP53 checkpoint, rendering cells to a more aggressive phenotype as evidenced by proliferation and apoptosis rates - and ASPP2kappa expression results in acquisition of genomic mutations, a first initiating step in leukemogenesis.

3. Study have provided evidence that ASPP2 has an inhibitory influence on triplenegative breast cancer (TNBC) growth and metastasis, and that this may rely on using the PI3K/AKT pathway in a p53independent manner.

4. the abnormal expression of ASPP2 may play an important role for development and metastasis in esophageal squamous cell carcinoma.

5. These findings identify TP53BP2 as a strong candidate causative gene for central nervous system (CNS) defects in 1q41q42 microdeletion syndrome.

6. Results showed that protein expression levels of ASPP2 and P53 were significantly higher in esophageal squamous cell carcinoma tissues than in paired noncancerous tissues.

7. Expression levels of TP53BP2, FBXO28, and FAM53A genes were associated with patient survival specifically in ER-positive, TP53-mutated tumors.

8. These data together implicated a critical impact of MiR-205/ASPP2 on promoting epithelial-mesenchymal transition.

9. ASPP2 is a key regulator of BECN1-dependent autophagy.

10. ASPP2 suppresses invasion, peritoneal dissemination and TGF-beta1-induced EMT by inhibiting Smad7 degradation mediated by ITCH in gastric cancer cells.

11. Our results suggest that Gal-1 and ASPP2 functionally compete in nanocluster for active Ras on the plasma membrane. ASPP2 dominates the biological outcome, thus switching from a Gal-1 supported growth-promoting setting to a senescence inducing and stemness suppressive program in cancer cells. Our results support Ras nanocluster as major integrators of tumour fate decision events.

12. ASPP2 suppresses p53 target gene transactivation, promoter occupancy, and endogenous p53 target gene expression in response to DNA damage

13. In this study, in recombinant adenovirus-ASPP2-infected HepG2 cells, ASPP2 overexpression induces amphiregulin expression in a p53-dependent manner

14. Downregulated expression of ASPP2 is associated with hepatocellular carcinoma.

15. miR-548d-3p/TP53BP2 pathway is critically involved in the proliferation and apoptosis of breast cancer cells and may be new therapeutic target of breast cancer cells.

16. ASPP1/2-PP1 complexes are required for chromosome segregation and kinetochore-microtubule attachments.

17. ASSP2 expression is lower in cancerous tissues and decreased ASPP2 lead to higher cancer cells proliferation and autophagic flux, which contribute to the gemcitabine resistance.

18. this study revealed a novel function of ASPP2 in modulating autophagy and apoptosis.

19. ASPP2 may participate in the lipid metabolism of non-alcoholic steatohepatitis and attenuate liver failure.

20. These results identify previously uncharacterized regions distributed throughout the protein sequence of ASPP2 as determinants of CagA binding, providing mechanistic insight into apoptosis reprogramming by CagA.

Zebrafish Tumor Protein P53 Binding Protein 2 (TP53BP2) interaction partners

1. These findings uncover a novel role of Aspp2 in regulating vertebrate embryonic growth.

Mouse (Murine) Tumor Protein P53 Binding Protein 2 (TP53BP2) interaction partners

1. These results suggest that ASPP2 plays an important role in p53-mediated neuronal apoptosis under gp120 stress.

2. These findings identify TP53BP2 as a strong candidate causative gene for central nervous system (CNS) defects in 1q41q42 microdeletion syndrome.

3. SPP2 dominates the biological outcome, thus switching from a Gal-1 supported growth-promoting setting to a senescence inducing and stemness suppressive program in cancer cells. Our results support Ras nanocluster as major integrators of tumour fate decision events.

4. ASPP2 may participate in the lipid metabolism of non-alcoholic steatohepatitis and attenuate liver failure.

5. ASPP2 prevents beta-catenin from transactivating ZEB1 directly by forming an ASPP2-beta-catenin-E-cadherin ternary complex

6. findings suggest that the identified STAT1/ASPP2 pathway may connect tumor suppression and cell polarity to neuroinflammation

7. our studies demonstrate the role of Siah2 in regulation of tight junction integrity and cell polarity under hypoxia, through its regulation of ASPP2 stability.

8. ASPP2 is a tumor suppressor that suppresses squamous cell carcinoma via inflammatory signaling through NF-kappaB-mediated repression of p63.

9. Our study demonstrates a novel role for ASPP1 and ASPP2 in the death of retinal ganglion cells.

10. regulates epithelial cell polarity in cooperation with PAR-3 to form an active PAR complex

11. Consistent with its role in cell polarity, ASPP2 influences interkinetic nuclear migration and lamination during CNS development.

12. ASPP2 is a haploinsufficient tumor suppressor that shares overlapping function(s) with p53 in mouse development and tumor suppression.

13. 53BP2S interacts and modulates the insulin signals mediated by insulin receptor substrates.

14. ASPP2(+/-) mice appeared developmentally normal, they displayed an increased incidence of a variety of spontaneous tumors as they aged

15. [review] potential ASPP2-mediated pathways found by gene expression profiling