anti-Ubiquitin Specific Peptidase 28 (USP28) Antibodies

Human Ubiquitin Specific Peptidase 28 (USP28) interaction partners

1. The authors identified 53BP1 and USP28 as essential components acting upstream of p53, evoking p21-dependent cell cycle arrest in response not only to centrosome loss, but also to other distinct defects causing prolonged mitosis.

2. USP28 controls activation of both the TP53 branch and the GATA4/NFkB branch that controls the senescence-associated secretory phenotype (SASP)

3. 53BP1-USP28 cooperation is essential for normal p53-promoter element interactions and gene transactivation-associated events, yet dispensable for 53BP1-dependent DNA double-strand repair regulation.

4. USP28-53BP1-p53-p21 signaling pathway is also required to arrest cell growth after a prolonged prometaphase.

5. analysis of centrinone resistance identified a 53BP1-USP28 module as critical for communicating mitotic challenges to the p53 circuit and TRIM37 as an enforcer of the singularity of centrosome assembly.

6. These results showed that USP28 is overexpressed in human glioblastomas and it contributes to glioma tumorigenicity.

7. Data indicte that deubiquitinating enzyme USP28 was targeted by microRNA miR-4295.

8. findings provide a first insight into understanding how the enzymatic activity of Usp28 is regulated by its non-catalytic UBR and endogenous ligands.

9. Dual regulation of Fbw7 activity by Usp28 is a safeguard mechanism for maintaining physiological levels of proto-oncogenic Fbw7 substrates, which is equivalently disrupted by loss or overexpression of Usp28.

10. identified Usp28 as a c-MYC target gene highly expressed in colorectal cancers, which indicates that USP28 and c-MYC form a positive feedback loop that maintains high c-MYC protein levels in tumors

11. USP28 has a chain preference activity for Lys(11), Lys(48), and Lys(63) diubiquitin linkages

12. Usp28 expression was indentified as a independent predictors of survival (P = 0.001) and potentially valuable in prognostic evaluation of bladder cancer

13. Study reveals a critical mechanism underlying the epigenetic regulation by USP28.

14. USP28 is not a critical factor in double-strand break metabolism and is unlikely to be an attractive target for therapeutic intervention aimed at chemotherapy sensitization.

15. USP28 gene expression is down regulated by oxidative stress through the mediation of reactive oxygen species

16. A new pathway that could be targeted at the level of GSK-3, Fbw7, or USP28 to influence HIF-1alpha-dependent processes like angiogenesis and metastasis.

17. molecular cloning of USP28 & characterization of alternatively spliced products and tissue-specific isoforms

18. Using a human cell line that faithfully recapitulated the Chk2-p53-PUMA pathway, we show that USP28 is required to stabilize Chk2 and 53BP1 in response to DNA damage.

19. High expression levels of USP28 are found in colon and breast carcinomas, and stabilization of MYC by USP28 is essential for tumour-cell proliferation.

20. Usp28 dissociates from Fbw7alpha in response to UV irradiation, providing a mechanism how Fbw7-mediated degradation of Myc is enhanced upon DNA damage.

Mouse (Murine) Ubiquitin Specific Peptidase 28 (USP28) interaction partners

1. In mice, an unusually direct antagonism between an E3 ligase and a deubiquitinase, Fbw7 and Usp28, modulate intestinal homeostasis and cancer.

2. Dual regulation of Fbw7 activity by Usp28 is a safeguard mechanism for maintaining physiological levels of proto-oncogenic Fbw7 substrates, which is equivalently disrupted by loss or overexpression of Usp28.

3. identified Usp28 as a c-MYC target gene highly expressed in colorectal cancers, which indicates that USP28 and c-MYC form a positive feedback loop that maintains high c-MYC protein levels in tumors