anti-PDZ Binding Kinase (PBK) Antikörper

Human PDZ Binding Kinase (PBK) Interaktionspartner

1. Results show that TOPK is highly expressed in hematopoietic tumor cell lines and in primary chronic myeloid leukemia tumors. Its expression induces the kinase activity of BCR/ABL.

2. PBK/TOPK provides stability of an oncoprotein, c-MYC.

3. Study identified PDZ binding kinase as a novel gene up-regulated in peritumoural brain zone of glioblastoma (GBM) with a strong role in conferring aggressiveness, including radio-chemoresistance, thus contributing to recurrence in GBM tumours.

4. Data found that the PBK/TOPK appears to be overexpressed in nucleus or cytoplasm in different colorectal cancer (CRC) patients. Patients with low-scoring and cytoplasmic expression, with negative nuclear expression, and advanced stage, or with low total expression were revealed to have a relatively poor prognosis. PBK/TOPK expression and localization might be used as an independent prognostic marker for CRC patients.

5. a novel interplay between AR and PBK that results in increased AR and ARVs expression that executes AR-mediated growth and progression of aggressive prostate cancer (PrCa), with implications for the development of PBK inhibitors for the treatment of aggressive PrCa.

6. Results found that PBK/TOPK was upregulated and phosphorylated in HTLV1-transformed Tcell lines and ATLLderived Tcell lines. In addition, HTLV1 infection upregulated PBK/TOPK expression in PBMCs, suggesting that this kinase increases the rate of mitosis and expands malignant T cells.

7. Findings strongly suggest that phosphorylated T-lymphokine-activated killer cell-originated protein kinase may be a potent biomarker to determine the outcome of patients with primary central nervous system lymphoma and to develop novel drugs to treat primary central nervous system lymphoma.

8. the expression of TOPK be a novel alternative biomarker to categorize the malignancy of gliomas.

9. CDK1-mediated mitotic phosphorylation of PDZ-binding kinase is involved in cytokinesis and inhibits its oncogenic activity.

10. Data suggest that T-LAK cell-originated protein kinase (TOPK) might play a pivotal role in breast cancer invasion and metastasis.

11. our study provide convincing evidences that FoxM1-regulated PBK exerts oncogenic activities towards HCC via the activation of beta-Catenin pathway.

12. High TOPK expression is associated with liver cancer.

13. The role of T-LAK cell-originated protein kinase directly promotes metastasis of colorectal cancer by modulating p53-related protein kinase.

14. TOPK protein and transcriptional levels of FOXM1 were reduced by TOPK inhibitor treatment.

15. Results indicate that src-family kinase (Src) is a upstream kinase of T-LAK cell-originated protein kinase (TOPK).

16. Upregulation of proteasome subunit beta type 8 PSMB8 and PDZ binding kinase PBK was confirmed by real-time reverse transcription-PCR analysis.

17. MiR-770-5p and PBK levels were inversely correlated in xenograft model mice.

18. TOPK knockdown did not alter radiation response in normal tissues, but significantly enhanced radiosensitivity in cancer cells.These findings have clinical relevance, as elevated TOPK protein expression was associated with poorer clinical outcomes in prostate cancer patients treated with radical radiotherapy. TOPK disruption may cause tumour-specific radiosensitisation in multiple different tumour types.

19. Determined the crystal structure of PBK, which has two phospho-mimicking mutations T9E and T198E. The structural data indicated that PBK may assemble into an inactive dimer in alkaline conditions. Analytical size-exclusion chromatography and analytical ultracentrifugation confirmed that PBK exists in a conformational transition between dimers and monomers at different pH conditions.

20. PBK/TOPK plays a crucial role in tumour malignant potential through its overexpression and highlight its usefulness as a prognostic factor and potential therapeutic target in gastric cancer.

Mouse (Murine) PDZ Binding Kinase (PBK) Interaktionspartner

1. this study shows that remote ischemic postconditioning protects against renal ischemia/reperfusion injury via activation of TOPK/PTEN/Akt signaling pathway

2. T-LAK cell-originated protein kinase (TOPK) phosphorylation of MKP1 protein prevents solar ultraviolet light-induced inflammation through inhibition of the p38 protein signaling pathway.

3. The TOPK protein is expressed mainly in the cytosol of spermatocytes and spermatids, but not in spermatids and spermatogonia in situ.

4. Melanoma cell lines expressing with high levels of TOPK are more resistant to As(3+)-induced apoptosis. Therefore, inhibition of TOPK activity combined with As(3+) treatment may be helpful in the treatment of melanomas.