Death-Associated Protein Kinase 3 Proteins (DAPK3)

Human Death-Associated Protein Kinase 3 (DAPK3) interaction partners

1. For the first time, the present study showed that anacardic acid induces cell apoptosis of prostatic cancer through autophagy by ER stress/DAPK3/Akt signaling pathway.

2. Activation of AKT negatively regulates the pro-apoptotic function of DAPK3 in prostate cancer.

3. Methylation of DAPK3 at CpG1 but not CpG2 was lower in men with type 2 diabetes compared with healthy control men. Moreover, a glucose challenge was associated with lower CpG1 and CpG2 methylation in DAPK3 in both men with type 2 diabetes and healthy men.

4. DAPK3 controls proliferation, migration and tumor growth through activation of ERK/c-Myc signaling in lung adenocarcinoma cells.

5. The results revealed mutations caused a significant structural variation in DAPK3, concentrated in flexible loops forming part of the ATP binding pocket which have been associated with very low kinase activity, and the cellular progression towards cancer

6. Cellular and mouse modeling studies show that DAPK3 is a tumor suppressor gene and is important in early development. Also, its expression is downregulated in more aggressive breast cancer relative to less aggressive and normal patient samples.

7. ROCK1 and ZIPK have diverse, but predominantly distinct regulatory functions in vascular SMC and that ROCK1-mediated activation of ZIPK is not involved in most of these functions.

8. DAPK3 plays a central role in preventing miR-17/miR-20a depletion-induced genome instability and in miR-17/miR-20a overexpression-triggered tumor formation.

9. These findings indicated that ZIPK may also be involved in the regulation of the cell cycle in human cells, by interacting with HsCdc14A.

10. findings suggest that ZIPK plays a role in the progression and completion of cytokinesis through MRLC phosphorylation

11. Depletion of ZIPK resulted in impairment of cultured VSMC migration and contraction.

12. ZIPK has a crucial role in regulation of ubiquitination and degradation of the AR

13. Interaction of RhoD and ZIP kinase modulates actin filament assembly and focal adhesion dynamics.

14. ZIPK may serve as a transcriptional regulator of canonical Wnt/beta-catenin signaling through interaction with NLK/TCF4.

15. Results suggest that DAPK3 is a tumor suppressor in which loss-of-function mutations promote increased cell survival, proliferation, cellular aggregation.

16. The NLS2 of human ZIPK functions the nucleus-directing motif, but only upon dephosphorylation of the adjacent T299 residue.

17. Dlk plays a positive role in modulating death-related signaling pathways.

18. These results suggest that ZIPK, in collaboration with Daxx and Par-4, mediates a novel nuclear pathway for apoptosis

19. data identify hZIPK as the unique SMPP-1-associated kinase expressed in human vesicular smooth muscle and support a role for Rho in promoting the hZIPK-MBS interaction

20. The specific expression pattern of TCP10L and interaction with DAPK-3 implies that TCP10L might play crucially important roles in spermatogenesis through its interaction with DAPK-3.

Mouse (Murine) Death-Associated Protein Kinase 3 (DAPK3) interaction partners

1. Cellular and mouse modeling studies show that DAPK3 is a tumor suppressor gene and is important in early development.

2. DAPK3 plays a central role in preventing miR-17/miR-20a depletion-induced genome instability and in miR-17/miR-20a overexpression-triggered tumor formation.

3. The C-terminal domain (NLS2 motif)of ZIPK of murine is nonfunctional for transport.

4. ZIPK may act as a cardiac RLC kinase and thereby affect contractility.

5. murine ZIPK underwent specific divergence from a conserved consensus