anti-Vaccinia Related Kinase 1 (VRK1) Antibodies

Caenorhabditis elegans (C. elegans) Vaccinia Related Kinase 1 (VRK1) interaction partners

1. vrk-1 has a role in early uterine development in Caenorhabditis elegans

2. By coordinating VRK-1- and PP2A-mediated signaling on BAF, Lem4 and LEM-4L (Y55F3BR.8) controls postmitotic nuclear envelope formation in a function conserved from worms to humans.

3. Genome-wide analysis of germ cell proliferation in C. elegans identifies vrk-1 as a key regulator of cep-1/p53.

4. Data show that expression of the fibroblast growth factor-like protein EGL-17 and its receptor EGL-15 is reduced in vrk-1 mutants, suggesting that VRK-1 might act at least partially through activation of FGF signaling.

Human Vaccinia Related Kinase 1 (VRK1) interaction partners

1. The protective DNA damage response induced by ionizing radiation is impaired by the combination of olaparib with depletion of VRK1, and can be used to reduce doses of radiation and their associated toxicity

2. Our findings showed that circVRK1 suppressed ESCC progression by regulating miR-624-3p/PTEN axis and PI3K/AKT signaling pathway, suggesting the potential therapeutic value of circVRK1 for ESCC.

3. Nonsense mutation of VRK1 gene is associated with distal spinal muscular atrophy.

4. Structural characterization of human vaccinia-related kinases, VRK1 and VRK2, bound to small-molecule inhibitors, has been reported.

5. VRK1-mediated mesenchymal to epithelial transition might facilitate the colonization of distal sites by metastatic breast cancer cells, providing some insight into the frequent association of VRK1 overexpression with breast malignancies and the correlation between VRK1 overexpression and poor clinical outcome.

6. VRK1 and AURKB for a complex that inhibits their kinase activity and H3 histone phosphorylation. In locations where the two kinases interact, there is a different pattern of histone modifications, indicating that there is a local difference in chromatin during mitosis because of the local complexes formed by these kinases and their asymmetric intracellular distribution.

7. that knockdown of VRK1 would inhibit the proliferation of glioma cells

8. this study not only provides a resource for investigating the unidentified functions of VRK1/VRK3, but also an insight into the regulatory roles of VRK1/VRK3 in biological processes.

9. Block the activation of the VRK1 promoter by Sox2.

10. VRK1 and BANF1 yielded AUCs of 0.790 and 0.735, respectively.

11. VRK1 AND VRK2 expression are predictive of tumor response to neoadjuvant chemoradiation therapy in rectal adenocarcinoma.

12. VRK1 was lowly expressed in adherent MM cells and highly expressed in suspended cells. In addition, VRK1 was positively correlated with the proliferation of MM cells by regulating the expression of cell cycle-related protein, such as cyclinD1, CDK2 and p27(kip1).

13. we conclude that VRK1 may be a candidate prognostic biomarker as well as a potential therapeutical target of hepatocellular carcinoma

14. VRK1 may act as a tumor promoter by controlling the level of cell cycle regulators associated with G1/S transition and could potentially serve as a therapeutic target and/or prognostic biomarker for HCC.

15. VRK1 is a novel regulator of CBs dynamics and stability in cell cycle by protecting coilin from ubiquitination and degradation in the proteasome, and propose a model of CB dynamics.

16. VRK1 regulation of NBS1 contributes to the stability of the repair complex and permits the sequential steps in DNA damage response.

17. VRK1 is a novel chromatin component that reacts to its alterations and participates very early in DNA damage response, functioning by itself or in cooperation with Ataxia Telangiectasia Mutated Proteins.

18. VRK1 deficiency in human and mouse leads to downregulation of amyloid-beta precursor protein (APP). APP overexpression rescues the phenotype caused by Vrk1 knockdown, suggesting that VRK1 affects neuronal migration through an APP-dependent mechanism.

19. VRK1 can contribute to make these tumors more resistant to DNA damage-based therapies, such as ionizing radiation or doxorubicin, which is consistent with its association to a poor prognosis in ER positive breast cancer.

20. VRK1 deficiency disrupts nuclear envelope morphology and leads to BAF retention on mitotic chromosomes.

Mouse (Murine) Vaccinia Related Kinase 1 (VRK1) interaction partners

1. Together, these studies of the partial KO Vrk1 mice reveal that even moderately reduced levels of Vrk1 expression result in minor neurological impairment and indicate new neuronal pathways likely involving VRK1.

2. VRK1 self-represses its activity to phosphorylate PXR through cyclin-dependent kinase 2 (CDK2) in high glucose conditions, resulting in the repression of the PCK1 gene. This PXR phosphorylation was also observed in fasting mouse livers. Thus, the VRK1-CDK2-PXR-PP2Calpha-SGK2 pathway can be a novel physiological cell signaling that regulates gluconeogenesis in response to glucose.

3. VRK1 deficiency in human and mouse leads to downregulation of amyloid-beta precursor protein (APP). APP overexpression rescues the phenotype caused by Vrk1 knockdown, suggesting that VRK1 affects neuronal migration through an APP-dependent mechanism.

4. Data suggest that VRK1 is required for both follicle development and oocyte growth in mammalian female reproduction system.

5. Protein kinase Cdelta regulates phosphorylation and down-regulation of Vaccinia-related kinase 1 (VRK1), thereby contributing to cell cycle arrest and apoptotic cell death in a p53-dependent manner.

6. reduction of VRK1 activity causes a delay in meiotic progression during oogenesis

7. VRK1 is required for the proliferation and differentiation of undifferentiated spermatogonia, which are essential for spermatogenic cell maintenance

8. Depletion of VRK1 leads to progressive male infertility as a result of a cessation of spermatogonial proliferation.

9. VRK genes play a role during embryonic development of hematopoiesis

10. can perform the functions of B1 kinase required for vaccinia virus genome replication, most likely due to overlapping specificity for cellular and/or viral substrates

11. These findings collectively support a role of VRK1 as a novel mitotic histone H3 kinase in mammals.