anti-DEK Oncogene (DEK) Antibodies

Human DEK Oncogene (DEK) interaction partners

1. DEK is overexpressed in HGSOCs, and decreasing DEK levels significantly reduces cell viability and tumor growth, resulting in apoptotic cell death.

2. These findings define DEK as an important and multifunctional mediator of homologous recombination.

3. DEK is detected in spontaneously forming neutrophil extracellular traps (NETs) from juvenile idiopathic arthritis patient synovial neutrophils, and DEK-targeted aptamers reduce NETs formation.

4. High DEK proto-oncogene protein (DEK) expression associated with complete response to neoadjuvant chemoradiotherapy.

5. High DEK expression is associated with cervical cancer tumorigenesis and metastasis.

6. The results of the present study demonstrated that EMT of colorectal carcinoma cells was partially mediated by DEK, which likely affected the invasive ability of colorectal carcinoma cells. In addition, cell proliferation and apoptosis were susceptible to DEK silencing.

7. RNA-sequencing proved to be a valuable tool for the detection of a fusion of genes DEK and NUP214 in a leukemia that showed cryptic cytogenetic rearrangement of chromosome band 9q34.

8. DEK overexpression enhanced carcinogenesis, including field cancerization, in OSCC by stimulating the G1 /S phase transition and promoting DNA replication.

9. DEK and LCMR1 were demonstrated to cooperate in the inhibition of apoptosis in lung cancer cells.

10. High DEK expression is associated with breast cancer angiogenesis .

11. our study indicates that DEK expression is required for tumorigenesis and metastasis of hepatocellular carcinoma

12. High DEK expression is associated with melanoma progression.

13. DEK correlates with IL6 expression in HPV16+/p16+ oropharyngeal squamous cell carcinomas (OPSCC).

14. data support a scenario whereby overexpression of the human DEK oncogene reprograms keratinocyte metabolism to fulfill energy and macromolecule demands required to enable and sustain cancer cell growth

15. Decreased DEK expression in plasma cells suggests a potential role of this gene in plasma cell development and lack of detectable DEK protein by IHC could be used as a biomarker for normal and malignant plasma cells

16. Our data indicated DEK plays multiple roles to facilitate tumor growth and maintenance. It can be used as a potential target for astrocytic tumor diagnosis and gene therapy.

17. High DEK expression is associated with pancreatic ductal adenocarcinoma.

18. AP-2a is an important transcription factor of DEK expression, which is correlated with the methylation level of the DEK core promoter in hepatocellular carcinoma .

19. miR-592 targets DEK transcript and suppresses hepatocellular carcinoma cell growth

20. Results find that DEK binds to transcription start sites with a dual role in activation and repression of highly and ubiquitously expressed genes.

Mouse (Murine) DEK Oncogene (DEK) interaction partners

1. These findings define DEK as an important and multifunctional mediator of homologous recombination.

2. DEK is crucial to the development of arthritis in mouse models, thus making it an appropriate target for aptamer-based therapy.

3. DEK was expressed throughout the brain in both sexes, including the medial prefrontal cortex (prelimbic, infralimbic and dorsal peduncular). DEK was also abundant in all amygdalar subdivisions (basolateral, central and medial) and in the hippocampus including the CA1, CA2, CA3, dentate gyrus (DG), ventral subiculum and entorhinal cortex.

4. Dek contributes to esophageal squamous cell carcinoma tumorigenesis at least partially through keratinocyte intrinsic pathways which promote cellular and tumor growth.

5. Data suggests that DEK participates in the process of embryo implantation and might play a role in influencing stromal cell decidualization through mediating cell proliferation, apoptosis and DNA damage.

6. DEK expression during normal hematopoiesis did reveal a relationship with specific cell types implicating a distinct function during myeloid differentiation

7. Studies demonstrate that DEK overexpression, due in part to Ron receptor activation, drives breast cancer progression through the induction of Wnt/beta-catenin signaling.

8. Results highlight a novel function of DEK as a guardian of chromatin by restricting widespread histone access, and in particular by modulating differential H3.3 loading in specific chromatin areas.

9. data demonstrate that DEK stimulates HNSCC cellular growth and identify DeltaNp63 as a novel DEK effector

10. DEK has potent effects on HSCs, HPCs, and hematopoiesis, information of biological and potential clinical interest.

11. The hallmark of translocation in acutte myeloid leukemiaa is the expression of the DEK/CAN fusion protein.

12. DEK is a neuroblastoma tumor antigen.

13. Our conclusion is that DEK could serve as an architectural protein at the promoter or enhancer sites of a subfraction of human genes.

14. Overexpression of the cellular DEK protein promotes epithelial transformation in vitro and in vivo.