anti-Dual Specificity Phosphatase 5 (DUSP5) Antibodies

Zebrafish Dual Specificity Phosphatase 5 (DUSP5) interaction partners

1. Dusp-5 and Snrk-1 control angioblast populations in the lateral plate mesoderm with Dusp-5 functioning downstream of Snrk-1

Human Dual Specificity Phosphatase 5 (DUSP5) interaction partners

1. DUSP5 functions in the feedback inhibition of ERK1/2 signaling in response to TNFalpha, which resulted in increased inflammatory gene expression.

2. Data show that dual specificity phosphatase 5 (DUSP5) is a downstream target of p68 RNA helicase (p68).

3. Methylation the DUSP5 gene promoter can serve as an additional means of identifying CIMP-high colorectal cancers.

4. DUSP5 expression in skeletal muscle was ninefold higher immediately after exercise and returned to pre-exercise level within 2 h.

5. Findings indicate that zinc-finger protein X-linked (ZFX) promotes colorectal cancer (CRC) progression by suppressing dual specificity phosphatase 5 (DUSP5) expression and suggest that ZFX is a prognostic biomarker and potentially useful therapeutic target in stage II/III CRC patients.

6. Results show that DUSP5 and DUSP6 mRNA are overexpressed in human PTCs, especially in BRAFV600E mutated papillary thyroid carcinomas (PTCs), and positively control cell migration and invasion.

7. role of the secondary binding site in assembling the DUSP5-pERK pre-reactive complex was further demonstrated by molecular dynamics simulations that showed that the remote C197-C219 disulfide linkage controls the structure of the secondary binding pocket based on its redox state (i.e., disulfide/dithiol) and, in turn, the enzymatic activity of DUSP5

8. The DUSP5 S147P protein is hypoactive compared to the DUSP5 wild-type protein.

9. Data indicate that cells from Burkitt's lymphoma, leukemia, neuroblastoma and Ewing sarcoma showed a higher dual-specificity phosphatase 5 pseudogene 1 (DUSP5P1)/dual specificity phosphatase 5 (DUSP5 ratio than normal cells.

10. DUSP1, DUSP4, and DUSP5 differentially modulate endothelial MAPK signaling pathways downstream of Tie-2 receptors.

11. DUSP5 methylation may serve as a prognostic marker for gastric cancer (GC), but this requires validation in a larger set of GC samples.

12. Studies indicate that dual-specificity MAP kinase phosphatases (MKPs) DUSP6/MKP-3 and DUSP5 are localized in the cytoplasm and nuclear compartments.

13. DUSP5 and DUSP6 selectively control ERK pathway activity and proliferation.

14. the differential up-regulation of MKP3 by Ets2 and of DUSP5 by c-Jun may converge in similar functional roles for these MAP kinase phosphatases in the growth arrest versus proliferation decisions of breast cancer cells

15. In FD-Fms cells, overexpression of human DUSP5 increased M-CSF-dependent proliferation & decreased differentiation. Overexpression in multipotent EGER-Fms cells increased M-CSF-induced proliferation & caused granulocytic, not macrophage, differentiation.

16. DUSP5 is a direct target of p53.

17. DUSP5 inactivates ERK2 and causes both nuclear translocation and sequestration of inactive ERK2.

18. the crystal structure of the catalytic domain of DUSP5 in an active conformation.

19. These results suggest the existence of an ERK1/2-driven negative feed-back regulation of ERK5 signaling in epidermal growth factor-stimulated HK-2 cells, which is mediated by MKP-3, DUSP5 and/or MKP-1.

20. proper regulation of DUSP5 activity is critical for normal immune system development, IL-2 actions, and tolerance

Mouse (Murine) Dual Specificity Phosphatase 5 (DUSP5) interaction partners

1. 257 genes among 55,681 genes examined were up-regulated after 30-min treatment of GT1-7 cells with GnRH. These up-regulated genes included four dual-specificity MAPK phosphatases (DUSPs), DUSP1, DUSP2, DUSP5, and DUSP6.

2. feedback interactions within the ERK pathway can regulate cell proliferation and transformation, and suggest oncogene-specific roles for DUSP5 in controlling ERK signaling and cell fate

3. This study shown that the Dusp15 promoter is sufficient for oligodendroglial expression and jointly activated by Sox10 and Myrf in an oligodendroglial cell line.

4. Dual specificity phosphatase 5 knockout (Dusp5-/- ) T cells display increased proliferation, increased apoptosis, and altered metabolic profiles, suggesting that DUSP5 is a pro-survival protein in T cells.

5. DUSP5 phosphatase is regulated at the transcriptional level by the MAPK pathway and that serum responsive element is involved in the regulation of this early response gene.

6. results suggest an in vivo role for DUSP5 as a tumor suppressor by modulating the oncogenic potential of activated Ras in the epidermis

7. After SSH between cDNA libraries from FD-Fms cells stimulated by M-CSF in the presence or the absence of U0126, we isolated DUSP5. DUSP5 expression is induced by M-CSF in various myeloid cells & acts as a specific negative-feedback regulator of ERK1/2.

8. proper regulation of DUSP5 activity is critical for normal immune system development, IL-2 actions, and tolerance