anti-Dual Specificity Phosphatase 16 (DUSP16) Anticorps

Human Dual Specificity Phosphatase 16 (DUSP16) interaction partners

1. Chemotherapy increased DUSP9 expression and decreased DUSP16 expression in a HIF1-dependent manner.

2. The crystal structure of JNK1 bound to the catalytic domain of MKP7 at 2.4-A resolution, providing high-resolution structural insight into the FXF-docking interaction, is reported.

3. The DUSP16 ablation leads to a G1/S transition arrest, reduced incorporation of 5-bromodeoxyuridine, enhanced senescence-associated beta-galactosidase activity, and formation of senescence-associated heterochromatic foci.

4. analysis of the interaction of the MAPK binding domain of DUSP16 with p38alpha

5. PPARdelta-mediated messenger RNA stabilization of mitogen-activated protein kinase phosphatase (MKP)-7 was responsible for the GW501516-mediated inhibition of JNK signaling.

6. Data indicate that the activities of phosphoprotein phosphatases MKP5 and MKP7 were determined in the system.

7. Data indicate that LRP6, BCL2L14, DUSP16, CREBL2, and CDKN1B were involed in centromeric (12p11.21-12p13.2) deletion in ETV6-RUNX1 B-cell precursor acute lymphoblastic leukemia (BCP-ALL).

8. MKP-7, a negative regulator of JNK, regulates VCAM-1 expression in activated endothelial cells through IRF-1 but not GATA6.

9. DUSPs 10 and 16 are positive regulators of activation, apparently acting by modulating cross-talk between the p38 and ERK pathways.

10. DUSP16 is a new epigenetically regulated determinant of JNK activation in BL.

11. MKP-7 down-regulates ERK-dependent gene expression by blocking nuclear accumulation of phospho-ERK.

12. context-dependent role for DUSP16 on cell transformation and apoptosis.

13. activation of the ERK pathway strongly blocks JNK activation through stabilization of MKP-7 mediated by phosphorylation

14. MKP7 binds beta-arrestin 2 via amino acids 394-443 of MKP7, the same region that interacts with JIP-1

15. identification of an intricate SDF-1alpha-induced signaling cascade that involves eNOS, JNK3, and MKP7and enhances endothelial migration

Mouse (Murine) Dual Specificity Phosphatase 16 (DUSP16) interaction partners

1. Ablation of Dusp16 enhanced axonal degeneration in response to trophic withdrawal, suggesting that it has a protective function. Moreover, axonal skin innervation was severely reduced while neuronal elimination was increased in the Dusp16 knockout. Mechanistically, Dusp16 negatively regulates the transcription factor p53 and antagonizes the expression of the pro-degenerative factor, Puma.

2. MAPK phosphatase 7 regulates T cell differentiation via inhibiting ERK-mediated IL-2 expression.

3. ADCY5 repression by miR-17 facilitated the translocation of EGFR and MKP7 from membrane into cytoplasmic and mitochondrial fractions.

4. Production of IL-10 and its inhibitory effect on IL-12 production were unaltered in Dusp16tp/tp macrophages.

5. the functional role of DUSP16 in Th1/Th2 balance.

6. the contrasting effects of acute and chronic stress on insulin sensitivity are driven by changes in subcellular distribution of MKP7 and activated JNK

7. DUSP16 is an important regulator of JNK activity and effector functions of CD4 and CD8 T cells.

8. JIP-1 targets MKP-7 to dephosphorylate JNK.