anti-Dual Specificity Phosphatase 9 (DUSP9) Anticorps

Human Dual Specificity Phosphatase 9 (DUSP9) interaction partners

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

2. SNP rs5945326 in DUSP9 gene may be not associated with the risk of gestational diabetes mellitus

3. The results of this study, combined with previous studies, suggested that therapeutic intervention to increase the expression or activity of DUSP9 may enable the activation of anti-proliferation signals in malignant cells.

4. A possible use for DUSP9 as CIMP marker.

5. DUSP9 protein levels were markedly suppressed in severe pre-eclampsia, but not in severe IUGR. This suppression might be attributable to the prolonged hypoxic conditions found in pre-eclampsia.

6. The DUSP9 locus is a common susceptibility locus for type 2 diabetes across different ethnicities, and 6 loci identified in South Asian genome-wide association studies also have significant effect on susceptibility to Japanese type 2 diabetes.

7. decreased expression of DUSP-9 is associated with poor prognosis in ccRCC.

8. DUSP9/MKP-4 is a bona fide target of PKA signaling and attenuation of DUSP9/MKP-4 function can mediate cross-talk between the PKA pathway and MAPK signaling through both ERK1/2 and p38alpha in vivo

9. 2.7 A resolution crystal structure of the catalytic domain of MKP-4 (MKP-4C) is presented

10. microtubule disruption by MKP4 provides a novel mechanism for tumor suppression by a cytosolic MKP

Mouse (Murine) Dual Specificity Phosphatase 9 (DUSP9) interaction partners

1. Data demonstrate the epigenetic similarity of sex-matched ESCs and EGCs and identify DUSP9 as a regulator of female-specific hypomethylation.

2. we have identified in this study the MAPK phosphatase Dusp9 as selectively expressed in mouse pDCs.

3. these findings identify DUSP9 as a critical mediator of BMP signaling to control appropriate ERK activity critical for ESC fate determination.

4. DUSP9/MKP-4 is a bona fide target of PKA signaling and attenuation of DUSP9/MKP-4 function can mediate cross-talk between the PKA pathway and MAPK signaling through both ERK1/2 and p38alpha in vivo

5. negatively regulates insulin signaling and, consequently, may contribute to the pathogenesis of insulin resistance

6. DUSP9/MKP-4 is essential for placental organogenesis but is otherwise dispensable for mammalian embryonic development.

7. microtubule disruption by MKP4 provides a novel mechanism for tumor suppression by a cytosolic MKP

8. Data show that Dusp9 transcripts is expressed in partially overlapping patterns that correspond to regions of active FGF signaling, suggesting combinatorial roles in negative regulation of this pathway during ear development.

9. Dusp9 has a protective effect against the development of insulin resistance through its ability to dephosphorylate and inactivate crucial mediators of stress-induced insulin resistance, such as ERK and JNK