anti-Dual Specificity Phosphatase 1 (DUSP1) 抗体

Human Dual Specificity Phosphatase 1 (DUSP1) interaction partners

1. Data suggest that high circulating DUSP1 levels reflect a chronic subclinical inflammation and underlying residual cardiovascular disease risks even in the treated population.

2. A2B adenosine receptor in MDA-MB-231 breast cancer cells diminishes ERK1/2 phosphorylation by activation of MAPK-phosphatase-1

3. Study reports the crystal structure of the human DUSP1 catalytic domain at 2.49 A resolution. The protein was crystallized as a (maltose-binding protein) MBP fusion protein in complex with a monobody that binds to MBP. Sulfate ions occupy the phosphotyrosine and putative phosphothreonine binding sites in the DUSP1 catalytic domain.

4. The molecular structure of DUSP1 crystallized as MBP fusion protein has been reported.

5. High DUSP1 expression is associated with apatinib resistance by activating the MAPK pathway in gastric cancer.

6. SIN attenuated LPS-induced inflammatory injury by regulation of miR-101, MKP-1 and JNK pathway.

7. miR-202-3p is upregulated in type 1 gastric neuroendocrine neoplasms (g-NENs) lesions and might play important roles in the pathogenesis of type 1 g-NENs by targeting DUSP1.

8. Downregulation of the expression of DUSP1 or protein phosphatase 1 led to a decline in the beta2adrenergic receptormediated dephosphorylation of ERK1/2.

9. the expression of DUSP1 was lower in OA FLSs than in normal FLSs, and DUSP1 may inhibit the expression of OA-associated mediators, MMP-13 and COX-2, by suppressing the activation of p38 MAPK and JNK pathways in OA FLSs.

10. Curcumin suppressed CXCL5 expression by direct inhibition of IKKbeta phosphorylation, and inhibition of p38 MAPK via induction of negative regulator MKP-1.

11. MKP-1 is a redox-regulated master controller of monocyte function and macrophage phenotype. (Review)

12. We propose a signaling cascade involving ARID1A, GADD45B and DUSP1 as mediators of the romidepsin effects in GCC cells.

13. this work indicates that suppression of JNK1/2 activity by MKP-1 maintains PARP-1 levels and suggests that MKP-1-mediated cisplatin resistance can be bypassed by PARP-1 inhibition.

14. Mean morning and evening DUSP1 mRNA levels showed significant increase during Ramadan compared to Shabaan, however, its diurnal rhythm was maintained. Morning IL-1alpha mRNA expression remained significantly higher than in the evening during Ramadan, but was markedly decreased compared to Shabaan.

15. Methylation-mediated silencing of the DUSP-1 promoter does not appear to be associated with reduced expression, indicating the involvement of other factors in specific suppression of DUSP-1 in diabetes-associated cardiac hypertrophy.

16. Increased MAP2K6, MAP4K3, and DUSP1 gene expressions in post-chemotherapy samples indicate a poor clinical outcome in osteosarcoma patients.

17. The aim of this review is to shed light on the role of four different phosphatases (PTEN, PP2A, CDC25 and DUSP1) in five different solid tumors (breast cancer, lung cancer, pancreatic cancer, prostate cancer and ovarian cancer), in order to better understand the most frequent and aggressive primary cancer of the central nervous system, glioblastoma.

18. Dual-specific phosphatase (DUSP1) was found to inhibit gallbladder cancer (GBC) cell proliferation, migration and invasion.

19. The results presented here emphasize the importance of MKP-1 as a mediator of therapeutic effects of glucocorticoids in inflammatory lung diseases as well as its potential as a novel anti-inflammatory drug target.

20. we show that IL-1 induces robust p38a activation both in the nucleus and in the cytoplasm/membrane.Following stimulation, p38a activity returns to a basal level in absence of receptor degradation. While nuclear pulse is controlled by MKP1 through a negative feedback to pp38, its basal activity is controlled by both TAB1 and MKP1 through a positive feedback loop.

Cow (Bovine) Dual Specificity Phosphatase 1 (DUSP1) interaction partners

1. MKP-1 is the specific phosphatase induced by AngII and involved in the negative feedback mechanism ensuring adequate ERK1/2-mediated aldosterone production in response to the hormone.

Mouse (Murine) Dual Specificity Phosphatase 1 (DUSP1) interaction partners

1. Data show that dual specificity phosphatase 1 (MKP-1) was a pivotal feedback regulator controlling both MAP kinases and NF-kappaB pathway.

2. Data suggest a critical role for MAP kinase phosphatase 1 (MKP-1) in the regulation of skin inflammation.

3. this study shows that Mkp-1 protects mice against toxin-induced liver damage by promoting the Nrf2 cytoprotective response

4. Results provide evidence that Mkp-1 plays an important role in the regulation of both the inflammatory response and metabolic programming during host defense against bacterial infection.

5. Results indicate that the upregulation of anterior cingulate cortex (ACC, areas 24a and 24b) MKP-1 is necessary for the expression of depressive symptoms induced by chronic pain, chronic stress, and optogenetic activation of the ACC.

6. The results suggested that DUSP1 gene silencing promoted the release of proinflammatory cytokines through activation of the MAPK signaling pathway in mice with acute pancreatitis.

7. The cardiac ischemia/reperfusion injury - induced DUSP1 deficiency promoted the activation of JNK which upregulated the expression of the mitochondrial fission factor (Mff).

8. Study demonstrates that MKP-1 serves as a master-regulator of macrophage phenotype and function and its dysregulation by metabolic stress may be a major contributor to atherogenesis and the progression of atherosclerotic plaques.

9. FAM3D inhibits glucagon secretion via MKP1-dependent suppression of ERK1/2 signaling.

10. these data show that MKP-1 is an important endogenous suppressor of innate immune responses involved in the regulation of blood-testis barrier barrier dynamic

11. MKP-1 regulates IL-1beta production through stabilization of HIF-1alpha. The induction of HIF-1alpha protein in MKP-1 deficiency is partly due to p38MAPK activation in response to LPS.

12. this work identifies a previously unrecognized role for DUSP1 in regulating autophagy.

13. c-FOS and DUSP1 expression levels determine the threshold of tyrosine kinase inhibitor (TKI) efficacy, such that growth-factor-induced expression of c-FOS and DUSP1 confers intrinsic resistance to TKI therapy in a wide-ranging set of leukemias.

14. PTHrP counteracts the pro-apoptotic actions of reactive oxygen species by a mechanism dependent on MKP1-induced dephosphorylation.

15. A2AR signaling regulates both basal and LPS-induced DUSP1 levels in macrophages via activating the adenylate cyclase pathway.

16. these data suggest an important role for DUSPs in regulating MAPK dephosphorylation, with an emphasis on DUSP1, during early adipogenesis

17. Loss of DUSP1 does not cause changes in cartilage degeneration and gait in a mouse model of spontaneous osteoarthritis at 21 months of age.

18. Nr4a1 induction is dependent on ERK1/2 and that MKP-1 negatively regulates this induction.

19. MKP-1 negatively regulates chemokine-driven osteoclast formation and subsequent bone resorption in response to LPS stimulation

20. results suggest that the p38alpha-MKP-1 signaling axis links IL-17R signaling in tissue-resident cells to autoimmune inflammation dependent on infiltrating T(H)17 cells.

Pig (Porcine) Dual Specificity Phosphatase 1 (DUSP1) interaction partners

1. Agonist stimulation of vascular smooth muscle increases PKC activity, which, in turn, increases MKP-1 activity and maintains MAPK1 activity at submaximal values.