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Lef1 (show LEF1 ELISA Kits) has a role in regulating Dusp6 in formation of the zebrafish posterior lateral line primordium
During fin development, dusp6, a known MAPK/ERK (show MAPK1 ELISA Kits) regulator, is induced in the mesoderm by FGF8 (show FGF8 ELISA Kits) signaling, through the PI3 (show PI3 ELISA Kits)/Akt (show AKT1 ELISA Kits) pathway.
Mkp3 encodes a feedback attenuator of the FGF pathway, the expression of which is initiated at an early stage so as to ensure correct FGF signaling levels at the time of axial patterning.
Retinoic acid-dependent control of MAP kinase phosphatase-3 is necessary for early kidney development.
Results show that DUSP5 (show DUSP5 ELISA Kits) and DUSP6 mRNA are overexpressed in human PTCs, especially in BRAFV600E mutated papillary thyroid carcinomas (PTCs), and positively control cell migration and invasion.
Authors demonstrate the broad applicability of this recombination-based method and they proved its potential to identify new drug targets via the identification of the tumor suppressor DUSP6 as potential synthetic lethal target in melanoma cell lines with BRAF (show BRAF ELISA Kits) V600E mutations and high DUSP6 expression.
PICSAR has a role in promoting cSCC (show CYP11A1 ELISA Kits) progression via activation of extracellular signal-regulated kinase 1/2 (show MAPK3 ELISA Kits) signaling pathway by downregulating DUSP6 expression
DUSP6 rs2279574 SNPs was not associated with chemoradiotherapy response, whereas tumor regression, weight loss, clinical stage, and cigarette smoking were independent prognostic predictors for these Chinese patients with non-small cell lung cancer.
DNA samples from each patient were genotyped for DUSP6 and TOP2A (show TOP2A ELISA Kits) SNPs
Suppression of the FOXA1 (show FOXA1 ELISA Kits)/DUSP6 signaling pathway may contribute to the development of Hirschsprung disease.
These observations led us to conclude that increased TSH signaling overcomes OIS and is essential for B-RafV600E-induced papillary thyroid carcinogenesis.
Dusp6 expression was higher in progestin-sensitive atypical endometrial hyperplasia groups compared with progestin-resistant groups. After treatment, Dusp6 expression was upregulated in progestin-sensitive groups, but not in progestin-resistant groups.
Our results suggest that DUSP6 gene expression in tumour samples may be a prognostic marker in NSCLC
DUSP6 downregulated the expression of matrix metallopeptidase 3 (show MMP3 ELISA Kits).
DUSP6 deficiency has limited impact on the regulation of energy metabolism, but impairs systemic glucose tolerance.
this study shows that CCL2 (show CCL2 ELISA Kits) supports the classical activation of macrophages, with miR (show MLXIP ELISA Kits)-9 mediated down-regulation of Dusp6 and enhanced ERK (show EPHB2 ELISA Kits)-mediated signal transduction possibly mediating this enhanced pro-inflammatory gene expression
Mitogen-activated protein kinase phosphatase 3 upregulation requires the activation of the Erk1/2 (show MAPK1/3 ELISA Kits) pathway, which correlates with the shutdown of this pathway.
MKP3 could be an important factor in the regulation of brown adipocyte differentiation.
DUSP6 regulates CD4 (show CD4 ELISA Kits)+ T-cell activation and differentiation by inhibiting the TCR-dependent ERK1/2 (show MAPK1/3 ELISA Kits) activation and restraining spontaneous colitis in IL-10 (show IL10 ELISA Kits)-deficient mice.
exercised obese mice had a lower expression of MKP-3 and FoxO1 (show FOXO1 ELISA Kits)/MKP-3 association in the liver
c-Myb (show MYB ELISA Kits) plays an important role in H-Ras (show HRAS ELISA Kits)-induced MKP-3 transcription
Mice lacking MKP-3 protein develop an abnormal persistent state of mechanical allodynia following plantar incision, concurrent with long-lasting spinal phosphorylation of ERK-1 (show MAPK3 ELISA Kits)/2 and p38 (show CRK ELISA Kits).
Depletion of DUSP6 reduced the viability of cancer cell lines and increased the cytotoxicity of EGFR (show EGFR ELISA Kits) and other targeted inhibitors, and cytotoxic agents.
LH/hCG (show CGA ELISA Kits) tightly up-regulates MKP-3 which in turn, dephosphorylates ERK1/2 (show MAPK1/3 ELISA Kits) and drives p21 expression.
The protein encoded by this gene is a member of the dual specificity protein phosphatase subfamily. These phosphatases inactivate their target kinases by dephosphorylating both the phosphoserine/threonine and phosphotyrosine residues. They negatively regulate members of the mitogen-activated protein (MAP) kinase superfamily (MAPK/ERK, SAPK/JNK, p38), which are associated with cellular proliferation and differentiation. Different members of the family of dual specificity phosphatases show distinct substrate specificities for various MAP kinases, different tissue distribution and subcellular localization, and different modes of inducibility of their expression by extracellular stimuli. This gene product inactivates ERK2, is expressed in a variety of tissues with the highest levels in heart and pancreas, and unlike most other members of this family, is localized in the cytoplasm. Two transcript variants encoding different isoforms have been found for this gene.
dual specificity phosphatase 6
, dual specificity protein phosphatase 7
, dual specificity protein phosphatase 6
, MAP kinase phosphatase X17C
, Dual specificity protein phosphatase 6
, dual specificity protein phosphatase 6-like
, MAP kinase phosphatase 3
, dual specificity protein phosphatase PYST1
, mitogen-activated protein kinase phosphatase 3
, serine/threonine specific protein phosphatase