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Human Polyclonal DUSP6 Primary Antibody pour ELISA, WB - ABIN545057
Karlsson, Mathers, Dickinson, Mandl, Keyse: Both nuclear-cytoplasmic shuttling of the dual specificity phosphatase MKP-3 and its ability to anchor MAP kinase in the cytoplasm are mediated by a conserved nuclear export signal. dans The Journal of biological chemistry 2004
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Human Monoclonal DUSP6 Primary Antibody pour IF, IHC (p) - ABIN560670
Okudela, Yazawa, Woo, Sakaeda, Ishii, Mitsui, Shimoyamada, Sato, Tajiri, Ogawa, Masuda, Takahashi, Sugimura, Kitamura: Down-regulation of DUSP6 expression in lung cancer: its mechanism and potential role in carcinogenesis. dans The American journal of pathology 2009
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Human Polyclonal DUSP6 Primary Antibody pour IHC - ABIN966015
Groom, Sneddon, Alessi, Dowd, Keyse: Differential regulation of the MAP, SAP and RK/p38 kinases by Pyst1, a novel cytosolic dual-specificity phosphatase. dans The EMBO journal 1996
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Human Polyclonal DUSP6 Primary Antibody pour ELISA, WB - ABIN4334835
Geetha, Mihaly, Stockenhuber, Blasi, Uhrin, Binder, Freissmuth, Breuss et al.: Signal integration and coincidence detection in the mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) cascade: concomitant activation of receptor tyrosine kinases and of ... dans The Journal of biological chemistry 2011
DUSP6 is a tumor suppressor in Non-small cell lung cancer.
The authors that the Dusp6 mRNA, which encodes an ERK1/2 phosphatase, is translationally repressed by 4EHP and a specific miRNA, miR-145.
Oxidative stress, ER stress, and mitochondrial dysfunction induced by Ab could be restored by DUSP6 overexpression. Additionally, the Ab-induced ERK1/2 activation was reversed. In summary, DUSP6 might have a neuroprotective effect on Abeta-induced cytotoxicity, probably via ERK1/2 activation.
A dual specificity phosphatase, DUSP6, that negatively regulates phosphorylation of (P)-ERK is up-regulated in EGFR- or KRAS-mutant lung adenocarcinoma (LUAD), potentially protecting cells with mutations in the RAS signaling pathway, a proposal supported by experiments with DUSP6-specific siRNA and an inhibitory drug
In primary human umbilical vein endothelial cells in which endogenous DUSP6 was ablated, DUSP6 facilitated TNF-alpha-induced ICAM-1 expression and endothelial leukocyte interaction. DUSP6-promoted endothelial inflammation is independent of ERK signaling. Inducible DUSP6 leads to activation of canonical nuclear factor (NF)-kappaB-mediated transcription of ICAM-1 gene in TNF-alpha-stimulated human ECs.
Individuals are carrying DUSP6 rs2279574 AA and AC genotypes associated with an increased risk in developing lung squamous carcinoma in Han Chinese and with advanced NSCLC stages.
DUSP6 expression in skeletal muscle was reduced by 43% just after exercise and remained below pre-exercise level after 2 h recovery.
Data show that oxidative stress and MAP kinase phosphatase 3 (MKP3) inhibition play a critical role in procyanidin B2 3,3''-di-O-gallate (B2G2)-induced cell death in prostate cancer (PCa) cells through sustained activation of both ERK1/2 and AMPKalpha.
High DUSP6 expression is associated with Lung Squamous Cell Carcinoma.
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.
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 V600E mutations and high DUSP6 expression.
PICSAR has a role in promoting cSCC progression via activation of extracellular signal-regulated kinase 1/2 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 SNPs
Suppression of the FOXA1/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.
These results therefore indicate that p53-mediated up-regulation of MKP-3 contributes to the establishment of the senescent cellular phenotype through dephosphorylating ERK1/2
data identify DUSP6 as an important regulator of ERK activity in the setting of muscle growth and muscular dystrophy
DUSP6 is important for TNF-alpha-induced endothelial ICAM-1 expression in aorta and in vein. Genetic deletion of Dusp6 in pulmonary circulation significantly alleviated the susceptibility of mice to lung injury caused by neutrophil recruitment during experimental sepsis induced by TNF-alpha or lipopolysaccharide.
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.
findings suggest that DUSP6 connects TCR signaling to activation-induced metabolic commitment toward glycolysis and restrains TFH cell differentiation via inhibiting IL-21 production.
mitogen-activated kinase phosphatase-3 overexpression resulted in a significant reduction of hypothalamic FoxO1 phosphorylation after insulin stimulation.
DUSP6 may be a useful strategy to prevent neuronal death in neurodegenerative diseases.
This study demonstrates that dusp6 deficiency is a strong genetic factor shaping gut microbiota, and that it confers obesity protection by ameliorating the gut microbiota response to diet-mediated stress.
DUSP6 deficiency has limited impact on the regulation of energy metabolism, but impairs systemic glucose tolerance.
this study shows that CCL2 supports the classical activation of macrophages, with miR-9 mediated down-regulation of Dusp6 and enhanced ERK-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 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+ T-cell activation and differentiation by inhibiting the TCR-dependent ERK1/2 activation and restraining spontaneous colitis in IL-10-deficient mice.
exercised obese mice had a lower expression of MKP-3 and FoxO1/MKP-3 association in the liver
c-Myb plays an important role in H-Ras-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-1/2 and p38.
Depletion of DUSP6 reduced the viability of cancer cell lines and increased the cytotoxicity of EGFR and other targeted inhibitors, and cytotoxic agents.
LH/hCG tightly up-regulates MKP-3 which in turn, dephosphorylates ERK1/2 and drives p21 expression.
dual specificity phosphatases (Dusps) 6 and 14 are up-regulated by activation of beta-catenin in murine liver cells
Constitutively active FOXO1 can rescue the hypoglycemic effect caused by reduced hepatic MKP-3 expression in vivo.
Insulin likely promotes MKP-3 protein degradation through activation of MEK/ERK pathway in liver cells.
loss of dusp6 affects gametogenesis and/or parentally-directed early development.
Dusp6 attenuates Ras/MAPK signaling during regeneration and suppressing Dusp6 can enhance cardiac repair.
Lef1 has a role in regulating Dusp6 in formation of the zebrafish posterior lateral line primordium
During fin development, dusp6, a known MAPK/ERK regulator, is induced in the mesoderm by FGF8 signaling, through the PI3/Akt 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.
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.
MAP kinase phosphatase 3
, dual specificity protein phosphatase 6
, dual specificity protein phosphatase PYST1
, mitogen-activated protein kinase phosphatase 3
, serine/threonine specific protein phosphatase
, MAP kinase phosphatase X17C
, dual specificity phosphatase 6
, Dual specificity protein phosphatase 6
, dual specificity protein phosphatase 6-like