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Dual specificity phosphatase 6

MKP-3, DUSP6, Pyst1
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ERK, MAPK, ERK1, CAN, MKP-1
Papers on MKP-3
ERK Signal Suppression and Sensitivity to CH5183284/Debio 1347, a Selective FGFR Inhibitor.
New
Ishii et al., Kamakura, Japan. In Mol Cancer Ther, Dec 2015
Because the mitogen-activated protein kinase (MAPK) pathway functions downstream of FGFR, we searched for a pharmacodynamic marker of FGFR inhibitor efficacy in a collection of cell lines with the ERK signature and identified dual-specificity phosphatase 6 (DUSP6) as a candidate marker.
MAP kinase phosphatase 3 inhibits brown adipocyte differentiation via regulation of Erk phosphorylation.
New
Lee et al., Taejŏn, South Korea. In Mol Cell Endocrinol, Dec 2015
Here, we identified that MAP kinase phosphatase 3 (MKP3) has a novel role as regulator of brown adipocyte differentiation.
Differential expression profiles and roles of inducible DUSPs and ERK1/2-specific constitutive DUSP6 and DUSP7 in microglia.
New
Choi et al., Seoul, South Korea. In Biochem Biophys Res Commun, Dec 2015
In contrast to the inducible DUSPs which also dephosphorylate p38 MAPK and JNK in the major inflammatory pathways, constitutive DUSP6 and DUSP7 are specific to ERK1/2 and have not been studied in microglia and other immune cells to date.
RAS-MAPK dependence underlies a rational polytherapy strategy in EML4-ALK-positive lung cancer.
New
Impact
Bivona et al., San Francisco, United States. In Nat Med, Sep 2015
Reactivation of the MAPK pathway via either a gain in the number of copies of the gene encoding wild-type K-RAS (KRAS(WT)) or decreased expression of the MAPK phosphatase DUSP6 promoted resistance to ALK inhibitors in vitro, and each was associated with resistance to ALK inhibitors in individuals with EML4-ALK-positive lung adenocarcinoma.
Erk Negative Feedback Control Enables Pre-B Cell Transformation and Represents a Therapeutic Target in Acute Lymphoblastic Leukemia.
New
Impact
Müschen et al., San Francisco, United States. In Cancer Cell, Aug 2015
Studying negative feedback regulation of Erk in genetic experiments at three different levels, we found that Spry2, Dusp6, and Etv5 were essential for oncogenic transformation in mouse models for pre-B acute lymphoblastic leukemia (ALL).
Silencing of DUSP6 gene by RNAi-mediation inhibits proliferation and growth in MDA-MB-231 breast cancer cells: an in vitro study.
Fang et al., Shanghai, China. In Int J Clin Exp Med, 2014
BACKGROUND: Dual-specificity phosphatase 6 (DUSP6) is a negative feedback mechanism of the mitogen-activated protein (MAP) kinase superfamily (MAPK/ERK, SAPK/JNK, p38), that is associated with cellular proliferation and differentiation.
Interleukin-1 loop model for pathogenesis of Langerhans cell histiocytosis.
Review
Yoshino et al., Yonago, Japan. In Cell Commun Signal, 2014
However, phosphorylated ERK (pERK) is rapidly dephosphorylated by dual specificity phosphatase 6 (DUSP6), and limited proliferation is predicted in BRAF mutant cells.
Impacts of activation of the mitogen-activated protein kinase pathway in pancreatic cancer.
Review
Furukawa, Tokyo, Japan. In Front Oncol, 2014
Mutations of KRAS or BRAF and epigenetic abrogation of DUSP6 contribute synergistically to the constitutive activation of MAPK.
Extracellular signal-regulated kinases 1/2 as regulators of cardiac hypertrophy.
Review
Kehat et al., Haifa, Israel. In Front Pharmacol, 2014
These models include direct manipulation of ERK1/2 such as overexpression, mutagenesis or knockout models, manipulations of upstream kinases such as MEK1 and manipulations of the phosphatases that dephosphorylate ERK1/2 such as DUSP6.
Identification of mutant genes with high-frequency, high-risk, and high-expression in lung adenocarcinoma.
Mei et al., Shanghai, China. In Thorac Cancer, 2014
CONCLUSION: For the mutant genes with high-frequency-risk-expression, CTNND1, DUSP6, MDH1 and RBM5 were identified.
[Congenital hypogonadotropic hypogonadism and Kallmann syndrome in males].
Review
Young et al., Cluj-Napoca / Kolozsvár, Romania. In Presse Med, 2014
Mutations in KAL1, FGFR1/FGF8/FGF17, PROK2/PROKR2, NELF, CHD7, HS6ST1, WDR11, SEMA3A, SOX10, IL17RD2, DUSP6, SPRY4, and FLRT3 have been associated with KS but sometimes also with its milder hyposmic/normosmic CHH clinical variant.
Reproduction, smell, and neurodevelopmental disorders: genetic defects in different hypogonadotropic hypogonadal syndromes.
Review
Beckers et al., Liège, Belgium. In Front Endocrinol (lausanne), 2013
KS is associated with mutations in KAL1, FGFR1/FGF8, FGF17, IL17RD, PROK2/PROKR2, NELF, CHD7, HS6ST1, FLRT3, SPRY4, DUSP6, SEMA3A, NELF, and WDR11 genes that are related to defects in neuronal migration.
Decline in miR-181a expression with age impairs T cell receptor sensitivity by increasing DUSP6 activity.
Impact
Goronzy et al., Stanford, United States. In Nat Med, 2012
The defective ERK signaling was caused by the dual specific phosphatase 6 (DUSP6), whose protein expression increased with age due to a decline in repression by miR-181a.
PP2A and DUSP6 are involved in sphingosylphosphorylcholine-induced hypopigmentation.
GeneRIF
Kim et al., Seoul, South Korea. In Mol Cell Biochem, 2012
DUSP6 and PP2A participate in the regulation of melanogenesis
Dual specificity phosphatase 6 as a predictor of invasiveness in papillary thyroid cancer.
GeneRIF
Jo et al., Taejŏn, South Korea. In Eur J Endocrinol, 2012
A link between DUSP6 expression and high-risk features of papillary thyroid carcinoma suggested that DUSP6 is an important independent factor affecting the signaling pathways in established papillary thyroid carcinoma.
Caspase-3 cleavage of DUSP6/MKP3 at the interdomain region generates active MKP3 fragments that regulate ERK1/2 subcellular localization and function.
GeneRIF
Pulido et al., Valencia, Spain. In J Mol Biol, 2012
caspase-3 cleavage of MKP3 down-regulates MKP3 full length and renders active MKP3 fragments, which may participate in novel regulatory pathways controlling the subcellular localization and activation of ERK1/2 during apoptosis.
Increased levels of DUSP6 phosphatase stimulate tumourigenesis in a molecularly distinct melanoma subtype.
GeneRIF
Melton et al., Edinburgh, United Kingdom. In Pigment Cell Melanoma Res, 2012
DUSP6 is important in melanoma and it plays a different role in the distinct subtype of mouse melanoma compared with that in classic human melanoma.
Mutation analysis of MESP2, HES7 and DUSP6 gene exons in patients with congenital scoliosis.
GeneRIF
Qiu et al., Nanjing, China. In Stud Health Technol Inform, 2011
MESP2, HES7 and DUSP6 genes may not be involved in the etiopathogenesis of sporadic and non-syndromic CS in Chinese Han population.
A five-gene signature and clinical outcome in non-small-cell lung cancer.
Impact
Yang et al., Taipei, Taiwan. In N Engl J Med, 2007
We selected five genes (DUSP6, MMD, STAT1, ERBB3, and LCK) for RT-PCR and decision-tree analysis.
MKP3 mediates the cellular response to FGF8 signalling in the vertebrate limb.
Impact
GeneRIF
Izpisúa Belmonte et al., Los Angeles, United States. In Nat Cell Biol, 2003
During fin development, dusp6, a known MAPK/ERK regulator, is induced in the mesoderm by FGF8 signaling, through the PI3/Akt pathway.
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