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Dual specificity phosphatase 16

MKP-7, DUSP16, MAPK phosphatase 7
This gene encodes a mitogen-activated protein kinase phosphatase that 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. The encoded protein specifically regulates the c-Jun amino-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) pathways.[provided by RefSeq, May 2010] (from NCBI)
Top mentioned proteins: JNK, MAPK, AP-1, p38, V1a
Papers on MKP-7
DUSP16 ablation arrests the cell cycle and induces cellular senescence.
New
Hui et al., Shanghai, China. In Febs J, Dec 2015
In particular, we showed that DUSP16 ablation leads to a G1 /S transition arrest, reduced incorporation of 5-bromodeoxyuridine, enhanced senescence-associated β-galactosidase activity, and formation of senescence-associated heterochromatic foci.
MAPK phosphatase 7 regulates T cell differentiation via inhibiting ERK-mediated IL-2 expression.
New
Dong et al., Beijing, China. In J Immunol, May 2015
In this study, we show that MKP7, also known as dual-specificity phosphatase 16, was required for CD4(+) T cell responses in vivo.
Discovery of novel DUSP16 phosphatase inhibitors through virtual screening with homology modeled protein structure.
Ryu et al., Seoul, South Korea. In J Biomol Screen, 2014
Recently, dual-specificity phosphatase 16 (DUSP16) emerged as a promising therapeutic target protein for the development of anti-atherosclerosis and anticancer medicines.
Structure of Mycobacterium smegmatis Eis in complex with paromomycin.
Suh et al., Seoul, South Korea. In Acta Crystallogr Sect F Struct Biol Commun, 2014
Both Mtb Eis and Msm Eis are active as aminoglycoside acetyltransferases, while only Mtb Eis functions as an N(ℇ)-acetyltransferase to acetylate Lys55 of dual-specificity protein phosphatase 16 (DUSP16)/mitogen-activated protein kinase phosphatase 7 (MKP-7), leading to the suppression of host immune responses.
NADPH oxidase-generated reactive oxygen species are required for stromal cell-derived factor-1α-stimulated angiogenesis.
Patterson et al., Chapel Hill, United States. In Arterioscler Thromb Vasc Biol, 2014
Here, we identified that NOX5 is the dominant NOX required for SDF-1α-induced c-Jun N-terminal kinase 3 activation and that NOX5 and MAP kinase phosphatase 7 (MKP7; the c-Jun N-terminal kinase 3 phosphatase) associate with one another but decrease this interaction on SDF-1α treatment.
Gene trap mice reveal an essential function of dual specificity phosphatase Dusp16/MKP-7 in perinatal survival and regulation of Toll-like receptor (TLR)-induced cytokine production.
Lang et al., Erlangen, Germany. In J Biol Chem, 2014
Here, we investigated the function of Dusp16/MKP-7 in the innate immune system.
miR-17 extends mouse lifespan by inhibiting senescence signaling mediated by MKP7.
Yang et al., Toronto, Canada. In Cell Death Dis, 2013
We demonstrate that miR-17 targets both ADCY5 and IRS1, upregulating the downstream signals MKP7, FoxO3, LC3B, and HIF1α, and downregulating mTOR, c-myc, cyclin D1, and JNK.
Haploinsufficiency of ETV6 and CDKN1B in patients with acute myeloid leukemia and complex karyotype.
Steinemann et al., Hannover, Germany. In Bmc Genomics, 2013
ETV6 and CDKN1B had reduced expression levels in CK-AML patients with deletion in 12p13 as compared to CK-AML without deletion in 12p13, while the other genes (BCL2L14, LRP6, DUSP16 and GPRC5D) located within the minimal deleted region in 12p13 had very low or missing expression in CK-AML irrespective of their copy number status.
A docking study of enhanced intracellular survival protein from Mycobacterium tuberculosis with human DUSP16/MKP-7.
Jang et al., Seoul, South Korea. In J Synchrotron Radiat, 2013
Mtb Eis activates JNK-specific dual-specificity protein phosphatase 16 (DUSP16)/mitogen-activated protein kinase phosphatase-7 (MKP-7) through the acetylation on Lys55, thus inactivating JNK by dephosphorylation.
PPARδ inhibits UVB-induced secretion of MMP-1 through MKP-7-mediated suppression of JNK signaling.
Seo et al., Seoul, South Korea. In J Invest Dermatol, 2013
Finally, in HR-1 hairless mice exposed to UVB, administration of GW501516 significantly reduced wrinkle formation and skin thickness, downregulated MMP-1 and JNK phosphorylation, and restored the levels of MKP-7, types I and III collagen.
Structural basis for the regulation of the mitogen-activated protein (MAP) kinase p38α by the dual specificity phosphatase 16 MAP kinase binding domain in solution.
Peti et al., In J Biol Chem, 2013
Here we describe the interaction of the MAPK binding domain of DUSP16 with p38α and show that despite belonging to the same dual specificity phosphatase (DUSP) family, its interaction mode differs from that of DUSP10.
Abnormalities of the der(12)t(12;21) in ETV6-RUNX1 acute lymphoblastic leukemia.
Moorman et al., Newcastle upon Tyne, United Kingdom. In Genes Chromosomes Cancer, 2013
The centromeric deletion encompassed the following genes: LRP6, BCL2L14, DUSP16, CREBL2, and CDKN1B.
PI3K/Akt-independent negative regulation of JNK signaling by MKP-7 after cerebral ischemia in rat hippocampus.
Guo et al., Nanjing, China. In Bmc Neurosci, 2012
RESULT: Mitogen-activated protein kinase phosphatase 7 (MKP-7) was upregulated significantly at 4 h of reperfusion postischemia in rat hippocampi.
Mycobacterium tuberculosis Eis protein initiates suppression of host immune responses by acetylation of DUSP16/MKP-7.
Suh et al., Seoul, South Korea. In Proc Natl Acad Sci U S A, 2012
We have discovered that Mtb Eis is an efficient N(ε)-acetyltransferase, rapidly acetylating Lys55 of dual-specificity protein phosphatase 16 (DUSP16)/mitogen-activated protein kinase phosphatase-7 (MKP-7), a JNK-specific phosphatase.
Dual specificity phosphatases 10 and 16 are positive regulators of EGF-stimulated ERK activity: indirect regulation of ERK signals by JNK/p38 selective MAPK phosphatases.
GeneRIF
McArdle et al., Bristol, United Kingdom. In Cell Signal, 2012
DUSPs 10 and 16 are positive regulators of activation, apparently acting by modulating cross-talk between the p38 and ERK pathways.
MKP-7, a negative regulator of JNK, regulates VCAM-1 expression through IRF-1.
GeneRIF
Kim et al., Chinju, South Korea. In Cell Signal, 2012
MKP-7, a negative regulator of JNK, regulates VCAM-1 expression in activated endothelial cells through IRF-1 but not GATA6.
Functional involvement of dual specificity phosphatase 16 (DUSP16), a c-Jun N-terminal kinase-specific phosphatase, in the regulation of T helper cell differentiation.
GeneRIF
Matsuguchi et al., Kagoshima, Japan. In J Biol Chem, 2011
the functional role of DUSP16 in Th1/Th2 balance.
DUSP16 is an epigenetically regulated determinant of JNK signalling in Burkitt's lymphoma.
GeneRIF
Crook et al., London, United Kingdom. In Br J Cancer, 2010
DUSP16 is a new epigenetically regulated determinant of JNK activation in BL.
Acute oxidative stress can reverse insulin resistance by inactivation of cytoplasmic JNK.
GeneRIF
Bose et al., Cambridge, United States. In J Biol Chem, 2010
the contrasting effects of acute and chronic stress on insulin sensitivity are driven by changes in subcellular distribution of MKP7 and activated JNK
Dual-specificity MAP kinase phosphatases (MKPs) and cancer.
Review
Keyse, Dundee, United Kingdom. In Cancer Metastasis Rev, 2008
The final group consists of three MKPs DUSP8/hVH-5, DUSP10/MKP-5 and DUSP16/MKP-7 all of which preferentially inactivate the stress-activated p38 and JNK MAP kinases.
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