Post-translational regulation of mitogen-activated protein kinase phosphatase-2 (MKP-2) by ERK

Peng, Dong; Zhou, Jun; Wu, Gen Sheng

doi:10.4161/cc.9.23.13957

Cited by 23 publications

(9 citation statements)

References 29 publications

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“…Previous reports have suggested that transcription of the DUSP4 gene can be regulated by oxidative stress and TGFβ, which both upregulate its expression in some cell types [18,19]. The DUSP4 gene is also subject to transcriptional suppression following promoter hypermethylation [14], and the DUSP4 protein may be regulated by phosphorylation and proteasomal degradation [20]. In our previous study, we found that DUSP4 was downregulated following 2 h exposure to TNF-α.…”

Section: Discussionmentioning

confidence: 69%

Tumor necrosis factor-α-mediated suppression of dual-specificity phosphatase 4: crosstalk between NFκB and MAPK regulates endothelial cell survival

et al. 2013

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We investigated the effects of tumor necrosis factor-α (TNF-α) exposure on mitogen-activated protein kinase signalling in human microvascular endothelial cells. TNF-α caused a significant suppression of a dual specificity phosphatase, DUSP4, that regulates ERK1/2 activation. Thus, we hypothesized that suppression of DUSP4 enhances cell survival by increasing ERK1/2 signalling in response to growth factor stimulation. In support of this concept, TNF-α preexposure increased growth factor-mediated ERK1/2 activation, whereas overexpression of DUSP4 with an adenovirus decreased ERK1/2 compared to an empty adenovirus control. Overexpression of DUSP4 also significantly decreased cell viability, lessened recovery in an in vitro wound healing assay, and decreased DNA synthesis. Pharmacological inhibition of NFκB activation or a dominant-negative construct of the inhibitor of κB significantly lessened TNF-α-mediated suppression of DUSP4 expression by 70–84 % and attenuated ERK activation, implicating NFκB-activation in the TNF-α-mediated suppression of DUSP4 that contributes to ERK1/2 signalling. Taken together, our findings show that DUSP4 attenuates ERK signalling and reduces cell viability, suggesting that the novel crosstalk between NFκB and MAPK pathways contributes to cell survival.

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Section: Discussionmentioning

confidence: 69%

Tumor necrosis factor-α-mediated suppression of dual-specificity phosphatase 4: crosstalk between NFκB and MAPK regulates endothelial cell survival

et al. 2013

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“…The G protein-coupled receptor [41] and survival motor neuron protein [42] mediate signal transduction. MKP is a dual-specificity phosphatase family that is involved in the MAPK signaling pathway, and includes MKP-2 that dephosphorylates and inactivates mitogen-activated protein kinases (MAPKs) [43].…”

Section: Discussionmentioning

confidence: 99%

Annotation of the Transcriptome from Taenia pisiformis and Its Comparative Analysis with Three Taeniidae Species

Yang

et al. 2012

PLoS ONE

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Background Taenia pisiformis is one of the most common intestinal tapeworms and can cause infections in canines. Adult T. pisiformis (canines as definitive hosts) and Cysticercus pisiformis (rabbits as intermediate hosts) cause significant health problems to the host and considerable socio-economic losses as a consequence. No complete genomic data regarding T. pisiformis are currently available in public databases. RNA-seq provides an effective approach to analyze the eukaryotic transcriptome to generate large functional gene datasets that can be used for further studies.Methodology/Principal FindingsIn this study, 2.67 million sequencing clean reads and 72,957 unigenes were generated using the RNA-seq technique. Based on a sequence similarity search with known proteins, a total of 26,012 unigenes (no redundancy) were identified after quality control procedures via the alignment of four databases. Overall, 15,920 unigenes were mapped to 203 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Through analyzing the glycolysis/gluconeogenesis and axonal guidance pathways, we achieved an in-depth understanding of the biochemistry of T. pisiformis. Here, we selected four unigenes at random and obtained their full-length cDNA clones using RACE PCR. Functional distribution characteristics were gained through comparing four cestode species (72,957 unigenes of T. pisiformis, 30,700 ESTs of T. solium, 1,058 ESTs of Eg+Em [conserved ESTs between Echinococcus granulosus and Echinococcus multilocularis]), with the cluster of orthologous groups (COG) and gene ontology (GO) functional classification systems. Furthermore, the conserved common genes in these four cestode species were obtained and aligned by the KEGG database.ConclusionThis study provides an extensive transcriptome dataset obtained from the deep sequencing of T. pisiformis in a non-model whole genome. The identification of conserved genes may provide novel approaches for potential drug targets and vaccinations against cestode infections. Research can now accelerate into the functional genomics, immunity and gene expression profiles of cestode species.

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“…ERK activation has also been shown to be involved in learning of various hippocampus-dependent tasks (Menard et al, 2015; Peng et al, 2010; Xia and Storm, 2012). A previous study indicated that training in novel object recognition or in fear conditioning resulted in SCOP degradation and ERK activation in hippocampus 5 min after training (Shimizu et al, 2007).…”

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confidence: 99%

A calpain-2 selective inhibitor enhances learning & memory by prolonging ERK activation

et al. 2016

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While calpain-1 activation is required for LTP induction by theta burst stimulation (TBS), calpain-2 activation limits its magnitude during the consolidation period. A selective calpain-2 inhibitor applied either before or shortly after TBS enhanced the degree of potentiation. In the present study, we tested whether the selective calpain-2 inhibitor, Z-Leu-Abu-CONH-CH2-C6H3 (3, 5-(OMe)2 (C2I), could enhance learning and memory in wild-type (WT) and calpain-1 knockout (C1KO) mice. We first showed that C2I could reestablish TBS-LTP in hippocampal slices from C1KO mice, and this effect was blocked by PD98059, an inhibitor of ERK. TBS resulted in PTEN degradation in hippocampal slices from both WT and C1KO mice, and C2I treatment blocked this effect in both mouse genotypes. Systemic injection of C2I 30 min before training in the fear-conditioning paradigm resulted in a biphasic dose-response curve, with low doses enhancing and high doses inhibiting freezing behavior. The difference between the doses needed to enhance and inhibit learning matches the difference in concentrations producing inhibition of calpain-2 and calpain-1. A low dose of C2I also restored normal learning in a novel object recognition task in C1KO mice. Levels of SCOP, a ERK phosphatase known to be cleaved by calpain-1, were decreased in dorsal hippocampus early but not late following training in WT mice; C2I treatment did not affect the early decrease in SCOP levels but prevented its recovery at the later time-point and prolonged ERK activation. The results indicate that calpain-2 activation limits the extent of learning, an effect possibly due to temporal limitation of ERK activation, as a result of SCOP synthesis induced by calpain-2-mediated PTEN degradation.

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Post-translational regulation of mitogen-activated protein kinase phosphatase-2 (MKP-2) by ERK

Cited by 23 publications

References 29 publications

Tumor necrosis factor-α-mediated suppression of dual-specificity phosphatase 4: crosstalk between NFκB and MAPK regulates endothelial cell survival

Tumor necrosis factor-α-mediated suppression of dual-specificity phosphatase 4: crosstalk between NFκB and MAPK regulates endothelial cell survival

Annotation of the Transcriptome from Taenia pisiformis and Its Comparative Analysis with Three Taeniidae Species

A calpain-2 selective inhibitor enhances learning & memory by prolonging ERK activation

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