Specific regulation of JNK signalling by the novel rat MKK7γ1 isoform

Haeusgen, Wiebke; Herdegen, Thomas; Waetzig, Vicki

doi:10.1016/j.cellsig.2010.07.002

Cited by 15 publications

(15 citation statements)

References 76 publications

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“…5B). These results are also supported by a previous study showing that JNK1 is mainly located in the cytosol in PC12 cells (61). Similar to JNK1, JNK2 was mainly detected in the cytosol, but it also showed considerable nuclear localization.…”

Section: Jnk Interacts With Proteins Of Different Molecular Functionssupporting

confidence: 80%

Quantitative Proteomics Reveals Dynamic Interaction of c-Jun N-terminal Kinase (JNK) with RNA Transport Granule Proteins Splicing Factor Proline- and Glutamine-rich (Sfpq) and Non-POU Domain-containing Octamer-binding Protein (Nono) during Neuronal Differentiation

Sury

McShane

Hernández-Miranda

et al. 2015

Molecular & Cellular Proteomics

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The c-Jun N-terminal kinase (JNK) is an important mediator of physiological and pathophysiological processes in the central nervous system. Importantly, JNK not only is involved in neuronal cell death, but also plays a significant role in neuronal differentiation and regeneration. For example, nerve growth factor induces JNK-dependent neuronal differentiation in several model systems. The mechanism by which JNK mediates neuronal differentiation is not well understood. Here, we employed a proteomic strategy to better characterize the function of JNK during neuronal differentiation. We used SILAC-based quantitative proteomics to identify proteins that interact with JNK in PC12 cells in a nerve growth factor-dependent manner. Intriguingly, we found that JNK interacted with neuronal transport granule proteins such as Sfpq and Nono upon NGF treatment. We validated the specificity of these interactions by showing that they were disrupted by a specific peptide inhibitor that blocks the interaction of JNK with its substrates.

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Section: Jnk Interacts With Proteins Of Different Molecular Functionssupporting

confidence: 80%

Quantitative Proteomics Reveals Dynamic Interaction of c-Jun N-terminal Kinase (JNK) with RNA Transport Granule Proteins Splicing Factor Proline- and Glutamine-rich (Sfpq) and Non-POU Domain-containing Octamer-binding Protein (Nono) during Neuronal Differentiation

Sury

McShane

Hernández-Miranda

et al. 2015

Molecular & Cellular Proteomics

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“…They phosphorylate and activate a number of nuclear and non-nuclear proteins, including the transcription factor AP-1, ATF-2, c-Myc, as well as cell apoptotic proteins (Fas, Bim, Bcl-xl). 53,54 These proteins control a diversity of cellular responses, such as proliferation, differentiation, cell death and survival. 55 Our data shows that miR-20a-5p regulates Bim expression and mycobacterial induced apoptosis in a JNK2-dependent manner.…”

Section: Cells Infected With Mir-20a-5p Lentivirus and Decreased In mentioning

confidence: 99%

Down-regulation of miR-20a-5p triggers cell apoptosis to facilitate mycobacterial clearance through targeting JNK2 in human macrophages

et al. 2016

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Induction of cell apoptosis is one of the major host defense mechanisms through which macrophages control Mycobacterium tuberculosis (Mtb) infection. However, the mechanisms underlying macrophage apoptosis triggered by Mtb infection are still largely unknown. In this study, a microarray profiling survey revealed 14 miRNAs were down-regulated in CD14C monocytes from active pulmonary tuberculosis patients, and only the reduction of miR-20a-5p could be reversed after successful anti-tuberculosis treatment. Validation of miR-20a-5p expression was confirmed using real time qPCR. Moreover, miR-20a-5p expression also decreased in differentiated THP-1 macrophages after mycobacterial infection in vitro. Functional assays through forced or inhibited expression of miR-20a-5p in THP-1 macrophages demonstrated that miR-20a-5p functioned as a negative regulator of mycobacterial-triggered apoptosis. Importantly, inhibition of miR-20a-5p expression resulted in more efficient mycobacterial clearance from infected THP-1 macrophages while miR-20a-5p overexpression promoted mycobacterial survival. Mechanistically, miR-20a-5p was demonstrated to regulate Bim expression in a JNK2-dependent manner, unlike Bcl2, and luciferase assay showed JNK2 was a novel direct target of miR-20a-5p. Together, our findings indicate that downregulation of miR-20a-5p triggers macrophage apoptosis as a novel mechanism for host defense against mycobacterial infection.

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“…JNK1 and JNK2 differentially regulate c-Jun stability and phosphorylation, thereby differentially affecting cellular proliferation. 29,35 JNK levels and activity are tightly controlled during the cell cycle to ensure…”

Section: O N O T D I S T R I B U T Ementioning

confidence: 99%

“…38 In response to oxidative stress, JNK1 promotes cellular survival through regulation of c-Myc and p21 expression and phosphorylation of JNK2. 32,35 In addition to p53 phosphorylation, activated JNK2 is a positive regulator of p53 expression. 35 JNK2 also phosphorylates FOXO family members Figure 3.…”

Section: P53-regulated Alterations In Response To Genotoxic Stressmentioning

confidence: 99%

“…32,35 In addition to p53 phosphorylation, activated JNK2 is a positive regulator of p53 expression. 35 JNK2 also phosphorylates FOXO family members Figure 3. Genotoxic stress-induced activation of p53 initiates reversible cell cycle arrest by inducing p21 activation and translocation of FOXO into cytosol (cFOXO: cytosolic FOXO).…”

Section: P53-regulated Alterations In Response To Genotoxic Stressmentioning

confidence: 99%

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Genotoxic stress-mediated cell cycle activities for the decision of cellular fate

Erol¹

2011

Cell Cycle

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Specific regulation of JNK signalling by the novel rat MKK7γ1 isoform

Cited by 15 publications

References 76 publications

Quantitative Proteomics Reveals Dynamic Interaction of c-Jun N-terminal Kinase (JNK) with RNA Transport Granule Proteins Splicing Factor Proline- and Glutamine-rich (Sfpq) and Non-POU Domain-containing Octamer-binding Protein (Nono) during Neuronal Differentiation

Quantitative Proteomics Reveals Dynamic Interaction of c-Jun N-terminal Kinase (JNK) with RNA Transport Granule Proteins Splicing Factor Proline- and Glutamine-rich (Sfpq) and Non-POU Domain-containing Octamer-binding Protein (Nono) during Neuronal Differentiation

Down-regulation of miR-20a-5p triggers cell apoptosis to facilitate mycobacterial clearance through targeting JNK2 in human macrophages

Genotoxic stress-mediated cell cycle activities for the decision of cellular fate

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