| Annotated protein: | Mitogen-activated protein kinase 10 (MAP kinase 10) (MAPK 10) (EC 2.7.11.24) (SAPK-beta) (Stress-activated protein kinase JNK3) (c-Jun N-terminal kinase 3) (p54-beta). Gene symbol: MAPK10. Taxonomy: Rattus norvegicus (Rat). Uniprot ID: P49187 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ MAPK10 |
| Ontology domain: | Cellular Component |
| SynGO term: | postsynaptic Golgi apparatus (GO:0150051) |
| Synapse type(s): | hippocampus, glutamatergic |
| Annotated paper: | Yang G, et al. "JNK3 couples the neuronal stress response to inhibition of secretory trafficking" Sci Signal. 2013 Jul 9;6(283):ra57 PMID:23838184 |
| Figure(s): | Figure 1, 2 |
| Annotation description: | Fig.1: "Stress-induced palmitoylation drives JNK3 to the Golgi complex" - "Together, these results indicate that palmitoylation promoted the association of JNK3 with the Golgi complex independently of its kinase activity." Fig.2: "Golgi-associated JNK3 mediates stress-induced reduction of surface AMPAR" - "Expression of JNK3 Parlm or coexpression of JNK3 with zD17 in either rat hippocampal neurons or COS7 cells induced the entrapment of VSVG in the Golgi complex (fig. S4, A and B). The disruption of VSVG secretion was independent of JNK3 kinase activity because VSVG accumulation in the Golgi also occurred in cells overexpressing the kinase-deficient mutants of JNK3 and JNK3 Parlm (Fig. 2A and fig. S4B)" - "Given that the palmitoylation of JNK3 in primary neurons was increased after NMDA treatment (Fig. 1F), we investigated whether JNK3 inhibited stress-induced secretory trafficking in neurons by monitoring the trafficking of AMPAR GluR1 in response to NMDA-induced neuronal stress" - "A significant and gradual reduction of surface, but not total, GluR1 was detected in rat hippocampal or cortical neurons challenged with NMDA despite the presence of the JNK inhibitors SP600125 or NIMoE (Fig. 2C and fig. S6, B and C). This reduction of surface GluR1 was mostly prevented by short hairpin RNA (shRNA)-mediated knockdown of endogenous JNK3 (Fig. 2D), which could be reversed by overexpressing the shRNA-resistant kinase-deficient JNK3 mutant (JNK3 KD) but not the kinase-deficient JNK3 KD-CS mutant, which cannot be palmitoylated (Fig. 2E)." 23/2/2018 PIm - The application of NMDA and the transport of AMPARs places this data in synaptic context. |
| Evidence tracking, Biological System: | Cultured neurons Non-neuronal tissue |
| Evidence tracking, Protein Targeting: | Over-expression |
| Evidence tracking, Experiment Assay: | Confocal Western blot Biochemical fractionation (generic) |
| Annotator(s): | Hana Goldschmidt (ORCID:0000-0002-5676-366X) Richard Huganir (ORCID:0000-0001-9783-5183) |
| Lab: | Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA and Kavli Neuroscience Discovery Institute, Johns Hopkins University, Baltimore, MD 21205, USA |
| SynGO annotation ID: | 2720 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |