| Annotated protein: | Calcium/calmodulin-dependent protein kinase type IV (CaMK IV) (EC 2.7.11.17) (CaM kinase-GR). Gene symbol: CAMK4. Taxonomy: Mus musculus (Mouse). Uniprot ID: P08414 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ CAMK4 |
| Ontology domain: | Biological Process |
| SynGO term: | postsynaptic modulation of chemical synaptic transmission (GO:0099170) |
| Synapse type(s): | hippocampus, glutamatergic cerebellum, GABAergic |
| Annotated paper: | Ho N, et al. "Impaired synaptic plasticity and cAMP response element-binding protein activation in Ca2+/calmodulin-dependent protein kinase type IV/Gr-deficient mice" J Neurosci. 2000 Sep 1;20(17):6459-72 PMID:10964952 |
| Figure(s): | Fig. 3C,D, Figure 5, Figure 6, Figure7A, D, Table 1 |
| Annotation description: | The paper examines the implications of the targeted deletion of Calcium /Calmodulin kinase IV. Figure 3C and figure 5B show impairment in LTP in CA1 neurons. The impairment is stronger if four tetanic stimulations are used (5B, in comparison to two stimulations in 3C). Figure 3D: no effect is seen on LTD in CA1 neurons. Figure 6 shows basal and depolarization-induced phosphorylation of CREB in primary cortical neurons of KO, het and WT E14 mice. Phosphorylation is low in the non-stimulated neurons but is dramatically increased upon depolarization of WT and HET neurons. No change is seen in the KO samples, implying that the major activity-dependent kinase phosphorylating CREB is Calcium /Calmodulin kinase IV. Figure 7A,C show (A) and quantify (C) decreased phospho-CREB staining of CA1 neurons of glutamate-perfused hippocampal slices of KO mice compared with WT littermates. Figure 5 and table 1 demonstrate an effect of Calcium /Calmodulin kinase IV KO on synaptic transmission and on LTD in cultured cultured Purkinje neurons. The effect is seen only at the late phase of LTP. Taking together, the paper shows that Calcium /Calmodulin kinase IV is necessary for the phosphorylation of CREB, and that Calcium /Calmodulin kinase IV signaling is important for the generation of proper LTP/LTD. |
| Evidence tracking, Biological System: | Intact tissue |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Field recordings Western blot |
| Annotator(s): | Noa Lipstein (ORCID:0000-0002-0755-5899) Cordelia Imig (ORCID:0000-0001-7351-8706) Vincent O'connor (ORCID:0000-0003-3185-5709) Nils Brose (ORCID:0000-0003-0938-8534) |
| Lab: | Department of Molecular Neurobiology, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany |
| Additional literature: | The paper examines the effect of a dominant negative (DN) or a constitutively active (CA) forms of Calcium /Calmodulin kinase IV and CREB. Figure 1b shows in dissociated hippocampal cultures that expression of CaMKIV-CA dramatically increased nuclear phospho-CREB staining following depolarization. The CaMKIV-DN levels decreased the levels of phosphorylation. Stereotaxic microinjections of the above-mentioned constructs (using viral-medicated carriers) were made into the CA1 region of the hippocampi of young adult rats and whole-celll voltage clamp was made in infected and non-infected pyramidal neurons. Figure 4 shows that the in vivo expression of CaMKIV-CA Enhances LTP but not LTD. Figure 6 shows that the in vivo expression of CREB-CA enhances LTP but not LTD. Taken together, the paper suggests that post-synaptic LTP in CA1 neurons is enhanced by the constitutively active forms of CaMKIV and CREB, likely through a signalling pathway involving CaMKIV, that leads to the phosphorylation of CREB. @ PMID:15748849 |
| SynGO annotation ID: | 3669 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |