p(HGNC:CAMKV)

Entity

Name

CAMKV

Namespace

hgnc

Namespace Version

20180906

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Tau Modifications Sections of NESTOR

These observations suggest that CaMKv blocks RhoA activity by preventing its interaction with Lfc. These results demonstrate that CaMKv regulates spine maintenance through RhoA inhibition. The suppression of the Lfc/RhoA pathway by AMPA receptors is implicated in dendritic spine maintenance10. Given that CaMKv expression is upregulated by synaptic activity, CaMKv may be a key signalling protein that transduces the signals from AMPA receptors to suppress RhoA during activity-dependent spine maintenance. Corroborating this, the AMPA receptor blocker NBQX attenuated CaMKv expression in neurons (Fig. 3i,j). Importantly, CaMKv overexpression completely rescued NBQX-induced spine loss (Fig. 3k,l). These findings collectively reveal that activity-dependent CaMKv expression and the subsequent inhibition of Lfc/RhoA are required to mediate AMPA receptor function in spine maintenance. PubMed:27796283

These findings suggest that CaMKv is required for both synaptic transmission and protein synthesis-dependent LTP in the hippocampus. PubMed:27796283

However, co-expression of the phospho-mimetic T345E failed to restore the defects in spine density after CaMKv depletion (Fig. 4l,m), suggesting that CaMKv phosphorylation by Cdk5 at Thr345 inhibits its function. PubMed:27796283

These observations suggest that CaMKv blocks RhoA activity by preventing its interaction with Lfc. These results demonstrate that CaMKv regulates spine maintenance through RhoA inhibition. The suppression of the Lfc/RhoA pathway by AMPA receptors is implicated in dendritic spine maintenance10. Given that CaMKv expression is upregulated by synaptic activity, CaMKv may be a key signalling protein that transduces the signals from AMPA receptors to suppress RhoA during activity-dependent spine maintenance. Corroborating this, the AMPA receptor blocker NBQX attenuated CaMKv expression in neurons (Fig. 3i,j). Importantly, CaMKv overexpression completely rescued NBQX-induced spine loss (Fig. 3k,l). These findings collectively reveal that activity-dependent CaMKv expression and the subsequent inhibition of Lfc/RhoA are required to mediate AMPA receptor function in spine maintenance. PubMed:27796283

These observations suggest that CaMKv blocks RhoA activity by preventing its interaction with Lfc. These results demonstrate that CaMKv regulates spine maintenance through RhoA inhibition. The suppression of the Lfc/RhoA pathway by AMPA receptors is implicated in dendritic spine maintenance10. Given that CaMKv expression is upregulated by synaptic activity, CaMKv may be a key signalling protein that transduces the signals from AMPA receptors to suppress RhoA during activity-dependent spine maintenance. Corroborating this, the AMPA receptor blocker NBQX attenuated CaMKv expression in neurons (Fig. 3i,j). Importantly, CaMKv overexpression completely rescued NBQX-induced spine loss (Fig. 3k,l). These findings collectively reveal that activity-dependent CaMKv expression and the subsequent inhibition of Lfc/RhoA are required to mediate AMPA receptor function in spine maintenance. PubMed:27796283

These findings suggest that CaMKv is required for both synaptic transmission and protein synthesis-dependent LTP in the hippocampus. PubMed:27796283

These findings suggest that CaMKv is required for both synaptic transmission and protein synthesis-dependent LTP in the hippocampus. PubMed:27796283