Kidins220/ARMS controls astrocyte calcium signaling and neuron-astrocyte communication.

ABSTRACT: Through their ability to modulate synaptic transmission, glial cells are key regulators of neuronal circuit formation and activity. Kidins220/ARMS (kinase-D interacting substrate of 220 kDa/ankyrin repeat-rich membrane spanning) is one of the key effectors of the neurotrophin pathways in neurons where it is required for differentiation, survival, and plasticity. However, its role in glial cells remains largely unknown. Here, we show that ablation of Kidins220 in primary cultured astrocytes induced defects in calcium (Ca²⁺) signaling that were linked to altered store-operated Ca²⁺ entry and strong overexpression of the transient receptor potential channel TRPV4. Moreover, Kidins220^-/- astrocytes were more sensitive to genotoxic stress. We also show that Kidi

SUBMITTER: Jaudon F 

PROVIDER: S-EPMC7206051 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature