Abnormal patterns of sleep and waking behaviors are accompanied by neocortical oscillation disturbances in an Ank3 mouse model of epilepsy-bipolar disorder comorbidity.
Study shows that simultaneous ablation of neuronal Neurofascin and Ankyrin G in young and adult mice reveals age-dependent increase in nodal stability in myelinated axons and differential effects on the lifespan.
Results suggested that exon 34 of AnkyrinG is an embryonic-stage-preferential exon that should be excluded from mature neurons and that Elavl3 regulates neuronal polarity through alternative splicing of this exon.
The loss of AnkG in the brain disrupts the excitation/inhibition balance of neurotransmitters hindering the synaptic plasticity of neurons and consequently leading to abnormal behavioral symptoms.
Studied effect of reduced expression of the large isoforms of Ank3 on cognition and behavior using a heterozygous knockout mouse model; found evidence for increased anxiety and observed specific neuroanatomical defects in heterozygous knockout mice including a smaller cingulate cortex granular retrosplenial cortex primary motor cortex and fimbria of the hippocampus.
This study proposed that psychiatric-related behavior in Ank3+/- mice is connected to a disturbance of the kinesin cargo system resulting in a dysfunction of neuronal ion channel and glutamate receptor transport. Lithium reverses this molecular signature suggesting the promotion of anterograde kinesin transport as part of its mechanism of action in ameliorating Ank3-related psychiatric-related behavior.
giant ankyrin-G promotes GABAergic synapse stability through opposing endocytosis of GABAA receptors and requires a newly described interaction with GABARAP a GABAA receptor-associated protein.
The giant exon of AnkG is required for assembly of the AIS and nodes of Ranvier and was a transformative innovation in evolution of the vertebrate nervous system that now is a potential target in neurodevelopmental disorders.
the structures of ANK repeats in complex with an inhibitory segment from the C-terminal regulatory domain and with a sodium channel Nav1.2 peptide are reported.
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