ArticleMolecular and cellular neurosciences2007
Dominant-negative suppression of Cav2.1 currents by alpha(1)2.1 truncations requires the conserved interaction domain for beta subunits.
Article in Molecular and cellular neurosciences, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Pin1 promotes human CaCell communication and signaling : CCS · 2024Article
- Ubiquitin Ligase RNF138 Promotes Episodic Ataxia Type 2-Associated Aberrant Degradation of Human CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- The first knockin mouse model of episodic ataxia type 2.Experimental neurology · 2014Article
- Age-related homeostatic midchannel proteolysis of neuronal L-type voltage-gated Ca²⁺ channels.Neuron · 2014Article
- Regulation of voltage-gated calcium channels by proteolysis.Sheng li xue bao : [Acta physiologica Sinica] · 2012Review
- Neuronal P/Q-type calcium channel dysfunction in inherited disorders of the CNS.Nature reviews. Neurology · 2012Review
- CaV2.1 channelopathies.Pflugers Archiv : European journal of physiology · 2010Review
- Alternative splicing in the synaptic protein interaction site of rat Ca(v)2.2 (alpha (1B)) calcium channels: changes induced by chronic inflammatory pain.Journal of molecular neuroscience : MN · 2009Article
- Functional contribution of alpha3L8' to the neuronal nicotinic alpha3 receptor.Journal of neuroscience research · 2008Article
- Novel mRNA isoforms of the sodium channels Na(v)1.2, Na(v)1.3 and Na(v)1.7 encode predicted two-domain, truncated proteins.Neuroscience · 2008Article
- A destructive interaction mechanism accounts for dominant-negative effects of misfolded mutants of voltage-gated calcium channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
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4 authors.
Funding
Abstract
Episodic ataxia type 2 (EA2) is an autosomal dominant disorder arising from CACNA1A mutations, which commonly predict heterozygous expression of Ca(v)2.1 calcium channels with truncated alpha(1)2.1 pore subunits. We hypothesized that alpha(1)2.1 truncations in EA2 exert dominant-negative effects on the function of wild-type subunits. Wild-type and truncated alpha(1)2.1 subunits with fluorescent protein tags were transiently co-expressed in cells stably expressing Ca(v) auxiliary beta subunits, which facilitate alpha1 subunit functional expression through high-affinity interactions with the alpha interaction domain (AID). Co-expression of wild-type subunits with truncations often resulted in severely reduced whole-cell currents compared to expression of wild-type subunits alone. Cellular image analyses revealed that current suppression was not due to reduced wild-type expression levels. Instead, the current suppression depended on truncations terminating distal to the AID. Moreover, only AID-bearing alpha(1)2.1 proteins co-immunoprecipitated with Ca(v) beta subunits. These results indicate that Ca(v) beta subunits may play a prominent role in EA2 disease pathogenesis.
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