Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Familial Hemiplegic Migraine Mutations Change α1ACa2+ Channel Kinetics

1 Mar 1998

Abstract excerpt

Missense mutations in the pore-forming human alpha1A subunit of neuronal P/Q-type Ca2+ channels are associated with familial hemiplegic migraine (FHM). The pathophysiological consequences of these mutations are unknown. We have introduced the four single mutations reported for the human alpha1A subunit into the conserved rabbit alpha1A (R192Q, T666M, V714A, and I1819L) and investigated possible changes in channel...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Ion channel regulation and function
Share to Migraine and Headache Studies
Share to Nicotinic Acetylcholine Receptors Study

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 9488686
DOI: 10.1074/jbc.273.10.5586

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Familial Hemiplegic Migraine Mutations Change α1ACa2+ Channel KineticsPMID 9488686Read ↗

Three new familial hemiplegic migraine mutants affect P/Q-type Ca(2+) channel kinetics.Semantic proximity Read ↗

Functional consequences of mutations in the human alpha1A calcium channel subunit linked to familial hemiplegic migraine.Semantic proximity Read ↗

Ca(V)2.1 P/Q-type calcium channel alternative splicing affects the functional impact of familial hemiplegic migraine mutations: implications for calcium channelopathies.Semantic proximity Read ↗

The hemiplegic migraine-associated Y1245C mutation in CACNA1A results in a gain of channel function due to its effect on the voltage sensor and G-protein-mediated inhibition.Semantic proximity Read ↗

Divergent sodium channel defects in familial hemiplegic migraineSemantic proximity Read ↗

Familial hemiplegic migraine type 1 mutations W1684R and V1696I alter G protein-mediated regulation of Ca(V)2.1 voltage-gated calcium channels.Semantic proximity Read ↗

Familial hemiplegic migraine: a ion channel disorder.Semantic proximity Read ↗

A structural analysis of the splice-specific functional impact of the pathogenic familial hemiplegic migraine type 1 S218L mutation on Cav2.1 P/Q-type channel gating.Semantic proximity Read ↗

Specific kinetic alterations of human CaV2.1 calcium channels produced by mutation S218L causing familial hemiplegic migraine and delayed cerebral edema and coma after minor head trauma.Semantic proximity Read ↗

Effects of familial hemiplegic migraine type 1 mutations on neuronal P/Q-type Ca2+ channel activity and inhibitory synaptic transmission.Semantic proximity Read ↗

A mutation in the first intracellular loop of CACNA1A prevents P/Q channel modulation by SNARE proteins and lowers exocytosis.Semantic proximity Read ↗

CaV2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.