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

Slow‐channel mutation in acetylcholine receptor αM4 domain and its efficient knockdown

9 May 2006

Abstract excerpt

OBJECTIVE: To identify the genetic basis of a slow-channel myasthenic syndrome, characterize functional properties of the mutant receptor, and selectively silence the mutant allele. METHODS: We performed nutation analysis, cloning, and patch-clamp analysis of the functional properties of the mutant receptor; screening for a small interfering RNA with check plasmid; and assessed of the efficacy of small...

Source

Identifiers

PMID: 16685696
DOI: 10.1002/ana.20861

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 31 Aug 2026.

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

0

discussions

0

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Slow‐channel mutation in acetylcholine receptor αM4 domain and its efficient knockdownPMID 16685696Read ↗

Novel beta subunit mutation causes a slow-channel syndrome by enhancing activation and decreasing the rate of agonist dissociation.Semantic proximity Read ↗

A novel congenital myasthenic syndrome due to decreased acetylcholine receptor ion-channel conductanceSemantic proximity Read ↗

Highly fatal fast-channel syndrome caused by AChR ε subunit mutation at the agonist binding site.Semantic proximity Read ↗

A mouse model of the slow channel myasthenic syndrome: Neuromuscular physiology and effects of ephedrine treatment.Semantic proximity Read ↗

Mutations in different functional domains of the human muscle acetylcholine receptor alpha subunit in patients with the slow-channel congenital myasthenic syndrome.Semantic proximity Read ↗

New mutations in acetylcholine receptor subunit genes reveal heterogeneity in the slow-channel congenital myasthenic syndrome.Semantic proximity Read ↗

Novel epsilon subunit mutation of the muscle acetylcholine receptor causing a slow-channel congenital myasthenic syndrome.Semantic proximity Read ↗

Mutation in the AChR ion channel gate underlies a fast channel congenital myasthenic syndromeSemantic proximity Read ↗

Slow-channel myasthenic syndrome caused by enhanced activation, desensitization, and agonist binding affinity attributable to mutation in the M2 domain of the acetylcholine receptor alpha subunit.Semantic proximity Read ↗

A novel fast-channel myasthenia caused by mutation in β subunit of AChR reveals subunit-specific contribution of the intracellular M1-M2 linker to channel gating.Semantic proximity Read ↗

Congenital myasthenic syndrome caused by decreased agonist binding affinity due to a mutation in the acetylcholine receptor epsilon subunit.Semantic proximity Read ↗

A beta-subunit mutation in the acetylcholine receptor channel gate causes severe slow-channel syndrome.Semantic proximity Read ↗

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