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  2. Monoclonal

SMC-309

KCNQ4 Antibody, Clone N43/6

Cannot supply to this region.

SKU:
SMC-309
Additional Names:
KCNQ4, Kv7.4, KVLQT4, Potassium voltage-gated channel subfamily KQT member 4, Voltage-gated potassium channel subunit Kv7.4, KQT-like 4, Potassium channel subunit alpha KvLQT4, Potassium voltage-gated channel KQT-like subfamily member 4, DFNA2, KCNQ4_HUMAN, Kcnq4, KCNQ 4, Potassium channel KQT like 4, Potassium voltage gated channel KQT like protein 4, Voltage gated potassium channel subunit Kv7.4
Application:
IHC, WB, IF, ICC, Microarray
Concentration:
1 mg/ml
Species Reactivity:
Human
Purification:
Protein G Purified
Storage Conditions:
-20[o]C
Supplier:
StressMarq Biosciences
Host:
Mouse
Reactivities:
Human, Mouse, Rat
ABP:
IMP-GEN-2015-06 < 10% Serum <100ml
Buffer:
PBS pH7.4, 50% glycerol, 0.09% sodium azide
Immunogen:
Fusion protein amino acids 2-77 of human KCNQ4
Clone:
N43/6 (Formerly sold as S43-6)
Uniprot:
P56696
Synonyms:
DFNA2;DFNA2A;KQT-like 4;KV7.4;potassium channel KQT-like 4;potassium channel subunit alpha KvLQT4;potassium channel, voltage gated KQT-like subfamily Q, member 4;potassium voltage-gated channel subfamily KQT member 4;potassium voltage-gated channel, KQT-like subfamily, member 4;Voltage-gated potassium channel subunit Kv7.4
Extra Details:
KCNQ4 encodes a voltage-gated potassium channel subunit that plays a vital role in regulating neuronal excitability, particularly in sensory systems. Predominantly expressed in the outer hair cells of the cochlea, KCNQ4 contributes to potassium ion efflux, maintaining the resting membrane potential and enabling precise auditory signal transduction. This channel is modulated by key signaling pathways: it is inhibited by M1 muscarinic acetylcholine receptors and activated by retigabine, a potassium channel opener with anticonvulsant properties. These regulatory mechanisms highlight KCNQ4's importance in maintaining excitatory-inhibitory balance in neurons. Mutations or dysfunction in KCNQ4 are strongly associated with progressive sensorineural hearing loss (DFNA2), but emerging evidence suggests broader implications in neurodegenerative disease. Disrupted potassium channel activity can lead to chronic neuronal hyperexcitability, oxidative stress, and eventual neurodegeneration-mechanisms shared across conditions such as Alzheimer's disease, epilepsy, and age-related hearing loss. Given its pharmacological responsiveness and role in sensory neuron stability, KCNQ4 is gaining attention as a potential therapeutic target. Enhancing its function may offer neuroprotective benefits by restoring ionic homeostasis and preventing excitotoxic damage in vulnerable neural circuits. As research into ion channelopathies expands, KCNQ4 stands out as a key player in both auditory neuroscience and the broader landscape of neurodegenerative disease research.
Shipping Conditions:
Blue Ice