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The protein encoded by KCNQ4 forms a potassium channel that is thought to play a critical role in the regulation of neuronal excitability, particularly in sensory cells of the cochlea. Additionally we are shipping KCNQ4 Proteins (7) and many more products for this protein.
Showing 10 out of 85 products:
Human Monoclonal KCNQ4 Primary Antibody for WB - ABIN393308
: in 1970
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Human Monoclonal KCNQ4 Primary Antibody for ICC, IF - ABIN361768
Hernandez, Zaika, Tolstykh, Shapiro: Regulation of neural KCNQ channels: signalling pathways, structural motifs and functional implications. in The Journal of physiology 2008
Show all 3 references for ABIN361768
Human Polyclonal KCNQ4 Primary Antibody for ELISA, WB - ABIN1451451
Kubisch, Schroeder, Friedrich, Lütjohann, El-Amraoui, Marlin, Petit, Jentsch: KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafness. in Cell 1999
Show all 2 references for ABIN1451451
Human Polyclonal KCNQ4 Primary Antibody for EIA, WB - ABIN374975
Oshima, Grimm, Corrales, Senn, Martinez Monedero, Géléoc, Edge, Holt, Heller: Differential distribution of stem cells in the auditory and vestibular organs of the inner ear. in Journal of the Association for Research in Otolaryngology : JARO 2007
analysis of mechanistic insights into the critical roles of Ca(2 (show CA2 Antibodies)+)/CaM (show CALM1 Antibodies) regulation of the Kv7.4 channel under physiological and pathological conditions
Interaction between G-protein betagamma subunits and Kv7.4 is crucial for channel responses to membrane voltage.
genotype-phenotype correlation is analogous to that in KCNQ1 (show KCNQ1 Antibodies) which causes autosomal dominant hereditary long QT syndrome 1 with milder phenotype and the autosomal recessive Jervell and Lange-Nielsen syndrome 1 with more severe phenotype
The study identified a novel KCNQ4 mutation in a five generation Chinese family and a known KCNQ4 mutation in a six generation Chinese family.
These findings suggest a protective role for Kv7.4 channels in the pulmonary circulation, limiting its reactivity to pressor agents and preventing hypoxia-induced pulmonary hypertension.
Identified the c.211delC mutation in the KCNQ4 gene and the c.2967C>A (p.H989Q) mutation in the TECTA (show TECTA Antibodies) gene to be associated with high-frequency sensorineural hearing loss in a Japanese family.
Kv7.4 currents are inhibited in a CB1 (show CNR1 Antibodies) pathway repressed by endocannabinoid 2-AG
In-frame deletion in KCNQ4 P-loop was identified in family members with autosomal dominant sensorineural hearing loss.
Differential protein kinase C (show PKC Antibodies)-dependent modulation of Kv7.4 and Kv7.5 (show KCNQ5 Antibodies) subunits of vascular Kv7 channels.
decreased cell surface expression and impaired conductance of the KCNQ4 channel are two mechanisms underlying hearing loss in DFNA2 (show GJB3 Antibodies)
REST as a crucial transcriptional regulator for the Kv7.4 potassium channel subunit (show KCNT1 Antibodies).
analysis of the vestibular role of KCNQ4 and KCNQ5 (show KCNQ5 Antibodies) K+ channels revealed by mouse models
Data show that in early pregnant mouse myometrium, the relative abundance of mRNA expression was KCNQ3 (show KCNQ3 Antibodies) > KCNQ4 > KCNQ5 (show KCNQ5 Antibodies) > KCNQ1 (show KCNQ1 Antibodies) > KCNQ2 (show KCNQ2 Antibodies).
evidence of the cellular etiology and mechanisms of SGN degeneration in DFNA2 (show GJB3 Antibodies).
KCNQ (show KCNQ1 Antibodies) channels set the resting membrane potential of inner hair cells in the isolated organ of Corti and maintain [Ca2 (show CA2 Antibodies)+]i at low levels
primary defect leading to high-frequency loss in DFNA2 (show GJB3 Antibodies) patients may be attributable to high levels of the dysfunctional Kcnq4_v3 variant in the spiral ganglion and inner hair cells in the basal hook region
Auditory function declined over several weeks in Kcnq4-/- mice and over several months in mice carrying the dominant negative allele.
Analyses of vestibular hair cells (HCs (show HLCS Antibodies)) of Bdnf (show BDNF Antibodies) conditional mutant mice, which are devoid of any innervation, demonstrate that regulation of Kcnq4 expression in vestibular HCs (show HLCS Antibodies) is independent of innervation.
Murine blood vessels exhibit a distinctive expression profile of KCNQ1 (show KCNQ1 Antibodies), KCNQ4, and KCNQ5 (show KCNQ5 Antibodies), with 'neuronal' KCNQ4 dominating
The protein encoded by this gene forms a potassium channel that is thought to play a critical role in the regulation of neuronal excitability, particularly in sensory cells of the cochlea. The current generated by this channel is inhibited by M1 muscarinic acetylcholine receptors and activated by retigabine, a novel anti-convulsant drug. The encoded protein can form a homomultimeric potassium channel or possibly a heteromultimeric channel in association with the protein encoded by the KCNQ3 gene. Defects in this gene are a cause of nonsyndromic sensorineural deafness type 2 (DFNA2), an autosomal dominant form of progressive hearing loss. Two transcript variants encoding different isoforms have been found for this gene.
potassium voltage-gated channel, KQT-like subfamily, member 4
, potassium voltage-gated channel KQT-like protein 4
, potassium channel KQT-like 4
, potassium channel subunit alpha KvLQT4
, potassium voltage-gated channel subfamily KQT member 4
, KQT-like 4
, potassium voltage-gated channel, subfamily Q, member 4
, voltage-gated potassium channel subunit Kv7.4