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anti-Human KCNQ4 Anticorps:
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Mammalian Monoclonal KCNQ4 Primary Antibody pour ISt, IHC - ABIN1304778
Sedivy, Joshi, Ghaly, Mizera, Zaloudikova, Brennan, Novotna, Herget, Gurney: Role of Kv7 channels in responses of the pulmonary circulation to hypoxia. dans American journal of physiology. Lung cellular and molecular physiology 2015
Show all 11 Pubmed References
Polyclonal KCNQ4 Primary Antibody pour ELISA, WB - ABIN539786
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. dans Journal of the Association for Research in Otolaryngology : JARO 2007
Mammalian Monoclonal KCNQ4 Primary Antibody pour ISt, IHC - ABIN1304779
Testai, Barrese, Soldovieri, Ambrosino, Martelli, Vinciguerra, Miceli, Greenwood, Curtis, Breschi, Sisalli, Scorziello, Canduela, Grandes, Calderone, Taglialatela: Expression and function of Kv7.4 channels in rat cardiac mitochondria: possible targets for cardioprotection. dans Cardiovascular research 2016
Results indicate that the KCNQ4 variant p.(Pro291Leu) causes early onset, progressive hearing loss in homozygous individuals and late onset, progressive mild to moderate hearing loss when inherited in a heterozygous state. It suggests that the same variant may affect the severity of the phenotype as well as the age of onset in mono-allelic or bi-allelic forms.
Results show that rs4660468 T allele of KCNQ4 involves with a higher risk of noise-induced hearing loss (NIHL) and it could be one biomarker of susceptibility for Chinese noise exposed workers. Furthermore, genetic variations of KCNQ4 and noise exposure jointly contribute to the NIHL risks by gene-environment interactions.
KCNQ4 gene polymorphisms associated with susceptibility to noise-induced hearing loss.
mutations in KCNQ4 gene are unlikely to be a major causative factor of ADNSHL in our studied patients from West Bengal, India, pointing to other genes might be responsible for ADNSHL in our studied patients
The fundamental processes that dictate Kv7.4 activity.
A novel KCNQ4 mutation, c.887 G > A (p.G296D), was identified in all five affected members in a Chinese family with autosomal dominant non-syndromic deafness 2. This mutation leads to a glycine-to-aspartic acid substitution at position 296 in the pore region of the KCNQ4 channel.
Tannic acid activates Kv7.4 and Kv7.3/7.5 K(+) channels resulting in vasodilation.
Gene and protein expression analyses show the predominance of KV7.4 channels over the other KV7 channel subtypes in human detrusor.
Kv7.4 channels are present and functional in cardiac mitochondria; their activation exerts a significant cardioprotective role
analysis of mechanistic insights into the critical roles of Ca(2+)/CaM 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 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
This study provides evidence that mouse Kv7 channels may contribute differently to regulating the functional properties of cerebral and coronary arteries.
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 gene to be associated with high-frequency sensorineural hearing loss in a Japanese family.
Kv7.4 currents are inhibited in a CB1 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-dependent modulation of Kv7.4 and Kv7.5 subunits of vascular Kv7 channels.
decreased cell surface expression and impaired conductance of the KCNQ4 channel are two mechanisms underlying hearing loss in DFNA2
Results indicate that midbrain Kcnq4 expression regulates alcohol-related behaviors and provide evidence that KV7.4 channels are a critical mediator of excessive alcohol drinking.
we provide strong evidence that Kv7.4 channels are a key modulator of the excitability of VTA dopaminergic neurons, which contributes to the development of depressive behaviour
is concluded that K(V)7 channels, via nifedipine sensitive channels, have a role in the regulation of basal renal vascular tone.
REST as a crucial transcriptional regulator for the Kv7.4 potassium channel subunit.
analysis of the vestibular role of KCNQ4 and KCNQ5 K+ channels revealed by mouse models
In 2 different rat and mouse models of hypertension, the functional impact of Kv7 channels was dramatically downregulated.
Data show that in early pregnant mouse myometrium, the relative abundance of mRNA expression was KCNQ3 > KCNQ4 > KCNQ5 > KCNQ1 > KCNQ2.
evidence of the cellular etiology and mechanisms of SGN degeneration in DFNA2.
KCNQ channels set the resting membrane potential of inner hair cells in the isolated organ of Corti and maintain [Ca2+]i at low levels
primary defect leading to high-frequency loss in DFNA2 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) of Bdnf conditional mutant mice, which are devoid of any innervation, demonstrate that regulation of Kcnq4 expression in vestibular HCs is independent of innervation.
Murine blood vessels exhibit a distinctive expression profile of KCNQ1, KCNQ4, and KCNQ5, with 'neuronal' KCNQ4 dominating
variations within the C terminus of splice variants produce profound differences in the voltage-dependent phenotype and functional expression of the channel
Results provide support for KCNQ4- or KCNQ5-encoded channels having an important functional impact in the vasculature.
K(v)7.4 and K(v)7.5 are expressed in different regions of the murine gastrointestinal tract and blockers of K(v)7 channels augment inherent contractile activity.
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