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anti-Human KCNQ4 Antikörper:
anti-Rat (Rattus) KCNQ4 Antikörper:
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Mammalian Monoclonal KCNQ4 Primary Antibody für ISt, IHC - ABIN1304778
Sedivy, Joshi, Ghaly, Mizera, Zaloudikova, Brennan, Novotna, Herget, Gurney: Role of Kv7 channels in responses of the pulmonary circulation to hypoxia. in American journal of physiology. Lung cellular and molecular physiology 2015
Show all 11 Pubmed References
Mammalian Monoclonal KCNQ4 Primary Antibody für 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. in Cardiovascular research 2016
Human Polyclonal KCNQ4 Primary Antibody für ELISA, WB - ABIN408705
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
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 (zeige KCNQ3 Antikörper)/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 (zeige CA2 Antikörper)+)/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 (zeige KCNQ1 Antikörper) 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
Kv7.4 currents are inhibited in a CB1 (zeige CNR1 Antikörper) pathway repressed by endocannabinoid 2-AG
REST as a crucial transcriptional regulator for the Kv7.4 potassium channel subunit (zeige KCNT1 Antikörper).
analysis of the vestibular role of KCNQ4 and KCNQ5 (zeige KCNQ5 Antikörper) K+ channels revealed by mouse models
Data show that in early pregnant mouse myometrium, the relative abundance of mRNA expression was KCNQ3 (zeige KCNQ3 Antikörper) > KCNQ4 > KCNQ5 (zeige KCNQ5 Antikörper) > KCNQ1 (zeige KCNQ1 Antikörper) > KCNQ2 (zeige KCNQ2 Antikörper).
evidence of the cellular etiology and mechanisms of SGN degeneration in DFNA2 (zeige GJB3 Antikörper).
KCNQ (zeige KCNQ1 Antikörper) channels set the resting membrane potential of inner hair cells in the isolated organ of Corti and maintain [Ca2 (zeige CA2 Antikörper)+]i at low levels
primary defect leading to high-frequency loss in DFNA2 (zeige GJB3 Antikörper) 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 (zeige HLCS Antikörper)) of Bdnf (zeige BDNF Antikörper) conditional mutant mice, which are devoid of any innervation, demonstrate that regulation of Kcnq4 expression in vestibular HCs (zeige HLCS Antikörper) is independent of innervation.
Murine blood vessels exhibit a distinctive expression profile of KCNQ1 (zeige KCNQ1 Antikörper), KCNQ4, and KCNQ5 (zeige KCNQ5 Antikörper), 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