Browse our anti-KCNQ4 (KCNQ4) Antibodies

Human Potassium Voltage-Gated Channel, KQT-Like Subfamily, Member 4 (KCNQ4) interaction partners

1. KCNQ4 gene polymorphisms associated with susceptibility to noise-induced hearing loss.

2. 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

3. The fundamental processes that dictate Kv7.4 activity.

4. 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.

5. Tannic acid activates Kv7.4 and Kv7.3 (show KCNQ3 Antibodies)/7.5 K(+) channels resulting in vasodilation.

6. Gene and protein expression analyses show the predominance of KV7.4 channels over the other KV7 channel subtypes in human detrusor.

7. Kv7.4 channels are present and functional in cardiac mitochondria; their activation exerts a significant cardioprotective role

8. analysis of mechanistic insights into the critical roles of Ca(2 (show CA2 Antibodies)+)/CaM regulation of the Kv7.4 channel under physiological and pathological conditions

9. Interaction between G-protein betagamma subunits and Kv7.4 is crucial for channel responses to membrane voltage.

10. 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

Mouse (Murine) Potassium Voltage-Gated Channel, KQT-Like Subfamily, Member 4 (KCNQ4) interaction partners

1. Kv7.4 currents are inhibited in a CB1 (show CNR1 Antibodies) pathway repressed by endocannabinoid 2-AG

2. REST as a crucial transcriptional regulator for the Kv7.4 potassium channel subunit (show KCNT1 Antibodies).

3. analysis of the vestibular role of KCNQ4 and KCNQ5 (show KCNQ5 Antibodies) K+ channels revealed by mouse models

4. 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).

5. evidence of the cellular etiology and mechanisms of SGN degeneration in DFNA2 (show GJB3 Antibodies).

6. 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

7. 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

8. Auditory function declined over several weeks in Kcnq4-/- mice and over several months in mice carrying the dominant negative allele.

9. 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.

10. Murine blood vessels exhibit a distinctive expression profile of KCNQ1 (show KCNQ1 Antibodies), KCNQ4, and KCNQ5 (show KCNQ5 Antibodies), with 'neuronal' KCNQ4 dominating