Rabbit Polyclonal Anti Kir7 1 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "The inwardly rectifying K+ channel KIR7.1 controls uterine excitability throughout pregnancy"
Article Title: The inwardly rectifying K+ channel KIR7.1 controls uterine excitability throughout pregnancy
Journal: EMBO Molecular Medicine
Figure Legend Snippet: Pharmacological inhibition of Kir7.1 in vitro in human and murine myometrium induces membrane depolarization and long-lasting contractions Representative membrane potential recording in current clamp configuration from a murine GD15 myometrial strip. (i) Addition of 10 μM VU590 depolarizes resting membrane potential (note slope change from resting potentials of preceding phasic bursts) and leads to a sustained plateau potential. (ii) Upon washout, spike potentials recover as plateau potential hyperpolarizes. (iii) On complete washout, phasic bursting resumes. Addition of 1 nM oxytocin and 10 μM VU590 to human myometrial strips stimulates long-lasting contractions. (i) Initial component of the response is phasic, followed by establishment of a tonic contraction.
Techniques Used: Inhibition, In Vitro, Stripping Membranes
Figure Legend Snippet: Knockdown of Kir7.1 in vivo significantly increases intrauterine pressure Mice in which Kir7.1 was knocked down (Anti-Kir7.1) had significantly increased intrauterine pressure when compared to mice injected with scrambled miRNA lentivirus (scrambled) from GD13 to GD18 (Fig 6 and Supplementary Fig S3 ). ( n = 6 per time point). * P
Techniques Used: In Vivo, Mouse Assay, Injection
Figure Legend Snippet: Pharmacological inhibition of Kir7.1 in vitro in human and murine myometrium stimulates longer-lasting contractions than oxytocin Dose- and gestation-dependent effect of VU590 on murine myometrial contractility [ n = 5, activity integral expressed as a fold-change of pre-treatment contractions (mean ± SD, per GD)]. * P
Techniques Used: Inhibition, In Vitro, Activity Assay
Figure Legend Snippet: Model of the role of Kir7.1 in maintenance of uterine quiescence In normal labour in the human myometrium, changes take place over a number of weeks that increase both the intrinsic electrical excitability of the cell (blue box) and, by altering cellular receptors and contractile machinery, the susceptibility to stimulation. Alterations in stimulation either by infection or gene-environment interaction can precipitate preterm labour (Cha et al , 2013 ); however, changes in control of the myometrial membrane potential or interference with functional gap junctions can affect labour even under normal endocrine conditions (Bond et al , 2000 ; Doring et al , 2006 ). In this study, we demonstrate that alteration of the function of a single potassium channel profoundly alters uterine contractility. Loss of Kir7.1 function depolarizes the plasma membrane and promotes voltage-gated calcium entry. In addition, the duration of the depolarization is extended, preventing the normal phasic contractions. In this way, the process of excitation-contraction coupling in uterine myocytes overrides pharmaco-contraction coupling. This effect could be used for therapeutic benefit. (Key: CPI-17 = C-kinase potentiated protein phosphatase-1 inhibitor. CX26 = Connexin 26. CX43 = Connexin 43. CX45 = Connexin 45. GEFs = Guanine nucleotide exchange factors. GPCR = G-protein coupled receptors. IP3 = inositol 1,4,5-trisphosphate. IP3R = inositol 1,4,5-trisphosphate receptor. MLC = Myosin light chain. MLCp = Phosphorylated myosin light chain. PIP2 = Phosphatidylinositol 4,5-bisphosphate. PLC β = Phospholipase C. RHOgtp = Ras homologue gene family, member A. RHO-K = Rho-associated, coiled-coil containing protein kinase 1.)
Techniques Used: Infection, Functional Assay, Planar Chromatography
Figure Legend Snippet: Stimulation of uterine contractions correlates with Kir7.1 inhibitory potency A The structures of the three compounds tested in this study. BNBI, a potent Kir1.1 inhibitor does not inhibit Kir7.1. MRT2000769 is structurally unrelated to VU590 and was identified as inhibiting Kir7.1 in a high throughput electrophysiology screen. VU590 is the first described inhibitor of Kir7.1. B, C Effects of BNBI (B) and MRT2000769 (C) on murine GD15 myometrial contractility.
Techniques Used: High Throughput Screening Assay
Figure Legend Snippet: Kir7.1 is expressed in uterine myocytes and is regulated in pregnancy in mice and humans mRNA expression of Kcnj13 in mice ( n = 5; mean ± SD, per GD) normalized to GD13. * P
Techniques Used: Mouse Assay, Expressing
Figure Legend Snippet: Knockdown of Kir7.1 in vitro depolarizes resting membrane potential A–C Representative membrane potential recordings in current clamp configuration from murine myometrial strips (A) treated with scrambled control miRNA (B) treated with Kir7.1 knockdown (Anti-Kir7.1) and (C) overexpressing Kir7.1 (+Kir7.1). D Resting membrane potential in current clamp configuration from murine myometrial strips ( n = 6; mean ± SD) from experiments depicted in (5A–C). * P
Techniques Used: In Vitro
Figure Legend Snippet: Knockdown of Kir7.1 in vitro increases myometrial activity and promotes tonic contractions A–C Representative time-force recordings of phasic contractions demonstrating (A) the effect of scrambled miRNA compared to (B) knockdown (Anti-Kir7.1) and (C) overexpression (+Kir7.1) of Kir7.1 on contractility in murine GD15 myometrial strips. D–F Mean data are summarized ( n = 8; mean ± SD, per group of experiments) as activity integral (area under the time-force curve) (D), contraction duration (E) and maximum force (F). * P
Techniques Used: In Vitro, Activity Assay, Over Expression
Figure Legend Snippet: A free-running simulation of the effect on the myometrial action potential waveform of increasing densities of Kir7.1 Time-dependent effect of increasing Kir7.1 channel densities on V m (mV, left) and [Ca] i (nM, right). Increasing density of Kir7.1 within experimentally determined values hyperpolarizes resting membrane potential, whereas decreasing membrane excitability during depolarizing excursions in V m leading to decreased calcium entry.
Figure Legend Snippet: Kir7.1 current in uterine myocytes decreases from mid-pregnancy to term Measurement of inwardly rectifying, VU590-sensitive current in freshly dissociated GD15 murine myometrial cells. Shown are voltage-clamp recordings in the presence and absence of 10 μM VU590. Current-voltage relation ( n = 5; mean ± SD, per data point) of current density [VU590 subtracted from control (vehicle alone)]. Current density (pA/pF) at −150 mV and 500 ms in freshly dissociated murine myometrial cells from GD15 and GD18 ( n = 5 mean ± SD, per GD). * P