Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
KCNJ13 encodes a member of the inwardly rectifying potassium channel family of proteins. Zusätzlich bieten wir Ihnen KCNJ13 Proteine (4) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 34 products:
the activity of Kir channels in the RPE is critically dependent on the regeneration of membrane PIP2 by PI4 kinases and that this may explain the dependence of these channels on hydrolyzable ATP.
These results suggest that the cellular defect of the Kir7.1 mutation is directly responsible for the pattern change in the jaguar/obelix mutant.
Kir7.1 mutations are associated with vision disorders to include novel insights into the molecular mechanism of disease pathobiology in Leber Congenital Amaurosis.
Juvenile or early-adult-onset cataract in the setting of a congenital vitreo-retinal dystrophy (zeige MERTK Antikörper) notable for fibrosis over the disc and clumped pigmentation in the posterior pole is a unique phenotype that suggests recessive KCNJ13 mutations.
Kir7.1 regulates the transition from quiescence to contractions in the pregnant uterus.
Kir7.1, R162W mutant showed a reduction of IKir7.1 and positive shift in '0' current potential.
Kir7.1 expression was found in 100% of choroid plexus tumors and was absent in endolymphatic sac (zeige ADCY10 Antikörper) tumors.
A homozygous nonsense mutation was found in the potassium channel subunit (zeige KCNT1 Antikörper) gene KCNJ13 that caused leber congenital amaurosis.
This study confirms the expression of Kir7.1 in human RPE (zeige RPE Antikörper), identifies a Kir7.1 splice variant resulting in predicted changes in protein sequence, and indicates that there is no functional interaction between this splice variant and full-length Kir7.1.
Kir7.1 channels are modulated by intracellular protons by diverse mechanisms; H26 is important for channel activation at physiological pH(i) and it influences an unidentified proton-induced inhibitory mechanism.
These results indicate that the KCNJ13 R162W mutation can cause Snowflake vitreoretinal degeneration and further show that vitreoretinal degeneration can arise through mutations in genes whose products are not structural components of the vitreous.
This study demonstrates the dual regulation of Kir7.1 channel function by PKA and PKC.
These results suggest that KCNJ13 expression is required for RPE (zeige RPE Antikörper) cells to maintain photoreceptor survival.
Coupling of MC4R (zeige MC4R Antikörper) to Kir7.1 may explain unusual aspects of the control of energy homeostasis by melanocortin signalling, including the gene dosage effect of MC4R (zeige MC4R Antikörper) and the sustained effects of AgRP (zeige AGRP Antikörper) on food intake.
This gene encodes a member of the inwardly rectifying potassium channel family of proteins. Members of this family form ion channel pores that allow potassium ions to pass into a cell. The encoded protein belongs to a subfamily of low signal channel conductance proteins that have a low dependence on potassium concentration. Mutations in this gene are associated with snowflake vitreoretinal degeneration. Alternate splicing results in multiple transcript variants.
potassium inwardly-rectifying channel, subfamily J, member 13
, inward rectifier potassium channel 13
, inwardly rectifying potassium channel 7.1
, inward rectifier potassium channel 13-like
, inward rectifier K(+) channel Kir7.1
, potassium channel, inwardly rectifying subfamily J member 13
, inwardly rectifying potassium channel Kir7.1