Abstract
Background: The KATP channel is formed of regulatory Sulfonylurea receptor subunits (SURx) and pore forming Kir6.x subunits. Transgenic mice overexpressing the KATP subunits SUR1 and gain of function Kir6.2(ΔN30, K185Q), controlled by cardiac specific α myosin heavy chain, demonstrate arrhythmias, premature death and do not deliver any double transgenic (DTG) pups. We hypothesized that KATP channel overexpression interferes with normal cardiac development accounting for in utero embryonic lethality.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
