<i>Adrbk1</i> (adrenergic receptor kinase, beta 1; also known as Grk2) is the main G-protein-coupled receptor kinase in developing embryos, and lack of GRK2 expression results in embryonic lethality before gestational day 15.5.  Homozygotes with this targeted mutation show defects which include failure of the heart to develop properly (thin myocardium syndrome).  This strain will be useful for delineating the role of GRK2 activity in developmental processes.  Heterozygotes exhibit altered adrenergic receptor-regulated heart function when tested as adults, and these mice can be useful for exploring the role of GRK2 function in the regulation of any G-protein coupled receptor subtype.  Homozygous embryos lack GRK2 immunoreactivity.  Heterozygote mouse brain and heart have 50% of normal GRK2 immunoreactivity.

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This <i>Adrbk1</i> (adrenergic receptor kinase, beta 1; also known as Grk2) targeted mutation strain may be useful for delineating the role of GRK2 activity in developmental processes. Homozygotes show defects which include failure of the heart to develop properly (thin myocardium syndrome) leading to embryonic lethality. Heterozygotes exhibit altered adrenergic receptor-regulated heart function as adults.


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