Sgk1 (serum/glucocorticoid regulated kinase) encodes a PI3K-dependent, serine-threonine kinase which is activated by cardiac insult (transverse aortic constriction, TAC) or heart failure. SGK1-DN mice express HA-tagged rat Sgk1 harboring a lysine to methionine substitution at residue 141, initially reported as 127, (K141M) under the cardiomyocyte-specific Myh6 promoter. The mutation results in inhibition of catalytic activity of the kinase, generating a kinase dead (KD) mutant. Hemizygous SGK1-DN mice are viable and fertile. Mice exhibit no phenotype under normal conditions. Following TAC-induced stress, SGK1-DN mice maintain an adaptive protective response characterized by compensatory hypertrophy, absence of fibrosis and preserved contractility. Mice carrying the constitutively active (CA) mutation in Sgk1 are available as MMRRC No. <a href="https://www.jax.org/strain/035476"">067426</a>.

SGK1-KD mice express a cardiac-specific Sgk1 (serum/glucocorticoid regulated kinase) gene modified to harbor a lysine to methionine substitution at residue 141, initially reported as 127, (K141M). The mutation disrupts the catalytic activity of the kinase, generating a kinase dead (KD) mutant. Following pressure overload induced by TAC (transverse aortic constriction), SGK1-KD mice develop a protective response from fibrosis and heart failure.

This strain is hosted by NIH's MMRRC, which partners with JAX for the distribution of this and other strains. For additional information and to purchase, please visit the MMRRC site.