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Open Access

Knock-in mice expressing cGKIα or cGKIβ selectively in smooth muscle

  • Silke Weber1Email author,
  • Susanne Feil1,
  • Sabine Brummer1,
  • Anna-Maria Knorn1,
  • Franz Hofmann1 and
  • Robert Feil1
BMC Pharmacology20055(Suppl 1):P59

Published: 16 June 2005


Protein KinaseSmooth MuscleSmooth Muscle CellTransgenic MouseHomologous Recombination

Many effects of NO and natriuretic peptides in smooth muscle cells (SMCs) are mediated by activation of cGMP synthesis and the cGMP-dependent protein kinase type I (cGKI). However, the molecular mechanisms of cGKI action, particularly the specific roles of the two cGKI isoforms, cGKIα and cGKIβ, are not clear. To analyze the functions of cGKI isoforms in SMCs, transgenic mice which express the cGKIα or cGKIβ isoform selectively in SMCs were generated (SM-cGKIα or SM-cGKIβ mice. The cGKIα or cGKIβ encoding sequences were integrated into the SMC-specific SM22α gene by homologous recombination in ES cells. Chimeric mice were generated by injection of correctly targeted ES cells into mouse blastocysts. After germline transmission of the modified alleles, the SM-cGKIα and SM-cGKIβ "knock-in" mouse lines could be established. These mouse lines are currently bred on a cGKI-deficient background to eliminate endogenous cGKI expression. This deletion/rescue strategy should help to clarify the specific functions of cGKIα and cGKIβ in SMCs.

Authors’ Affiliations

Institut für Pharmakologie und Toxikologie, TU München, Germany


© BioMed Central Ltd 2005