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Publication : Defective smooth muscle regulation in cGMP kinase I-deficient mice.

First Author  Pfeifer A Year  1998
Journal  EMBO J Volume  17
Issue  11 Pages  3045-51
PubMed ID  9606187 Mgi Jnum  J:48058
Mgi Id  MGI:1261684 Doi  10.1093/emboj/17.11.3045
Citation  Pfeifer A, et al. (1998) Defective smooth muscle regulation in cGMP kinase I-deficient mice. EMBO J 17(11):3045-51
abstractText  Regulation of smooth muscle contractility is essential for many important biological processes such as tissue perfusion, cardiovascular haemostasis and gastrointestinal motility. While an increase in calcium initiates smooth muscle contraction, relaxation can be induced by cGMP or cAMP. cGMP-dependent protein kinase I (cGKI) has been suggested as a major mediator of the relaxant effects of both nucleotides. To study the biological role of cGKI and its postulated cross-activation by cAMP, we inactivated the gene coding for cGKI in mice. Loss of cGKI abolishes nitric oxide (NO)/cGMP-dependent relaxation of smooth muscle, resulting in severe vascular and intestinal dysfunctions. However, cGKI-deficient smooth muscle responded normally to cAMP, indicating that cAMP and cGMP signal via independent pathways, with cGKI being the specific mediator of the NO/cGMP effects in murine smooth muscle.
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