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Molecular and Cellular Biology, June 2001, p. 3959-3963, Vol. 21, No. 12
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.12.3959-3963.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Reproductive Function in Protein Kinase Inhibitor-Deficient Mice

Mouna Belyamani,1,2 Esha A. Gangolli,1,2 and Rejean L. Idzerda1,2,3,*

Department of Medicine, Division of Metabolism, Endocrinology and Nutrition1 and Department of Pharmacology,3 University of Washington, Seattle, Washington 98195, and Veterans Affairs Puget Sound Health Care System, Seattle, Washington 981082

Received 15 March 2001/Accepted 28 March 2001

The protein kinase inhibitor (PKI) family includes three genes encoding small, heat-stable inhibitors of the cyclic AMP-dependent kinase PKA. Each PKI isoform contains a PKA inhibitory domain and a nuclear export domain, enabling PKI to both inhibit PKA and remove it from the nucleus. The PKIbeta isoform, also known as testis PKI, is highly expressed in germ cells of the testis and is found at more modest levels in other tissues. In order to investigate its physiological role, we have generated PKIbeta knockout mice by gene targeting. These mice exhibit a partial loss of PKI activity in testis but remain fertile with normal testis development and function. PKIbeta knockout females also reproduce normally. The PKIbeta mutants were crossed with our previously derived PKIalpha mutants to obtain double-knockout mice. Remarkably, these mice are also viable and fertile with no obvious physiological defects in either males or females.

* Corresponding author. Mailing address: University of Washington, Department of Medicine, Box 357138, Seattle, WA 98195. Phone: (206) 616-0481. Fax: (206) 616-0499. E-mail: idzerda{at}u.washington.edu.

Molecular and Cellular Biology, June 2001, p. 3959-3963, Vol. 21, No. 12
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.12.3959-3963.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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