m-Calpain is required for preimplantation embryonic development in mice |
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| Authors: | Previn Dutt Dorothy E Croall J Simon C Arthur Teresa De Veyra Karen Williams John S Elce Peter A Greer |
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| Institution: | (1) Division of Cancer Biology and Genetics, Queen's University Cancer Research Institute, Queen's University, Kingston, Ontario, K7L 3N6, Canada;(2) Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, K7L 3N6, Canada;(3) Department of Biochemistry, Queen's University, Kingston, Ontario, K7L 3N6, Canada;(4) Department of Biochemistry, Microbiology and Molecular Biology, University of Maine, Orono, Maine 04469-5735, USA;(5) MRC Phosphorylation Unit, University of Dundee, Perth Rd, Dundee, Angus, DD1 5EH, UK |
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| Abstract: | Background μ-calpain and m-calpain are ubiquitously expressed proteases implicated in cellular migration, cell cycle progression, degenerative
processes and cell death. These heterodimeric enzymes are composed of distinct catalytic subunits, encoded by Capn1 (μ-calpain) or Capn2 (m-calpain), and a common regulatory subunit encoded by Capn4. Disruption of the mouse Capn4 gene abolished both μ-calpain and m-calpain activity, and resulted in embryonic lethality, thereby suggesting essential roles
for one or both of these enzymes during mammalian embryogenesis. Disruption of the Capn1 gene produced viable, fertile mice implying that either m-calpain could compensate for the loss of μ-calpain, or that the
loss of m-calpain was responsible for death of Capn4
-/- mice. |
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