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J Biol Chem, Vol. 274, Issue 29, 20450-20456, July 16, 1999
From XCE, a new member of the endothelin-converting
enzyme and neutral endopeptidase family, is preferentially expressed in
specific areas of the central nervous system including spinal chord and medulla. To elucidate the importance and function of XCE, we disrupted its gene in mouse embryonic stem cells by homologous recombination and
created mice deficient in XCE. The resulting phenotype is characterized
by neonatal lethality. All XCE
Neonatal Lethality in Mice Deficient in XCE, a Novel Member of
the Endothelin-converting Enzyme and Neutral Endopeptidase Family
,,
Preclinical Cardiovascular Research, ¶ CNS
Research, and ** Toxicology, F. Hoffmann-La Roche Ltd., Pharma
Division, Grenzacherstrasse 124, 4070 Basel, Switzerland and the
Friedrich-Miescher Institute,
Maulbeerstrasse 66, 4058 Basel, Switzerland
/ homozygous mice died of
respiratory failure shortly after birth, and in most cases their lungs
were never ventilated. Apart from the atelectasis, anatomical and
histological examinations of embryonic day 18.5 XCE / embryos and
newborn homozygotes did not reveal any obvious abnormalities in organs
and tissues. Malformations that are related to the knock-out were also
not found in the skeletons of XCE / mice. In addition, XCE
knock-out animals showed no deficiency of pulmonary surfactant proteins
and had normal heart beat frequencies. Taken together, our results
demonstrate that XCE is an essential gene. The phenotype of the
XCE-deficient mice together with the central nervous system-specific
expression further suggest that XCE may play a vital role in the
control of respiration.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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