Previous Article | Next Article ![]()
Molecular and Cellular Biology, August 2006, p. 6272-6282, Vol. 26, No. 16
0270-7306/06/$08.00+0 doi:10.1128/MCB.00472-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Department of Developmental Neurobiology,1 Animal Resource Center, St. Jude Children's Research Hospital, Memphis, Tennessee 381052
Received 17 March 2006/ Returned for modification 15 April 2006/ Accepted 1 June 2006
The Crk adaptor protein, which is encoded by two splice variants termed CrkI and CrkII, contains both SH2 and SH3 domains but no catalytic region. It is thought to function in signal transduction processes involved in growth regulation, cell transformation, cell migration, and cell adhesion. Although the function of Crk has been studied in considerable detail in cell culture, its biological role in vivo is still unclear, and no Crk-knockout mouse model has been available. Therefore, we generated a complete null allele of Crk in mice by using the Cre-loxP recombination approach. The majority of Crk-null mice die at late stages of embryonic development, and the remainder succumb shortly after birth. Embryos lacking both CrkI and CrkII exhibited edema, hemorrhage, and cardiac defects. Immunohistochemical examination suggested that defects in vascular smooth muscle caused dilation and rupturing of blood vessels. Problems in nasal development and cleft palate were also observed. These data indicate that Crk is involved in cardiac and craniofacial development and that it plays an essential role in maintaining vascular integrity during embryonic development.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»