Mice homozygous for this E-selectin mutant allele (E-/-) are viable and fertile with normal circulating leukocyte and platelet profiles. While several transcripts are generated from the mutant locus (due to transcription from the endogenous promoter and/or bidirectional transcription initiated from the pgk promoter in the neo-resistance cassette), these frame-shifted transcripts are non-functional with several predicted stop codons. In contrast to wildtype mice, no protein product is detected in several tissues isolated from LPS-injected homozygous mice. Homozygous mice exhibit abnormal responses to inflammatory stimuli. E-selectin deficiency results in endostatin unresponsiveness (as shown in corneal angiogenesis (mixed B6;129 genetic background) and aortic explant (C57BL/6 congenic background) experiments). These E-selectin mutant mice may be useful in studying inflammation, leukocyte rolling, leukocyte-endothelial adhesion, angiogenesis, and cancer.
Of note, E-selectin mutant mice are also be available on a C57BL/6J congenic background (Stock No. 008236), a BALB/cJ congenic background (Stock No. 008237), on a mixed genetic background (Stock No. 002915), and along with other selectin mutations (Stock No. 002916, Stock No. 003806, and Stock No. 003807).
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype of these E-selectin mutant mice could vary from that originally described. We will modify the strain description if necessary as published results become available.
