The Lamc2 gene encodes for the gamma-2 subunit of laminin 5, which is an extracellular matrix glycoprotein found in cutaneous basement membranes. These mice carry a spontaneous mutation of Lamc2 that arose on the 129X1 background and is a single retroviral insertion (murine leukemia virus long terminal repeat) in intron 18. Onset of progressive skin blistering disease in homozygotes on the congenic C57BL/6J background (N11) is approximately 13 weeks. Homozygotes backcrossed to C57BL/6J for 11 generations exhibit ulcerated lesions and tissue granulation in ear skin, which develops into deformed pinna. Thickened epidermis (hyperplasia) and subepidermal separation, with little to no inflammation, occurs in the skin of the footpads and tail. 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. This is the case for the strain above. The PLoS Genet. 2014 Feb 13;10(2):e1004068 publication described mice that were backcrossed to C57BL/6 for 11 generations (N11), while this strain has been backcrossed further to N13 to reduce the 129X1 congenic segment linked to the mutation. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

This Lamc2jeb mutant mouse strain may be useful in studies of epidermolysis bullosa and is a model for Non-Herlitz Type Junctional Epidermolysis Bullosa.

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Our minimum guarantee for cryorecovery orders is 2 carriers. To ensure that your colony can be rapidly expanded upon arrival, additional carriers may be added to your order.