These Plg knock-out mice exhibit multiple spontaneous thrombotic lesions in liver, stomach, colon, rectum, lung, pancreas, and other tissues. They are suitable for use in applications related to studies of fibrinolysis and hemostasis.
Dr. Thomas Bugge, NIH/NIDCR
Mice homozygous for the Plgtm1 targeted mutation are viable and fertile. They show a progressive multi-organ pathology and die around 6 months of age. The pathology is characterized by wasting, rectal prolapse, impaired skin wound healing, gastointestinal ulceration, and thrombosis. No details of mammary gland morphology have been provided.
This mutation was generated by replacing a 9 kb fragment of the Plg gene with a vector containing Hprt. The 129-derived E14TG2a ES cell line was used.
|Allele Name||targeted mutation 1, Jay L Degen|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||Plg-; Plg0|
|Gene Symbol and Name||Plg, plasminogen|
|Strain of Origin||129P2/OlaHsd|
|Molecular Note||A PGK-HPRT minigene replaces proximal promoter sequences and the first two exons of the gene. Northern analysis and enzymatic activity assays were used to demonstrate the lack of a transcript and functional protein, respectively, in homozygous mutant animals.|
Homozygous mice are are viable and fertile, but develop progressive multi-organ pathology and die around 6 months of age. When maintaining a live colony, heterozygous mice may be bred together, to wildtype mice from the colony or to C57BL/6J inbred mice (Stock No. 000664). The expected coat color from breeding is black.
When using the Plg- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002830 in your Materials and Methods section.