Mice homozygous for both the hHGFki and Prkdcscid alleles, also called immunocompromised hHGFki mice, are viable and fertile. 

The hHGFki allele is a "humanized" knock-in mutation that replaces the mouse hepatocyte growth factor (HGF) coding region downstream of the signal sequence with the human HGF cDNA sequence. As a result, the endogenous mouse promoter drives expression of human HGF. While the human HGF activates both the human and murine form of its tyrosine kinase receptor (met proto-oncogene (MET; c-Met)), the murine HGF is unable to activate human MET. Mice homozygous for hHGFki express only the human form of HGF. In homozygous hHGFki mice, HGF expression from the knock-in allele is observed in developing embryo, as well as adult liver, kidney and lung. hHGFki homozygous mice exhibit an increase in serum HGF after clotting. 

Mice homozygous for the Prkdcscid mutation exhibit T- and B-cell deficiency.

Use of MICE only available to non-profit entities.

Of note, hHGFki;scid mice also harboring the Il2R&gamma;cnull mutation on the NOD-congenic background are available: NSG-hHGFki (Stock No. <a href="https://www.jax.org/strain/014553">014553</a>).

These hHGFki;scid mice harbor the "humanized" knock-in mutation (hHGFki) that replaces the mouse hepatocyte growth factor (HGF) coding factor, and the Prkdcscid mutation that results in T- and B-cell deficiency. These mice may be useful in studying the HGF/MET pathway in human tumor xenografts and mouse tumor allografts.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

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