The severe combined immunedeficient SCID mouse

The SCID mutation spontaneously occurs in BALB/c mice, where it impairs double-strand DNA break repair. V(D)J rearrangement is primarily affected, resulting in a defective coding joint formation which prevents the development of mature B and T cells. The molecular consequence of the SCID mutation is a genetically determined deficiency of the DNA-dependent protein kinase (DNA-PK) which induces DNA break repair by forming an activated complex with the DNA end-binding Ku proteins (p80 and p70) upon association with the damaged DNA.

there is improved human lymphocyte trafficking from the SCID mouse peritoneal cavity to peripheral tissues.

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