This is the original congenic background strain on which Dr. Mel Bosma discovered the spontaneous scid mutation.
Mice homozygous for the Prkdcscid mutation lack both T and B cells due to a defect in V(D)J recombination. Therefore, they easily accept foreign tissue transplants, including human tumors, making them effective models for testing new cancer treatments and as hosts for human immune system tissues (i.e., SCID-hu).
The C.B-17 scid mice exhibit extremely low levels of Ig in ~20% of the mice at 12 weeks of age. The incidence of Ig will increase as the mice age. Despite this "leakiness" C.B-17 scids do not mount an antibody response to challenge by immunogenic material.
Strain is similar to BALB/c except it carries the Igh-1b allele from the C57BL/Ka strain.
Taconic has identified cardiac calcinosis in the CB17SC with an incidence of up to 50% in males at 7 weeks. Cardiac calcinosis is an incidental finding which does not cause clinical illness. Certain inbred strains such as BALB/c are predisposed to developing cardiac calcinosis.
Genetic Background:
C.B-17 Background
Origin:
The C.B-17 scid spontaneous mutant model was derived by embryo transfer in 1989 and rederived in 1998 using donor females from the laboratory of Dr. Mel Bosma of the Fox Chase Cancer Center. The Taconic foundation colony was at F27 in 2005.
For some applications, weight may be critical. For orders where weight is critical, please place orders by weight, not by age. Taconic can accept orders by weight for this model. A minimum 3 gram span is required. All weights are weights at time of packing. Mice and rats can lose weight in transit. Orders for specific weight spans will be assessed a nominal fee. More detail on weight order policies is available.
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