| First Author | Butler A | Year | 1994 |
| Journal | Scand J Immunol | Volume | 40 |
| Issue | 3 | Pages | 355-8 |
| PubMed ID | 8091136 | Mgi Jnum | J:20603 |
| Mgi Id | MGI:68684 | Doi | 10.1111/j.1365-3083.1994.tb03473.x |
| Citation | Butler A, et al. (1994) Resistance to secondary amyloidosis in A/J mice is not significantly associated with allelic variants linked to the serum amyloid A gene cluster. Scand J Immunol 40(3):355-8 |
| abstractText | We have tested the hypothesis that structural allelic variants of serum amyloid A confer relative resistance to secondary amyloidosis in the A/J mouse. F2 mice, previously generated from amyloid-resistant (A/J) and amyloid-susceptible (C57BL/6J) strains and categorized with respect to amyloid susceptibility, were genotyped by polymerase chain reaction (PCR) amplification of the polymorphic D7Nds5 microsatellite. This microsatellite is closely linked to the SAA gene cluster and can discriminate between D7Nds5 alleles of A/J and C57BL/6J origin. The distribution of D7Nds5 genotypes in relation to splenic amyloid load did not deviate significantly from that expected of a random distribution, indicating that A/J amyloid resistance is not determined by variants at, or close to, D7Nds5. Therefore, structural alleles in the tightly-linked SAA gene cluster do not confer amyloid resistance in this mouse model. |
