| Primary Identifier | MGI:3689387 | Allele Type | Transgenic |
| Attribute String | Knockdown | Gene | Tg(B19-RNAi:Il3)241Ckn |
| Strain of Origin | FVB/N X (BALB/c x C57BL/6)F1 | Is Recombinase | false |
| Is Wild Type | false |
| description | Of 5 transgenic founder lines, two exhibited no abnormal phenotype and were not further characterized. One of the other founder mice died of neurologic disease at 3 months, without having bred. Founders 241 and 244 transmitted the transgene and both the lymphoproliferative and neurologic phenotypes to their progeny. The pathology of the neurologic and of the lymphoproliferative disorders differs between the two lines only in penetrance and in age of onset (3-6 months for line 241 compared to 6-12 months for line 244). |
| molecularNote | This transgene consists of the full length, 990-bp mouse interleukin 3 cDNA, in reverse (antisense) orientation, under control of the B19 parvovirus promoter and a T-cell dominant control region from the 3' end of the human CD2 gene. A human beta-globin gene segment including the 3' end of exon 2, all of intron 2 and exon 3, the polyadenylation signal and some 3' flanking DNA is present just downstream of the Il3 sequence. Interleukin 3 antisense RNA is detected by RT-PCR analysis in mature CD3+ T lymphocytes of transgenic animals both with lymphoproliferation and with no disease phenotype, in transgenic B220+IgM- pre-B cells, and in brains of both asymptomatic and neurologically affected transgenic mice. Il3 antisense transcripts are present in cultured splenocytes from asymptomatic transgenic mice following in vitro concanavalin A (ConA) stimulation, and ELISA of supernatants from these cultures demonstrates a 5-fold reduction in interleukin 3 secretion compared to similar cultures of control splenocytes. |
