| First Author | Bartholin L | Year | 2008 |
| Journal | Genesis | Volume | 46 |
| Issue | 12 | Pages | 724-31 |
| PubMed ID | 18821589 | Mgi Jnum | J:148747 |
| Mgi Id | MGI:3846301 | Doi | 10.1002/dvg.20425 |
| Citation | Bartholin L, et al. (2008) Generation of mice with conditionally activated transforming growth factor beta signaling through the TbetaRI/ALK5 receptor. Genesis 46(12):724-31 |
| abstractText | We generated a transgenic mouse strain (LSL-TbetaRI(CA)) containing a latent constitutively active TGFbeta type I receptor (TbetaRI/ALK5) by using a knock-in strategy into the X chromosome-linked hypoxanthine phosphoribosyl-transferase (Hprt) locus. Transgene expression, under the control of the ubiquitous CAG (human cytomegalovirus enhancer and chicken beta-actin) promoter, is repressed by a floxed transcriptional 'Stop' (LSL, Lox-Stop-Lox). In the presence of cre-recombinase, the 'Stop' is excised to allow TbetaRI(CA) transgene expression. We showed that restricted expression of TbetaRI(CA) in T lymphocytes efficiently activates TGFbeta signaling and rescues the T-cell autoimmune disorders of TGFbetaRII conditional knockouts. Unexpectedly, our study reveals that TGFbeta signaling upregulation controls T-cell activation but does not impair their development or their peripheral homeostasis. In addition to the information provided on TGFbeta effects on T-cell biology, LSL-TbetaRI(CA) mouse constitutes an attractive tool to address the effect of TGFbeta signaling upregulation in any cell type expressing the cre-recombinase. |
