| First Author | Davoodi-Semiromi A | Year | 2007 |
| Journal | Biochem Biophys Res Commun | Volume | 356 |
| Issue | 3 | Pages | 655-61 |
| PubMed ID | 17382905 | Mgi Jnum | J:121519 |
| Mgi Id | MGI:3710307 | Doi | 10.1016/j.bbrc.2007.03.028 |
| Citation | Davoodi-Semiromi A, et al. (2007) Truncated pStat5B is associated with the Idd4 locus in NOD mice. Biochem Biophys Res Commun 356(3):655-61 |
| abstractText | We investigate JAK-STAT5 activation and its relationship to full-length Stat5B (FL-Stat5) and constitutive phosphorylated carboxy-truncated Stat5B (ct-pStat5) in four different strains of mouse. Our electrophoresis mobility shift assays data indicate constitutive phosphorylation of full-length-Stat5 (p<0.001) and DNA binding in NOD but not in B6 mice. Our data suggest that the relative ratio of FL-Stat5: ct-Stat5 in NOD is 5- to 8-fold lower (p<0.0001) when compared with normal B6 mice. Additionally, EMSAs data from B6.NOD/c11 suggest contribution of Idd4 susceptibility locus on chromosome 11 in constitutive phosphorylation of Stat5 in NOD mice. The presence of ct-pStat5 in regulatory T cells of NOD mice suggests this form of Stat5 is associated with impaired function of Tregs in NOD mouse. In agreement with our previous report the JAK-Stat5B defective pathway in NOD mice along with other defective factors is associated with the pathogenesis of autoimmune type 1 diabetes in NOD mice. |
