| First Author | Allen CE | Year | 2007 |
| Journal | Gene Expr | Volume | 14 |
| Issue | 2 | Pages | 83-100 |
| PubMed ID | 18257392 | Mgi Jnum | J:266689 |
| Mgi Id | MGI:6256793 | Doi | 10.3727/105221607783417574 |
| Citation | Allen CE, et al. (2007) Disruption of ZAS3 in mice alters NF-kappaB and AP-1 DNA binding and T-cell development. Gene Expr 14(2):83-100 |
| abstractText | The large zinc finger proteins, ZAS, regulate the transcription of a variety of genes involved in cell growth, development, and metastasis. They also function in the signal transduction of the TGF-beta and TNF-alpha pathways. However, the endogenous protein of a representative member, ZAS3, is rapidly degraded in primary lymphocytes, which limits the determination of its physiological function in vitro. Therefore, we have generated mice with targeted disruption of ZAS3. Oligonucleotide-based microarray analyses revealed subtle but consistent differences in the expression of genes, many of which are associated with receptor or signal transduction activities between ZAS3+/+ and ZAS3-/- thymi. Gel mobility shift assays showed altered DNA binding activities of NF-kappaB and AP-1 proteins in ZAS3-deficient tissues, including the thymus. Lymphocyte analysis suggested a subtle but broad function of ZAS3 in regulating T-cell development and activation. In CD3+ ZAS3-/- thymocytes, the CD4/ CD8 ratio was decreased and CD69 expression was decreased. In peripheral CD4+ ZAS3-/- lymphocytes we observed an increased number of memory T cells. |
