| First Author | Xiao J | Year | 2018 |
| Journal | FEBS Lett | Volume | 592 |
| Issue | 18 | Pages | 3101-3110 |
| PubMed ID | 30098009 | Mgi Jnum | J:266331 |
| Mgi Id | MGI:6202796 | Doi | 10.1002/1873-3468.13221 |
| Citation | Xiao J, et al. (2018) Consequences of Cre-mediated deletion of Ciz1 exon 5 in mice. FEBS Lett 592(18):3101-3110 |
| abstractText | CIZ1 plays a role in DNA synthesis at the G1/S checkpoint. Ciz1 gene-trap null mice manifest motor dysfunction, cell-cycle abnormalities, and DNA damage. In contrast, it has previously been reported that mouse embryonic fibroblasts derived from presumed Ciz1 knock-out mice (Ciz1(tm1.1Homy/tm1.1Homy) ) generated by crossing Cre-expressing mice with exon 5-floxed mice (Ciz1(tm1Homy/tm1Homy) ) do not exhibit evidence of enhanced DNA damage following gamma-irradiation or cell-cycle defects. Here, we report that Ciz1(tm1.1Homy/tm1.1Homy) mice show loss of Ciz1 exon 5 but are neurologically normal and express abnormal transcripts (Ciz1(DeltaE5/DeltaE5) mice) that are translated into one or more proteins of approximate wild-type size. Therefore, Ciz1(tm1.1Homy/tm1.1Homy) mice (Ciz1(DeltaE5/DeltaE5) ) lose residues encoded by exon 5 but may gain function from novel amino acid sequences. |
