First Author | Matsuzaki T | Year | 2018 |
Journal | Genesis | Volume | 56 |
Issue | 4 | Pages | e23099 |
PubMed ID | 29508517 | Mgi Jnum | J:261688 |
Mgi Id | MGI:6155322 | Doi | 10.1002/dvg.23099 |
Citation | Matsuzaki T, et al. (2018) Generation and characterization of a mouse line carrying Reck-CreERT2 knock-in allele. Genesis 56(4):e23099 |
abstractText | Reck encodes a membrane-anchored glycoprotein implicated in the regulation of extracellular metalloproteinases, Notch-signaling, and Wnt7-signaling and shown to play critical roles in embryogenesis and tumor suppression. Precise mechanisms of its actions in vivo, however, remain largely unknown. By homologous recombination, we generated a new Reck allele, Reck(CreERT2) (MGI symbol: Reck<tm3.1(cre/ERT2)Noda>). This allele is defective in terms of Reck function but expected to induce loxP-mediated recombination in the cells committed to express Reck. Similarity in the expression patterns of the Reck(CreERT2) transgene and the endogenous Reck gene was confirmed in five tissues. In the adult hippocampus, induction of Reck expression after transient cerebral ischemia could be demonstrated using this allele. These results indicate the utility of this Cre-driver allele in further studies. |