| First Author | Mochizuki R | Year | 2003 |
| Journal | Biochem Biophys Res Commun | Volume | 310 |
| Issue | 4 | Pages | 1219-26 |
| PubMed ID | 14559245 | Mgi Jnum | J:86413 |
| Mgi Id | MGI:2679791 | Doi | 10.1016/j.bbrc.2003.09.153 |
| Citation | Mochizuki R, et al. (2003) Targeted disruption of the neurochondrin/norbin gene results in embryonic lethality. Biochem Biophys Res Commun 310(4):1219-26 |
| abstractText | Neurochondrin/norbin is a cytoplasmic protein involved in dendrite outgrowth. The expression of the gene has been restricted to neural, bone, and chondral tissues. To identify the functions of the gene in vivo, we have generated mice with a disrupted mutation in the neurochondrin/norbin gene. Histological analysis of heterozygous mutant mice indicates the possibility of specific functions of neurochondrin/norbin in chondrocyte differentiation. We defined the expression patterns of neurochondrin/norbin-lacZ fusion protein in the central nervous system. In the developing olfactory bulb, beta-galactosidase activity was detected in the mantle layer at 12.5 dpc and the strongest activity was detected in the presumptive mitral or tufted cell layer at 15.5 dpc. beta-Galactosidase activity was also detected in the lateral choroid plexus. In homozygous (-/-) mutant mice, the disruption of the neurochondrin/norbin gene leads to early embryonic death between 3.5 and 6.5 dpc. This result indicates that neurochondrin/norbin gene function is essential for the early embryogenesis. |
