| First Author | Mukhopadhyay R | Year | 2006 |
| Journal | FEBS Lett | Volume | 580 |
| Issue | 16 | Pages | 3889-94 |
| PubMed ID | 16797549 | Mgi Jnum | J:110338 |
| Mgi Id | MGI:3640037 | Doi | 10.1016/j.febslet.2006.06.017 |
| Citation | Mukhopadhyay R, et al. (2006) Targeted disruption of the mouse Asna1 gene results in embryonic lethality. FEBS Lett 580(16):3889-94 |
| abstractText | The bacterial ArsA ATPase is the catalytic component of an oxyanion pump that is responsible for resistance to arsenicals and antimonials. Homologues of the bacterial ArsA ATPase are widespread in nature. We had earlier identified the mouse homologue (Asna1) that exhibits 27% identity to the bacterial ArsA ATPase. To identify the physiological role of the protein, heterozygous Asna1 knockout mice (Asna1+/-) were generated by homologous recombination. The Asna1+/- mice displayed similar phenotype as the wild-type mice. However, early embryonic lethality was observed in homozygous Asna1 knockout embryos, between E3.5 (E=embryonic day) and E8.5 stage. These findings indicate that Asna1 plays a crucial role during early embryonic development. |
