| First Author | Paschaki M | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 4 | Pages | e62274 |
| PubMed ID | 23638021 | Mgi Jnum | J:200551 |
| Mgi Id | MGI:5508845 | Doi | 10.1371/journal.pone.0062274 |
| Citation | Paschaki M, et al. (2013) Transcriptomic analysis of murine embryos lacking endogenous retinoic acid signaling. PLoS One 8(4):e62274 |
| abstractText | Retinoic acid (RA), an active derivative of the liposoluble vitamin A (retinol), acts as an important signaling molecule during embryonic development, regulating phenomenons as diverse as anterior-posterior axial patterning, forebrain and optic vesicle development, specification of hindbrain rhombomeres, pharyngeal arches and second heart field, somitogenesis, and differentiation of spinal cord neurons. This small molecule directly triggers gene activation by binding to nuclear receptors (RARs), switching them from potential repressors to transcriptional activators. The repertoire of RA-regulated genes in embryonic tissues is poorly characterized. We performed a comparative analysis of the transcriptomes of murine wild-type and Retinaldehyde Dehydrogenase 2 null-mutant (Raldh2 (-/-)) embryos - unable to synthesize RA from maternally-derived retinol |
