| First Author | Fukamachi K | Year | 2001 |
| Journal | Biochem Biophys Res Commun | Volume | 287 |
| Issue | 1 | Pages | 257-63 |
| PubMed ID | 11549284 | Mgi Jnum | J:71670 |
| Mgi Id | MGI:2150548 | Doi | 10.1006/bbrc.2001.5579 |
| Citation | Fukamachi K, et al. (2001) Rat neuronal leucine-rich repeat protein-3: cloning and regulation of the gene expression. Biochem Biophys Res Commun 287(1):257-63 |
| abstractText | Rat neuronal leucine-rich repeat protein-3 (rNLRR-3) gene was isolated and cloned from fibrosarcoma cells overexpressing c-Ha-ras. Stable expression of constitutively active forms of Ras (H-Ras(V12) or v-H-Ras) led to a two- to fourfold increase in rNLRR-3 mRNA in rat normal fibroblasts (3Y1). When cells expressing H-Ras(V12) were treated with mitogen activated protein kinase (MAPK) kinase inhibitors (U0126, PD98059), suppression of rNLRR-3 mRNA correlated well with a reduction in MAPK activity. Epidermal growth factor (EGF) led to elevation of rNLRR-3 gene expression about 4 h after stimulation of normal fibroblasts. U0126 completely suppressed the induction by EGF of rNLRR-3 mRNA with abrogation of MAPK phosphorylation. U0126 inhibited the basal transcription of rNLRR-3. LY294002, a PI3 kinase inhibitor, showed a lesser effect on expression of the gene. These results indicate that rNLRR-3 gene expression is regulated mainly through the Ras-MAPK signaling pathway in fibroblasts. |
