| First Author | Bélanger LF | Year | 2003 |
| Journal | Mol Cell Biol | Volume | 23 |
| Issue | 14 | Pages | 4778-87 |
| PubMed ID | 12832465 | Mgi Jnum | J:84382 |
| Mgi Id | MGI:2667511 | Doi | 10.1128/MCB.23.14.4778-4787.2003 |
| Citation | Belanger LF, et al. (2003) Mek2 is dispensable for mouse growth and development. Mol Cell Biol 23(14):4778-87 |
| abstractText | MEK is a dual-specificity kinase that activates the extracellular signal-regulated kinase (ERK) mitogen-activated protein (MAP) kinase upon agonist binding to receptors. The ERK/MAP kinase cascade is involved in cell fate determination in many organisms. In mammals, this pathway is proposed to regulate cell growth and differentiation. Genetic studies have shown that although a single Mek gene is present in Caenorhabditis elegans, Drosophila melanogaster, and Xenopus laevis, two Mek homologs, Mek1 and Mek2, are present in the mammalian cascade. The inactivation of the Mek1 gene leads to embryonic lethality and has revealed the unique role played by Mek1 during embryogenesis. To investigate the biological function of the second homolog, we have generated mice deficient in Mek2 function. Mek2 mutant mice are viable and fertile, and they do not present flagrant morphological alteration. Although several components of the ERK/MAP kinase cascade have been implicated in thymocyte development, no such involvement was observed for MEK2, which appears to be nonessential for thymocyte differentiation and T-cell-receptor-induced proliferation and apoptosis. Altogether, our findings demonstrate that MEK2 is not necessary for the normal development of the embryo and T-cell lineages, suggesting that the loss of MEK2 can be compensated for by MEK1. |
