This Drosophila model of malignant glioma uses the GAL4/UAS system to drive expression of an activated form of Dmel\Ras85D (the allele Ras85DV12) in glial cells. The RAS proteins control signaling pathways that are key regulators of several aspects of normal cell growth and malignant transformation. The constitutively active Ras85DV12 is analogous to oncogenic mutations found in orthologous human RAS proteins KRAS, NRAS, and HRAS.
The human genes Hsap\HRAS and Hsap\KRAS have been introduced into flies, but have not been characterized in the context of this disease model.
Expression of activated Dmel\Ras85D in glial cells, effected by RNAi, results in numerous glial neoplasias detectable at the larval stage; brain tumors cause early lethality in the pupal stage.
See also 'cancer, multiple, RAS-related' (FBhh0000474).
[updated Feb. 2022 by FlyBase; FBrf0222196]
The RAS proteins are members of a large superfamily of low-molecular-weight GTP-binding proteins. The RAS proteins control signaling pathways that are key regulators of several aspects of normal cell growth and malignant transformation. Three members of the RAS family, HRAS, KRAS and NRAS, are found to be activated by mutation in human tumors. These three members are very closely related, having 85% amino acid sequence identity (Downward, 2003; pubmed:12509763).
Many to many: multiple paralogs and orthologs in both species.
Many to many: multiple paralogs and orthologs in both species.
Many to many: multiple paralogs and orthologs in both species.