Disease relevance of Epistasis, Genetic

• Genetic epistasis analysis indicates that OSR-1 regulates survival under osmotic stress via CaMKII and a conserved p38 MAP kinase signaling cascade and regulates osmotic avoidance and resistance to acute dehydration likely by distinct mechanisms [1].

High impact information on Epistasis, Genetic

• Based on genetic epistasis analysis, nsy-1 appears to act downstream of the CaMKII unc-43, and NSY-1 associates with UNC-43, suggesting that UNC-43/CaMKII activates the NSY-1 MAP kinase cassette [2].
• Genetic epistasis data are consistent with a model that Tsc1 and Tsc2 function together in the insulin signaling pathway [3].
• Genetic epistasis studies revealed an early requirement for RAN1 in the ethylene pathway [4].
• Genetic epistasis experiments indicate that shn functions downstream of the dpp signal and its receptors [5].
• Genetic epistasis analysis suggests that ksr-1 acts downstream of or in parallel to let-60 ras [6].

Biological context of Epistasis, Genetic

• Evidence for genetic epistasis in human insulin resistance: the combined effect of PC-1 (K121Q) and PPARgamma2 (P12A) polymorphisms [7].
• Genetic resistance to Friend leukemia virus in mice: masking of Fv-2 phenotype by an epistatic gene, Fv-4 [8].

Associations of Epistasis, Genetic with chemical compounds

• Genetic epistasis experiments demonstrate that bazooka acts downstream of discs large in tumor cell invasion [9].
• Genetic epistasis over mutations that eliminate detectable levels of serotonin reveals that egl-30 requires serotonin to regulate egg laying [10].
• Methods for site-directed mutagenesis, in vitro analysis of mutant proteins, and in vivo characterization of mutants in response to UV or gamma irradiation, MMS, HU, and temperature, as well as genetic epistasis are described [11].
• The combination of angiotensinogen 235 TT and angiotensin-converting enzyme DD showed further reduction (P=0.0377) when compared with angiotensinogen 235 TT alone, an example of genetic epistasis [12].

Gene context of Epistasis, Genetic

• Genetic epistasis experiments indicate that wg signaling operates by inactivating the zw3 repression of en autoactivation [13].
• By genetic epistasis, we demonstrate that PGRP-LC acts upstream of the imd gene [14].
• Genetic epistasis experiments indicate that lin-25 is required in the inductive signaling pathway downstream of let-60 Ras and the Raf/MAP kinase cascade [15].
• These results, together with genetic epistasis studies, suggest that postsynaptic Pum modulates synaptic function via direct control of eIF-4E expression [16].
• Although genetic epistasis experiments place IFT proteins downstream of the Hh receptor and upstream of the Gli transcription factors, the mechanism by which IFT regulates Gli function is unknown [17].

References