Therefore, although the presence of mutant monomers may increase the tissue damage found in individuals with MFS [26], the levels of normal fibrillin-1 seem to have the potential to modulate the pathogenic effects of mutated proteins.
This suggests that the high prevalence of mutant genotype may increase the susceptibility to oxidative stress associated diseases.
The presence of ectopic developing vulvae along the ventral mid-line of lin-15 mutant animals may increase the severity of the AVKR axonal defect by contributing post-outgrowth bundling defects during larval development.
These results implicate SPOP as a novel participant in DSB repair, suggest that SPOP mutation drives prostate tumorigenesis in part through genomic instability, and indicate that mutant SPOP may increase response to DNA-damaging therapeutics.
Furthermore, repeated treatment interruptions may accelerate the emergence of resistant mutant virus and may increase the infection of long term reservoirs such as macrophages which will accelerate progression to AIDS.
Thus, mutant K-Ras may increase the dependency of tumor cells on de novo lipogenesis and provide a biological basis for targeting these tumors, or a subset of them, with a FASN inhibitor.
Together, our data demonstrate that the average mitochondrial density in muscles is not decreased in both mutants of mtDNA replication, and in fact may increase in tam3/tam9 mutants.
Use of constitutively active Rho GTPase mutants to preferentially capture GAPs may increase the likelihood of identifying these regulators in platelets.
