The synthetic lethality interactions between these two genes may reflect their more general roles beyond CFS protection.
However, when Rad52 is depleted by shRNAs in FANCM KO cells, a strong proliferation defect is observed, suggesting a synthetic lethality interaction between these two genes.
Combined inactivation of FANCM and Rad52 leads to a strong cell proliferation defect, suggesting a synthetic lethality interaction between these two genes.
Comparison of the 16S rDNA and catA phylogenies revealed an absence of congruence between these two genes.
Suppression of Rad52 expression in combination with FANCM knockout drastically reduces cell and tumor growth, suggesting a synthetic lethality interaction between these two genes, which offers a potential targeted treatment strategy for FANCM-deficient tumors with Rad52 inhibition.
HLA DPB1 and DQA1 may play a direct role in immune response associated with HIV-1 infection, or the critical region may be located between these two genes.
To investigate the role of other segment polarity genes in the mutual control between these two genes, we have examined wingless and engrailed protein distribution in embryos mutant for each of the segment polarity genes.
The synchronously replicating gene LARP resides between these two genes.
Moreover, a significant correlation between these two genes existed in control, schizophrenia and bipolar subjects.
Therefore, a distinction between these two genes on association level is not possible.
However, we were also unable to demonstrate evidence for epistasis between these two genes (Table 10).
