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CNL is the most prominent mechanism of component disruption, with RBX1 being the most frequently disrupted component.
We found that RBX1 sustained an extremely high frequency of copy-number loss, representing a characteristic of NRF2 inhibitory complex component disruption unique to OVCA.
While the magnitude and frequency of KEAP1/CUL3/RBX1 complex component disruption were more prominent in the cohort we assessed, these results reveal the potential importance of alternative mechanisms of NRF2 activation in ovarian cancer and warrant consideration in future studies.
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We present our recent work on resource allocation problems for the monitoring and inspection of pipeline infrastructure networks in the face of component disruptions.
This work aims to combine new probabilistic and multiscale modeling approaches to provide insights into the performance of spatially distributed infrastructure subject to component disruptions from natural disasters or other sources.
Both chemotactic and phototactic behavior in R. centenum are under Che1 control, as strains with Che1 component disruptions have motility phenotypes similar to those of E. coli chemotactic mutants [ 39].
Moreover, we note that OVCA sustains a unique pattern of complex component gene disruption compared to other cancer types, including those for which NRF2 activation through complex disruption are well known.
A similar result was obtained by RNAi against unc-52, which encodes the basement membrane component perlecan; disruption of unc-52 results in embryonic arrest midway through elongation (paralyzed arrest at twofold, Pat, phenotype) (Rogalski et al. 1993).
Analysis of the frequency of KEAP1/CUL3/RBX1 E3-ubiquitin ligase complex component gene disruption in a broad spectrum of cancer types revealed that component gene alteration is a common phenomenon in cancer, albeit at varying frequencies, suggesting this NRF2 inhibitory complex is important to many cancer types).
They suggested that a remarkably high frequency of DNA and mRNA alterations may affect components of the KEAP1/CUL3/RBX1 complex, through a unique pattern of genetic mechanisms in the paper entitled " Unique pattern of component gene disruption in the NRF2 inhibitor KEAP1/CUL3/RBX1 E3-ubiquitin ligase complex in serous ovarian cancer".
Previous work allowed us to model psoriasis in skin-humanized mice through proper combinations of inflammatory cell components and disruption of barrier function.
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