Among these proteins, twelve were found to be upregulated in the models compared with the controls and these same proteins were found to be downregulated in the FSGD group compared with the models.
Differentially expressed proteins of the FSGD and model groups were catalogued based on GO enrichment analysis.
HP and AAT levels were significantly decreased (P < 0.001, P < 0.001, resp.) in the model group compared to the FSGD group.
We examined the therapeutic effect of FSGD in the adenine-induced CRF rats.
We presumed that HP and AAT could be applicable as markers in the progression of CRF and may be the candidate biomarkers of FSGD. Further research is needed to explore the role of these protein functions in pathogenesis.
Caption: Figure 4: The expressions of HP and AAT among the control, model, and FSGD groups obtained by the ELISA, Western blot, and RT-qPCR methods.
Although most duplicated genes tend to undergo beneficial mutation after FSGD, 3.3% to 7.2% of duplicated genes survive during evolution.
First, DNAH9A underwent duplication-degeneration- complementation (DDC) after FSGD. DDC is a temporary status between gene duplication and subfunctionalization (Amores et al., 1998; Wang et al., 2010).
Divergent duplication evolution in ray-finned fishes occurred after FSGD. Some fishes suffered beneficial mutation, whereas others preferentially preserved the duplicates, such as the DNAH9 duplicates in P.
From 2r to 3r: Evidence for a fish-specific genome duplication (fsgd).