Exact(13)
Martelli, A. et al. Clinical data and characterization of the liver conditional mouse model exclude neoplasia as a non-neurological manifestation associated with Friedreich's ataxia.
In 12 week PB promoted livers, the cell proliferation in PBP/MED1fl/fl livers was still higher than in liver conditional nulls.
As no predisposition to cancer could be observed in both cohorts, we revisited the phenotype of the liver conditional mouse model.
Using the PBP/MED1 liver conditional null (PBP/MED1ΔLiv) mice, we reported that PBP/MED1 is essential for liver regeneration and the peroxisome proliferator-activated receptor α ligand Wy-14,643-induced receptor-mediated hepatocarcinogenesis.
Furthermore, PBP/MED1 null hepatocytes in PBP/MED1 liver conditional null (PBP/MED1ΔLiv) mice did not develop hepatocellular carcinoma (HCC) when chronically exposed to a PPARα ligand, indicating that PBP/MED1 is essential for this receptor-mediated liver tumorigenesis (32).
Among the mouse models of FRDA, the liver conditional mouse model pointed to a tumor suppressor activity of frataxin leading to the hypothesis that individuals with FRDA might be predisposed to cancer.
Similar(46)
Scarb1tm1.1Thh, also known as hypomSCARB1-KOliver [43], was developed as a liver-conditional knockout using Cre recombinase loxP technology.
Alb/cre,Pdss2 loxP/loxP liver-conditional Pdss2 knockout mice that have normal renal function (Peng et al, 2008).
Liver-conditional and podocyte-conditional Pdss2 knockout mice were generated as previously described (Peng et al, 2008).
The influence of long-term probucol treatment on pathway-level expression alterations was also assessed in liver-conditional Pdss2 knockout mice.
In contrast, a trend towards decreased MnSOD enzyme activity in isolated liver mitochondria was seen in missense mutant or liver-conditional knockout mice treated long-term with probucol.
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