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), according to Phb1/Phb2 interdependence. While both models are liver-specific, our Phb2-KO is time-specific (Phb2fl/fl;Alb-Cre-ERT2), not constitutive. Specifically, we induced the KO in adult mice (8 weeks old), avoiding the absence of liver prohibitins at the embryonic and developmental stages.
Although unpublished, we also generated constitutive liver-specific Phb2-KO (Phb2fl/fl;Alb-Cre). In such a case, we likewise observed hepatocellular carcinoma with visible nodules on livers of 11-week-old Phb2-KO mice (see Fig. 1), compared with a similar observation in constitutive Phb1-KO by the age of 20 weeks (
In conclusion, similar constitutive KO models (Phb1-KO/low-Phb2 versus Phb2-KO/low-Phb1) exhibit similar phenotypes. So why does the abrogation of liver prohibitins at the embryonic stage not induce major metabolic defects? Compensatory mechanisms might be progressively induced, in particular over a period where the glycemia does not rely on hepatic glucose production. These fascinating prohibitin-dependent adaptations certainly deserve further investigation.
Phb1:Phb2 heterodimers in the mitochondria: Beyond functional interdependence.