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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: Hepatology. 2014 Oct 29;60(6):2065–2076. doi: 10.1002/hep.27348

Fig. 3. Adult-onset, hepatocyte-specific overexpression of NIK causes liver oxidative stress and hepatocyte death.

Fig. 3

(A-C) STOP-NIK males were sacrificed 18 days after GFP (Con) or albumin-Cre adenoviral infection. (A) Liver weight. BW: body weight. Con: n=6; Cre: n=6. (B) H & E staining of liver sections. (C) Liver sections were co-stained with TUNEL reagents and DAPI. Inserts: enlarged merged images. TUNEL-positive cells were normalized to DAPI-positive cells. Con: n=5; Cre: n=5. (D) STOP-NIK mice were infected with AAV-GFP or AAV-Cre, and liver sections (9 days after infection) were stained with TUNEL reagents and DAPI. AAV-GFP: n=3; AAV-Cre: n=3. (E) Liver extracts (18 days after adenoviral infection) were immunoblotted with the indicated antibodies. (F) Liver ROS levels (normalized to protein levels). a.u.: arbitrary units. Con: n=6; Cre: n=5; AAV-GFP: n=3; AAV-Cre: n=3. *p<0.05.