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Volume 37, Issue 4, Pages 422-424 (October 2002)
Sandgren EP, Palmiter RD, Heckel JL, Daugherty CC, Brinster RL, Degen JL. Complete hepatic regeneration after somatic deletion of an albumin–plasminogen activator transgene [Cell 1991;66:245–256] Markus Grompe Journal of Hepatology Volume 37, Issue 4, Pages (October 2002) DOI: /S (02)
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Fig. 1 Gross appearance of Alb-uPA transgenic mouse liver. Livers were removed from 5-week-old male mice. The liver to the left is from a non-transgenic control mouse, that in the center from a hemizygous transgenic mouse and that to the right from a homozygous transgenic mouse. Note the large red nodules in the hemizygote's liver and their absence from the homozygote's liver. (Reprinted with permission from Cell 1991;66:245–256). Journal of Hepatology , DOI: ( /S (02) )
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Fig. 2 Histopathology of Alb-uPA transgenic mouse liver. (A) Liver from a 4.5-week old non-transgenic control mouse. Note the uniform size and arrangement of the hepatocytes. (B) Liver from a 4.5-week old hemizygous transgenic spanning a red–white interface. Note the disarrayed hepatocytes of variable size in the red area (top). Hepatocytes in the white area (bottom) are generally small and show cytoplasmic vacuolization. (Reprinted with permission from Cell 1991;66:245–256). Journal of Hepatology , DOI: ( /S (02) )
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Fig. 3 Southern blot analysis of the Alb-uPA transgene. DNA was isolated from a purified population of red nodule hepatocytes. The blot was simultaneously probed with a control sequence (black arrow) and transgene specific probe (upper band in all lanes). Liver C is from a non-transgenic mouse. The kidney shows the pattern of the unrearranged locus. In all red nodules, the intensity of the transgene band is reduced. In addition the size is altered, demonstrating genomic rearrangement. (Reprinted with permission from Cell 1991;66:245–256). Journal of Hepatology , DOI: ( /S (02) )
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