MAPK8IP2 (5-1′, 2h-1′) inhibits apoptosis [30]. UBE2C (5-1′, 2h-1′, 4h-1′) facilitates progression of the cell cycle via APC activation and increased cyclin A [34]. UBE2M (hUbc12) is a conjugating enzyme for NEDD8, Selleckchem FHPI involved in the ubiquitinylation of cell-cycle factors involved in the G1/S transition [35]. IGFBP3 (5-1′) is associated with IGFBP5, which in turn may lead to cell cycle arrest in the G2/M phase [36]. CDK5 (10-1′) associated with MEK inhibitor CDK6 promotes cell cycle transition in the G1 phase [37]. Downregulated genes: MAPK13 (5-1′, 30-1′, 3h-1′, 4h-1′, 6h-1′) is one of several protein kinases activated by cellular stresses (including oxidative stress) and

cytokines IL-1

and TNFα and has been found to be a downstream carrier of the PKCdelta-dependent death signal [38]. Over expression of BTG3 (10-1′, 4h-1′) has been shown to impair serum-induced cell cycle progression from the G0/G1 to S phase [39]. UBE2C promotes progression of the cell cycle [34]. Bcl-rambo (2h-1′, 3h-1′, 4h-1′) is a Bcl-2 member that induces cell death [40]. MAPK6 (3h-1′, 6h-1′) – over expression of this gene in NIH 3T3 cells has been seen to inhibit DNA synthesis and G1 phase arrest [41] and the Selleck ICG-001 nucleocytoplasmic shuttling of ERK3 regulates its inhibitory action on cell cycle progression [42]. MDM2 transcriptional (3h-1′, 6h-1′) products form complexes with p53 in the G0/G1 phases of the cell cycle and inhibit the G1 arrest and inhibitory functions of p-53 [43]. Discussion In this study we find that an isolated increase in sinusoidal flow does not have the same Non-specific serine/threonine protein kinase macroscopic, microscopic or genetic impact on the liver

as that seen in the liver remnant after partial hepatectomy. Our findings indicate that increased sinusoidal flow may not be a sufficient stimulus in itself for the initiation of liver regeneration. On histological examination of the transition zone between the shunted and portally perfused sides (Fig. 3), we found the liver lobuli larger on the portally perfused side as previously observed by other investigators [44]. The expansion was the result of not only slightly congested sinusoids, but also by, in general, larger hepatocytes. These changes suggests to us that after three weeks of mainly portal perfusion (the right hepatic artery was intact) to segments I, V, VI, VII and VIII, the metabolic and hepatotrophic stimuli from the splanchninc blood results in selective growth of these segments, independently from the shunted contra lateral side (segments II, III and IV). The finding that the proliferative index and phosphohistone H3 distribution is similar in both sides at t = 3 weeks, suggests that this selective growth may be the result of hepatocyte hypertrophy.