However, the expression of some proteins is enhanced. One of them is the C/EBP homologous protein, also known as growth arrest and DNA damage-inducible gene 153 that mediates proapoptotic pathways emanating from the stressed ER. Previously it was shown that GRP78 expression was increased in a human hepatoma cell line that overproduced HBs proteins and in the liver of transgenic mice that expressed deletion mutant of large HBs. Hepatic fibrosis constitutes the wound healing response to liver injury. During fibrosis, hepatic stellate cell activation represents a critical event, because these cells become the primary source of extracellular matrix in the liver upon damage. Development of hepatic fibrosis after chemical liver injury is enhanced in BALB/c mice exhibiting a Th2 response compared to C57BL/6 mice, which demonstrated a primary Th1 response. Transgenic mice on fibrosis-resistant C57BL/6 genetic background, which over-produce HBs proteins, develop modest spontaneous liver fibrosis. Transcription factor c-Jun and signal transducer and activator of transcription 3 are implicated in several cellular processes including proliferation, survival, and cell transformation. They are activated in chemically induced murine liver tumours and in HCCs of humans, suggesting an important function for these proteins in the development of liver tumours. Here we VE-821 report that the production of HBV surface proteins stimulates the expression of CHOP in hepatocytes and could cause stronger liver damage in transgenic mice on BALB/c genetic background compared to C57BL/6. Furthermore, HBV transgenic mice develop hepatic fibrosis and the level of fibrosis depends on the genetic background. Although c-Jun transcription factor up-regulation and activation of STAT3 and PERK in the liver of transgenic mice might contribute to tumour development, CHOP expression might reduce tumorigenesis in transgenic mice on BALB/c genetic background. Rab5, the prototypical Rab GTPase identified and localized almost 25 years ago, operates as a master regulator of the endocytic pathway. Rab5 regulates homotypic endosome fusion molecular motor-driven vesicle movement on microtubules and Rab conversion, the process by which Rab GTPases along a transport pathway are kept in register. Rab5 also plays a central role in the internalization and trafficking of signal transducing cell surface receptors. Rab5 is encoded as three isoforms, Rab5A, Rab5B and Rab5C in mouse and human genomes. These isoforms are encoded by different genes and expressed in all tissues. Bucci et al. examined Rab5 isoform function in cultured cells and showed that expression of all three Rab5 isoforms independently affect endocytosis. Subsequently, Rab5 isoforms were found to be differentially phosphorylated, suggesting that they serve as more than a backup or redundant function in endocytosis. More recent work has extended the idea that the Rab5 isoforms have different, if overlapping, functions. Wainszelbaum et al. and Bhattacharya et al. reported that Rab5 isoforms are differentially induced by cytokines.