'One Health' for the people of Hong Kong and the world

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Adenoviral delivery of RNA decoys restores cellular proapoptotic protein PUMA expression by silencing Epstein-Barr virus-encoded miR-BART5 in nasopharyngeal carcinoma cells

Poster Session 1 - Vaccines and Anti-Viral Therapeutics: no. 3.17Epstein-Barr virus (EBV) encodes 48 mature microRNAs that play important roles in viral maintenance and promote host cell survival by regulating viral transcripts expression, inhibiting apoptosis or facilitating to evade cell immune surveillance. We have previously shown that EBV-encoded miR-BART5 targets and downregulates cellular pro-apoptotic protein p53-upregulated modulator of apoptosis (PUMA) to promote cellular survival of EBV-infected nasopharyngeal carcinoma (NPC) cells. Since compromising miR-BART5 might induce apoptosis of EBV-infected NPC cell, in this study we have established an adenoviral expression system to deliver anti-miR-BART5 decoys to NPC cells. The anti-miR-BART5 decoys comprised 6 tandem repeats of miR-BART5 binding sites and their expression was driven by EBVEBER2 promoter. They were designed to serve as a competitive inhibitor of miR-BART5 to reverse miR-BART5's inhibitory effects on PUMA in EBV-infected NPC cells. The RNA polymerase III-dependent EBER2 promoter is particularly strong in ...postprin

CRTC1 transcriptional coactivator is required for hepatitis B virus gene expression and replication

This journal suppl. entitled: Metabolism, Diet and Disease 2014: Cancer and metabolismConference Theme: Cancer and metabolismPoster Presentation: P31BACKGROUND: Chronic hepatitis B virus (HBV) infection occurs in over 400 million people worldwide, 15-40% of whom will terminally develop severe liver diseases including hepatocellular carcinoma. Although development of HCC is a multi-step process, high HBV DNA level is a major risk factor for disease progression. Transcription of HBV from the cccDNA template is essential for its replication and requires CREB transcription factor, a master regulator of cell metabolism. However, transcriptional coactivators that facilitate CREB-dependent activation of HBV transcription remain to be identified and characterized …published_or_final_versio

Ubiquitination and proteosome-dependent degradation of the activated form of human liver-enriched transcription factor CREB-H regulated by protein kinase A

Poster Presentation - Theme 1: Cell biologyCREB-H is a membrane-bound bZIP transcription factor which is mainly expressed in liver and small intestine. CREB-H plays important roles in the regulation of lipid metabolism, iron metabolism, gluconeogenesis and acute phase response. CREB-H is proteolytically activated by regulated intramembrane proteolysis to generate a C-terminal truncated form known as ...postprin

LKB1 tumor suppressor and salt-inducible kinases negatively regulate human T-cell leukemia virus type 1 transcription

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Perception and use of complementary and alternative medicine for low back pain

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Loss of yeast peroxiredoxin TSA1 induces genome instability through constitutive activation of DNA damage checkpoint and elevation of cellular dNTP levels

Session 4: Cancer, Cell Biology and Musculoskeletal System: session no. 4.11Peroxiredoxins are a family of antioxidant enzymes critically involved in cellular defense and signaling. Particularly, yeast peroxiredoxin Tsa1p is thought to play a role in the maintenance of genome integrity, but the underlying mechanism is not understood. In this study, we took a genetic approach to investigate the cause of genome instability in tsa1Delta cells. Strong genetic interactions of TSA1 with DNA damage checkpoint components DUN1, SML1, and CRT1 were found when mutant cells were analyzed for either sensitivity to DNA damage or rate of spontaneous base substitutions. An elevation in intracellular dNTP production was observed in tsa1Delta cells. This was associated with constitutive activation of the DNA damage checkpoint as indicated by phosphorylation of Rad9/Rad53p, reduced steady-state amount of Sml1p, and induction of RNR and HUG1 genes. In addition, defects in the DNA damage checkpoint did not modulate intracellular level of reactive oxygen species, but suppressed the mutator phenotype of tsa1Delta cells. On the contrary, overexpression of RNR1 exacerbated this phenotype by increasing dNTP levels. Taken together, our findings uncover a new role of TSA1 in preventing the overproduction of dNTPs, which is a root cause of genome instability