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An activating transcription factor 6 beta (ATF6β) regulates apoptosis of hemocyte during immune response in Crassostrea gigas.

The homeostasis of immune cells during immune response is viral for hosts to defend against invaders. Activating transcription factor 6 (ATF6) is an important transcription factor in the unfolded protein response (UPR) to maintaining cells homeostasis. In the present study, one ATF6 homologue was identified from Pacific oyster Crassostrea gigas (designated as CgATF6β). The full length cDNA of CgATF6β was of 2645 bp with a 1596 bp open reading frame (ORF) encoding a polypeptide of 531 amino acids. The deduced amino acid sequence of CgATF6β was predicted to contain a transmembrane region, a conserved basic leucine zipper (bZIP) domain, a site 1 proteases cleavage site, a site 2 protease cleavage site, and a Golgi localization signal. CgATF6β mRNA was constitutively expressed in hemocytes, gill, mantle, gonad, hepatopancreas and labial palp, with a slightly higher expression level in muscle (2.45-fold of that in gill, p < 0.05). After oysters were challenged with Vibrio splendidus, the mRNA expression levels of CgATF6β in hemocytes were significantly up-regulated at 3 h (2.68-fold of that in seawater group, p < 0.01) and peaked at 12 h (3.14-fold of that in seawater group, p < 0.01). The endogenic CgATF6β protein was mainly located in the cytoplasm of oyster hemocytes, and it was significantly transported into the nuclei of hemocytes at 1.5 h after the challenge with V. splendidus. After an injection with CgATF6β dsRNA, the mRNA expression of CgATF6β was knocked down to 0.26-fold of that in dsGFP group (p < 0.01). In CgATF6β dsRNA-injected oysters, the mRNA expressions of glucose-regulated protein 78 (GRP78), calnexin (CNX) and anti-apoptotic B-cell lymphoma-2 (Bcl-2) in hemocytes were significantly decreased at 12 h after V. splendidus challenge, which were 0.65-fold (p < 0.01), 0.54-fold (p < 0.01) and 0.17-fold (p < 0.01) of that in dsGFP-injected oysters, while the apoptotic rate of hemocytes was significantly up-regulated (1.97-fold of that in dsGFP group, p < 0.05). Collectively, these results suggested that CgATF6β was involved in apoptosis inhibition of oyster hemocytes upon V. splendidus challenge by regulating the expression of CgGRP78, CgCNX and CgBcl-2.

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Sex-determining region Y box 4 (SOX4) suppresses Hepatitis B virus replication by inhibiting hepatocyte nuclear factor 4α expression.

Hepatitis B virus (HBV) infection is still a health care crisis in the world, and a considerable number of chronic hepatitis B patients die of end-stage liver diseases, including liver cirrhosis and hepatocellular carcinoma. A previous study has reported that sex-determining region Y box 4 (SOX4) promotes HBV replication by binding to the AACAAAG motif in the viral genome. However, such SOX4 binding site was not found in the genome of the majority of HBV genotype strains. Further, we found that SOX4 inhibited rather than promoted the replication of most HBV strains. In line with this, HBV replication was significantly enhanced when the endogenous SOX4 was knocked down. Moreover, we demonstrated that the SOX4-induced suppression of HBV replication was mainly mediated by hepatocyte nuclear factor 4α (HNF4α). Taken together, our findings suggest that SOX4 plays an important antiviral role by inhibiting HNF4α expression in most HBV strains.

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Rabbit Anti-Polyprotein(H Rabbit Anti-Hepatitis C V Rabbit Anti-Hepatitis C V Benzyl 4,6-O-Benzylidene- Recombinant Tick-Borne En pCAMBIA2301 Vector (gusA 10 µl Extended Length Ba Human Mouse Rat Phospho-p 6 Benzylaminopurine ribos 2 Butylboronic acid CAS N Human anti hepatitis A vi 1-(Benzyl-d5)-4-[(6-benzy

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7-Deaza-7-fluoro modification confers on 4'-cyano-nucleosides potent activity against entecavir/adefovir-resistant HBV variants and favorable safety.

We designed, synthesized and identified a novel nucleoside derivative, 4'-C-cyano-7-deaza-7-fluoro-2'-deoxyadenosine (CdFA), which exerts potent anti-HBV activity (IC ∼26 nM) with favorable hepatocytotoxicity (CC ∼56 μM). Southern blot analysis using wild-type HBV (HBV)-encoding-plasmid-transfected HepG2 cells revealed that CdFA efficiently suppresses the production of HBV (IC = 153.7 nM), entecavir (ETV)-resistant HBV carrying L180M/S202G/M204V substitutions (HBV; IC = 373.2 nM), and adefovir dipivoxil (ADV)-resistant HBV carrying A181T/N236T substitutions (HBV; IC192.6 nM), whereas ETV and ADV were less potent against HBV and HBV (IC: >1,000 and 4,022.5 nM, respectively). Once-daily peroral administration of CdFA to human-liver-chimeric mice over 14 days (1 mg/kg/day) comparably blocked HBV and HBV viremia by 0.7 and 1.2 logs, respectively, without significant changes in body-weight or serum human-albumin levels, although ETV only slightly suppressed HBV viremia (CdFA vs ETV; p = 0.032). Molecular modeling suggested that ETV-TP has good nonpolar interactions with HBV reverse transcriptase (RT)'s Met204 and Asp205, while CdFA-TP fails to interact with Met204, in line with the relatively inferior activity against HBV of CdFA compared to ETV (IC: 0.026 versus 0.003 nM). In contrast, the 4'-cyano of CdFA-TP forms good nonpolar contacts with RT's Leu180 and RT's Met180, while ETV-TP loses interactions with RT's Met180, explaining in part why ETV is less potent against HBV than CdFA. The present results show that CdFA exerts potent activity against HBV, HBV and HBV with enhanced safety and that 7-deaza-7-fluoro modification confers potent activity against drug-resistant HBV variants and favorable safety, shedding light to further design more potent and safer anti-HBV nucleoside analogs.

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