Enterovirus 71 Activates GADD34 via Precursor 3CD to Promote IRES-Mediated Viral Translation.

Enterovirus 71 (EV71) is the major pathogen of hand, foot, and mouth disease. In severe cases, it can cause life-threatening neurological complications, such as aseptic meningitis and polio-like paralysis. There are no specific antiviral treatments for EV71 infections.

Identification of the internal ribosome entry sites in the 5'‑untranslated region of the gene.

The Fos proto‑oncogene, activator protein‑1 (AP‑1) transcription factor subunit () gene, a member of the immediate early gene family, encodes c‑Fos, which is a subunit of the AP‑1 transcription factor. The present study aimed to investigate the mechanism by which the translation efficiency of mRNA is upregulated when cellular protein synthesis is shut off. The result of western blotting revealed that the protein expression levels of c‑Fos were increased in rhabdomyosarcoma cells infected with enterovirus 71 (EV71) compared with uninfected cells.

Inhibition of NF-κB might enhance the protective role of roflupram on SH-SY5Y cells under amyloid β stimulation via PI3K/AKT/mTOR signaling pathway.

Alzheimer disease (AD) is a progressive neurodegenerative disease and mostly endanger the health of people older than 65 years. Accumulation of beta amyloid protein (Aβ) is the main characteristic of AD. Roflupram (ROF) could improve the behavior of AD in a mouse model.

Transcriptomic characteristics of bronchoalveolar lavage fluid and peripheral blood mononuclear cells in COVID-19 patients.

Circulating in China and 158 other countries and areas, the ongoing COVID-19 outbreak has caused devastating mortality and posed a great threat to public health. However, efforts to identify effectively supportive therapeutic drugs and treatments has been hampered by our limited understanding of host immune response for this fatal disease. To characterize the transcriptional signatures of host inflammatory response to SARS-CoV-2 (HCoV-19) infection, we carried out transcriptome sequencing of the RNAs isolated from the bronchoalveolar lavage fluid (BALF) and peripheral blood mononuclear cells (PBMC) specimens of COVID-19 patients.

Ribosome Profiling of Vaccinia Virus-Infected Cells.

Ribosome profiling is a method that determines genome-wide mRNA translation through measuring ribosome-protected mRNA fragments by deep sequencing. This method can be used to quantify gene expression at the translational level and precisely pinpoint ribosome loading onto mRNA with codon-level resolution. Genome-wide regulation of mRNA translation can also be determined if RNA-Sequencing (RNA-Seq) is carried out in parallel.

Vaccinia Virus Transcriptome Analysis by RNA Sequencing.

RNA-sequencing (RNA-Seq) using next-generation sequencing (NGS) technique is a powerful tool for simultaneous analysis of global transcripts from both vaccinia virus and host cell. Here, we describe an RNA-Seq method for analyzing the vaccinia virus transcriptome from virus-infected HeLa cells. We pay particular attention to vaccinia virus-specific aspects of sample preparation, sequencing, and data analyses, but our method could be modified to analyze transcriptomes of other cells or tissues infected with different poxviruses.

MicroRNA‑539 inhibits cell proliferation, colony formation and invasion in pancreatic ductal adenocarcinoma by directly targeting IGF‑1R.

MicroRNAs (miRNAs) possess oncogenic and tumour‑suppressive roles in the carcinogenesis and progression of pancreatic ductal adenocarcinoma (PDAC) by regulating the expression of numerous cancer‑related genes. Thus, the investigation on the expression and roles of miRNAs in PDAC may facilitate the identification of novel and effective targets for the clinical diagnosis and treatment of patients with PDAC. miRNA‑539 (miR‑539) has been studied in multiple types of human cancer.

Doxorubicin Loaded Silica Nanoparticles with Dual Modification as a Tumor-Targeted Drug Delivery System for Colon Cancer Therapy.

In the following study, we describe the preparation and characterization of poly(ethylene glycol) (PEG) and biotin modified, doxorubicin (DOX) loaded silica nanoparticles (Dox/SLN-PEG-Biotin), which was employed as a drug delivery system for colon cancer therapy. The DOX/SLN-PEG-Biotin exhibited small particle size and low cytotoxicity in vitro. Moreover, the Dox releases from DOX/SLN-PEG-Biotin followed a redox-sensitive behavior.

Interferon activates promoter of Nmi gene via interferon regulator factor-1.

N-Myc interactor (Nmi) is reported to participate in many activities, such as signaling transduction, transcription regulation, and antiviral responses. As Nmi may play important roles in interferon (IFN)-induced responses, we investigated the mechanism how Nmi protein is regulated. We identified and cloned the promoter of Nmi gene.

Excessive nNOS/NO/AMPK signaling activation mediated by the blockage of the CBS/H2S system contributes to oxygen‑glucose deprivation‑induced endoplasmic reticulum stress in PC12 cells.

Hypoxic‑ischemia stress causes severe brain injury, leading to death and disability worldwide. Although it has been reported that endoplasmic reticulum (ER) stress is an essential step in the progression of hypoxia or ischemia‑induced brain injury, the underlying molecular mechanisms are and have not yet been fully elucidated. Accumulating evidence has indicated that both nitric oxide (NO) and hydrogen sulfide (H2S) play an important role in the development of cerebral ischemic injury.

Enterovirus 71 3C Promotes Apoptosis through Cleavage of PinX1, a Telomere Binding Protein.

Unlabelled: Enterovirus 71 (EV71) is an emerging pathogen causing hand, foot, and mouth disease (HFMD) and fatal neurological diseases in infants and young children due to their underdeveloped immunocompetence. EV71 infection can induce cellular apoptosis through a variety of pathways, which promotes EV71 release. The viral protease 3C plays an important role in EV71-induced apoptosis.

HIV-1 Vpr protein activates the NF-κB pathway to promote G2/M cell cycle arrest.

Viral protein R (Vpr) plays an important role in the replication and pathogenesis of Human immunodeficiency virus type 1 (HIV-1). Some of the various functions attributed to Vpr, including the induction of G2/M cell cycle arrest, activating the NF-κB pathway, and promoting viral reverse transcription, might be interrelated. To test this hypothesis, a panel of Vpr mutants were investigated for their ability to induce G2/M arrest and to activate the NF-κB pathway.

HIV-1 Vpr stimulates NF-κB and AP-1 signaling by activating TAK1.

Background: The Vpr protein of human immunodeficiency virus type 1 (HIV-1) plays an important role in viral replication. It has been reported that Vpr stimulates the nuclear factor-κB (NF-κB) and activator protein 1 (AP-1) signaling pathways, and thereby regulates viral and host cell gene expression. However, the molecular mechanism behind this function of Vpr is not fully understood.

[Effect of RelB on HIV-1 Vpr-mediated transcription activation and cell G2/M arrest].

Vpr, an auxiliary protein of HIV-1(Human immunodeficiency virus type 1), exerts important functions to promote viral replication and AIDS progression. In this study, we performed a yeast two-hybrid screening assay using human cDNA library to further investigate the molecular mechanism of various functions of Vpr RelB, a key protein in NF-kappaB signaling pathway, was identified as a Vpr interaction protein by co-immunoprecipitation. Further investigations indicated that RelB not only promoted the Vpr-mediated activation of NF-kappaB reporter gene, but also enhanced the transactivation of HIV LTR.

HIV-1 Vpr activates both canonical and noncanonical NF-κB pathway by enhancing the phosphorylation of IKKα/β.

The human immunodeficiency virus type I (HIV-1) Vpr plays an essential role in viral replication. A number of studies have reported that Vpr modulates the nuclear factor-κB (NF-κB) pathway. Yet, the reported effects of Vpr on NF-κB signaling are controversial.