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milk by Streptococcus thermophilus . Food Biotechnol 2012,26(3):280–292.CrossRef 51. Smith JM, Smith NH, O’Rourke M, Spratt BG: How clonal are bacteria? Proc Natl Acad Sci U S A 1993,90(10):4384–4388.PubMedCentralPubMedCrossRef 52. Feil EJ, Cooper JE, Grundmann H, Robinson DA, Enright MC, Berendt T, Peacock SJ, Smith JM, Murphy M, Spratt BG, https://www.selleckchem.com/products/BKM-120.html Moore CE, Day NP: How clonal is Staphylococcus aureus ? J Bacteriol 2003, 185:3307–3316.PubMedCentralPubMedCrossRef Competing interests The authors declare that Epacadostat they have no competing interests. Authors’ contributions Conceived and designed the experiments: TD WJL ZHS HPZ. Performed the experiments: QL HYX YQS. Analyzed the data: ZHS YQS. Contributed reagents/materials/analysis tools: ZHS QL HYX YQS. Wrote the paper: TD HPZ. All authors read and approved the final manuscript.”
“Background EV71 is a positive-stranded RNA virus in the genus enterovirus of the family Picornaviridae,
usually leading to hand, foot, and mouth diseases (HFMD) and herpangina [1, 2]. Moreover, EV71 has also been associated with fatal pulmonary edema, severe neurological complications, including encephalitis, meningitis, about and a poliomyelitis-like syndrome [3, 4]. Increasing evidences have found it to be the major etiological agent causing current outbreaks of HFMD in the Asia-Pacific region, including mainland China [2, 5, 6]. However, the molecular pathogenesis of EV71 infection remains obscure. Mitogen-activated protein kinase (MAPK) belongs to a family of serine/threonine protein kinases. It is widely conserved among eukaryotes and involved in many cellular processes such as inflammation, proliferation,
differentiation, movement, and death [7–9]. To date, seven distinct groups of MAPKs have been characterized in mammalian cells, including extracellular regulated kinases (ERK1/2), JNK1/2/3, p38 MAPK (p38 α/β/γ/δ), ERK3/4, ERK5, ERK7/8 and Nemo-like kinase (NLK) [10–12]. Of these, the most extensive studies are ERK1/2, JNKs and p38 MAPKs. As previously reported, JNK1/2 and/or p38 MAPK pathways is required for infection and replication of human immunodeficiency virus type 1, encephalomyocarditis virus, coxsackievirus B3, hepatitis C virus, herpes simplex virus 1, and the severe acute respiratory syndrome coronavirus [13–18]. The diverse effects of JNK1/2 and p38 MAPK activation by these viruses include induction of apoptosis in infected cells and enhancement of viral replication.