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With the rapid proliferation of RNAi applications in basic and clinical sciences, the challenge has now become understanding how components of RNAi machinery function together in a regulated manner. Argonaute proteins are the central effectors of RNAi and are highly conserved among eukaryotes and some archaebacteria. These RNA-binding proteins use small guide RNAs to silence expression of genes at the mRNA and DNA levels. In Argonaute Proteins: Methods and Protocols, expert researchers in this burgeoning field provide detailed, up-to-date methods to study Argonaute protein functions and interactions in a wide variety of cell types ranging from yeast to mammalian systems, as well as in vitro. Written in the highly successful Methods in Molecular Biology™ series format, chapters include brief introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and key tips on troubleshooting and avoiding known pitfalls. Practical and authoritative, Argonaute Proteins: Methods and Protocols serves as a vital reference for both experienced and novice scientists approaching the vast complexities of RNAi research.
Biochemistry. --- Genetic engineering. --- Protein Science. --- Genetic Engineering. --- Biological chemistry --- Chemical composition of organisms --- Organisms --- Physiological chemistry --- Biology --- Chemistry --- Medical sciences --- Designed genetic change --- Engineering, Genetic --- Gene splicing --- Genetic intervention --- Genetic surgery --- Genetic recombination --- Biotechnology --- Transgenic organisms --- Composition
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Zika virus (ZIKV), one of the flavivirus family members transmitted by mosquitos, was declared a Public Health Emergency of International Concern by the WHO in February 2016 because of clusters of newborn microcephaly cases and other neurological disorders in Brazil. Most ZIKV infections result in a self-limited flu-like febrile disease, however, if contracted during pregnancy, the virus can also infect fetuses and cause a spectrum of birth defects known as congenital Zika syndrome. To date, no vaccines or antiviral drugs are licensed for ZIKV, and the virus has spread and become endemic to many tropical and sub-tropical countries. Included in this book are thirteen reports addressing diverse aspects of ZIKV–host interactions. These studies range from basic science to clinical research. It is expected that findings from these studies will contribute to a better understanding of the host cells interacting with ZIKV, and may serve as the basis for new diagnostics, antiviral therapies, and vaccine design.
Research & information: general --- Biology, life sciences --- Zika virus --- peroxisomes --- innate immune response --- interferon --- astrocytes --- fetal brain --- zika virus --- flaviviruses --- T cells --- host-pathogen interactions --- flavivirus --- tight junctions --- claudins --- ZO-1 --- blood-placental barrier --- placenta --- apoptosis --- viral replication --- Bcl-2 protein family --- ZIKV --- virus host interactions --- pathogenesis --- MR766 --- guinea pig --- subcutaneous --- vaginal --- sexual transmission --- virus transmission --- envelope protein --- glycosylation --- fusion loop --- viral fusion --- cell entry --- NS5 protein --- nuclear localization --- inflammation --- innate immunity --- extracellular vesicles --- cellular communication --- C6/36 cells --- human monocytes --- endothelial vascular cells --- protein–protein interaction --- non-structural viral proteins --- network --- JAK/STAT --- cytokine --- West Nile virus --- HSP90 --- NS5 --- virus–host interactions --- anti-viral signaling --- immune response --- inflammatory mediator --- Sertoli cells --- Leydig cells --- ZIKA virus --- arboviruses --- infertility --- IFN --- RIG-I --- MDA5 --- IFNAR1 --- zika --- host --- cell death --- peroxisome --- mosquito --- tight junction
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Zika virus (ZIKV), one of the flavivirus family members transmitted by mosquitos, was declared a Public Health Emergency of International Concern by the WHO in February 2016 because of clusters of newborn microcephaly cases and other neurological disorders in Brazil. Most ZIKV infections result in a self-limited flu-like febrile disease, however, if contracted during pregnancy, the virus can also infect fetuses and cause a spectrum of birth defects known as congenital Zika syndrome. To date, no vaccines or antiviral drugs are licensed for ZIKV, and the virus has spread and become endemic to many tropical and sub-tropical countries. Included in this book are thirteen reports addressing diverse aspects of ZIKV–host interactions. These studies range from basic science to clinical research. It is expected that findings from these studies will contribute to a better understanding of the host cells interacting with ZIKV, and may serve as the basis for new diagnostics, antiviral therapies, and vaccine design.
Zika virus --- peroxisomes --- innate immune response --- interferon --- astrocytes --- fetal brain --- zika virus --- flaviviruses --- T cells --- host-pathogen interactions --- flavivirus --- tight junctions --- claudins --- ZO-1 --- blood-placental barrier --- placenta --- apoptosis --- viral replication --- Bcl-2 protein family --- ZIKV --- virus host interactions --- pathogenesis --- MR766 --- guinea pig --- subcutaneous --- vaginal --- sexual transmission --- virus transmission --- envelope protein --- glycosylation --- fusion loop --- viral fusion --- cell entry --- NS5 protein --- nuclear localization --- inflammation --- innate immunity --- extracellular vesicles --- cellular communication --- C6/36 cells --- human monocytes --- endothelial vascular cells --- protein–protein interaction --- non-structural viral proteins --- network --- JAK/STAT --- cytokine --- West Nile virus --- HSP90 --- NS5 --- virus–host interactions --- anti-viral signaling --- immune response --- inflammatory mediator --- Sertoli cells --- Leydig cells --- ZIKA virus --- arboviruses --- infertility --- IFN --- RIG-I --- MDA5 --- IFNAR1 --- zika --- host --- cell death --- peroxisome --- mosquito --- tight junction
Choose an application
Zika virus (ZIKV), one of the flavivirus family members transmitted by mosquitos, was declared a Public Health Emergency of International Concern by the WHO in February 2016 because of clusters of newborn microcephaly cases and other neurological disorders in Brazil. Most ZIKV infections result in a self-limited flu-like febrile disease, however, if contracted during pregnancy, the virus can also infect fetuses and cause a spectrum of birth defects known as congenital Zika syndrome. To date, no vaccines or antiviral drugs are licensed for ZIKV, and the virus has spread and become endemic to many tropical and sub-tropical countries. Included in this book are thirteen reports addressing diverse aspects of ZIKV–host interactions. These studies range from basic science to clinical research. It is expected that findings from these studies will contribute to a better understanding of the host cells interacting with ZIKV, and may serve as the basis for new diagnostics, antiviral therapies, and vaccine design.
Research & information: general --- Biology, life sciences --- Zika virus --- peroxisomes --- innate immune response --- interferon --- astrocytes --- fetal brain --- zika virus --- flaviviruses --- T cells --- host-pathogen interactions --- flavivirus --- tight junctions --- claudins --- ZO-1 --- blood-placental barrier --- placenta --- apoptosis --- viral replication --- Bcl-2 protein family --- ZIKV --- virus host interactions --- pathogenesis --- MR766 --- guinea pig --- subcutaneous --- vaginal --- sexual transmission --- virus transmission --- envelope protein --- glycosylation --- fusion loop --- viral fusion --- cell entry --- NS5 protein --- nuclear localization --- inflammation --- innate immunity --- extracellular vesicles --- cellular communication --- C6/36 cells --- human monocytes --- endothelial vascular cells --- protein–protein interaction --- non-structural viral proteins --- network --- JAK/STAT --- cytokine --- West Nile virus --- HSP90 --- NS5 --- virus–host interactions --- anti-viral signaling --- immune response --- inflammatory mediator --- Sertoli cells --- Leydig cells --- ZIKA virus --- arboviruses --- infertility --- IFN --- RIG-I --- MDA5 --- IFNAR1 --- zika --- host --- cell death --- peroxisome --- mosquito --- tight junction
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