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Details

Autor(en) / Beteiligte
Titel
EZH2 phosphorylation regulates Tat-induced HIV-1 transactivation via ROS/Akt signaling pathway
Ist Teil von
  • FEBS letters, 2015-12, Vol.589 (24), p.4106-4111
Ort / Verlag
England: Elsevier B.V
Erscheinungsjahr
2015
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
  • •Tat induces HIV-1 transactivation through inhibiting EZH2.•Tat-induced EZH2 phosphorylation is ROS/Akt dependent.•EZH2 phosphorylation is correlated with Tat-induced transactivation. EZH2 plays a major role in HIV-1 latency, however, the molecular linkage between Tat-induced HIV-1 transactivation and EZH2 activity is not fully understood. It was shown Tat induced HIV-1 transactivation through inhibiting EZH2 activity. Tat decreased the levels of H3K27me3 and EZH2 occupy at the long terminal repeat (LTR) of HIV-1. We further showed for the first time that transfected with Tat construct resulted in an increase in phosphorylated EZH2 (p-EZH2), mediated by active Akt. ROS/Akt-dependent p-EZH2 was correlated with Tat-induced transactivation. Our study reveals that novel mechanisms allow Tat-induced HIV-1 transactivation by ROS/Akt-dependent downregulating the EZH2 epigenetic silencing machinery.
Sprache
Englisch
Identifikatoren
ISSN: 0014-5793
eISSN: 1873-3468
DOI: 10.1016/j.febslet.2015.11.033
Titel-ID: cdi_proquest_miscellaneous_1751488387
Format
Schlagworte
Adenosine - analogs & derivatives, Adenosine - pharmacology, AKT, Amino Acid Substitution, Chromatin Immunoprecipitation, Enhancer of zeste homolog 2, Enhancer of Zeste Homolog 2 Protein, Enzyme Inhibitors - pharmacology, Genes, Reporter - drug effects, HeLa Cells, HIV-1, HIV-1 - drug effects, HIV-1 - enzymology, HIV-1 - physiology, Humans, Mutagenesis, Site-Directed, Mutant Proteins - antagonists & inhibitors, Mutant Proteins - genetics, Mutant Proteins - metabolism, Phosphorylation - drug effects, Polycomb Repressive Complex 2 - antagonists & inhibitors, Polycomb Repressive Complex 2 - genetics, Polycomb Repressive Complex 2 - metabolism, Protein Processing, Post-Translational - drug effects, Protein Transport - drug effects, Proto-Oncogene Proteins c-akt - agonists, Proto-Oncogene Proteins c-akt - antagonists & inhibitors, Proto-Oncogene Proteins c-akt - genetics, Proto-Oncogene Proteins c-akt - metabolism, Reactive oxygen species, Reactive Oxygen Species - agonists, Reactive Oxygen Species - metabolism, Recombinant Fusion Proteins - chemistry, Recombinant Fusion Proteins - metabolism, RNA Interference, Signal Transduction - drug effects, tat Gene Products, Human Immunodeficiency Virus - agonists, tat Gene Products, Human Immunodeficiency Virus - antagonists & inhibitors, tat Gene Products, Human Immunodeficiency Virus - genetics, tat Gene Products, Human Immunodeficiency Virus - metabolism, Transcriptional Activation - drug effects, Virus Activation - drug effects

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