These data indicate that the LGYSG sequence is important for the interaction of H2 with A28 and suggest that this sequence is buried within the EFC complex.”
“This Letter to Editors refers to “”Prenatal dexamethasone exposure affects anxiety-like behaviour and neuroendocrine systems in an age dependent manner”" by M. Nagano et al. (2008) 60, 364-371. The letter points to unexpected decrease of glucocorticoid receptors, which is rather consistent with anxiolytic effects and
suggests that age, sex, and hormonal status of subjects may represent additional confounding variables. (C) 2008 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Epstein-Barr virus (EBV) infection is associated with many human this website malignancies. In vitro, EBV transforms primary B lymphocytes into continuously growing lymphoblastoid cell lines. EBV latent membrane protein 1 (LMP-1) is required for EBV transformation processes. Interferon regulatory factor 4 (IRF-4) is a transcription factor and has oncogenic potential. We find that high levels of IRF-4 are associated with EBV transformation of human primary B cells in vitro and
with EBV type III latency in which LMP-1 is expressed. We show that EBV LMP-1 stimulates IRF-4 expression in B lymphocytes. The stimulation of IRF-4 by LMP-1 requires signaling from LMP-1 and involves cellular NF-kappa B. The growth of EBV-transformed cells is inhibited HKI-272 in vitro when IRF-4 is specifically down-regulated. We further demonstrate that IRF-4 knockdown cells have lower proliferation but higher apoptotic PLEKHB2 rates than control cells. Finally, IRF-4 is expressed in significant numbers of specimens of primary central nervous
system (CNS) lymphomas (12/27 [44.4%]), an EBV-associated malignancy. The association between the expression levels of LMP-1 and IRF-4 is statistically significant (P = 0.011) in these CNS lymphomas. Our data suggest that IRF-4 may be a critical factor in EBV transformation and a useful target in the therapy of EBV-mediated neoplasia.”
“Long-lasting synaptic changes in transmission and morphology at the basis of memory storage, require delivery of newly synthesized proteins to affected synapses. Although many of these proteins are generated in the cell body, several key molecules for plasticity can be delivered in the form of silent mRNAs at synapses in extra somatic compartments where they are locally translated. One of such mRNAs encodes brain-derived neurotrophic factor (BDNF), a key molecule in neuronal development, learning and memory. A single BDNF protein is produced from several splice variants having a different 5′ untranslated region. These mRNA variants have a different subcellular localization (soma, proximal or distal dendritic compartment) and may represent a spatial code for a local control of BDNF availability.