1,720,983 research outputs found
Long-term stability of humanized telomeres in yeast in the presence and absence of Tel1p
No full textAlterazioni dell'omeostasi intracellulare del CA2+ indotte dal virus herpes simplex di tipo 1 (HSV-1) in colture primarie di neuroni coricali di ratto
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Calcium signaling triggered by Herpes Simplex Virus type-1 (HVS-1) in rat cortical neurons
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Herpes simplex virus type 1 infection in neurons leads to production and nuclear localization of APP intracellular domain (AICD): implications for Alzheimer’s disease pathogenesis
Full text linkSeveral data indicate that neuronal infection with herpes simplex virus type 1 (HSV-1) causes biochemical alterations reminiscent of Alzheimer’s disease (AD) phenotype. They include accumulation of amyloid-β (Aβ), which originates from the cleavage of amyloid precursor protein (APP), and hyperphosphorylation of tau protein, which leads to neurofibrillary tangle deposition. HSV-1 infection triggers APP processing and drives the production of several fragments including APP intracellular domain (AICD) that exerts transactivating properties. Herein, we analyzed the production and intracellular localization of AICD following HSV-1 infection in neurons. We also checked whether AICD induced the transcription of two target genes, neprilysin (nep) and glycogen synthase kinase 3β (gsk3β), whose products play a role in Aβ clearance and tau phosphorylation, respectively. Our data indicate that HSV-1 led to the accumulation and nuclear translocation of AICD in neurons. Moreover, results from chromatin immunoprecipitation assay showed that AICD binds the promoter region of both nep and gsk3β. Time course analysis of NEP and GSK3β expression at both mRNA and protein levels demonstrated that they are differently modulated during infection. NEP expression and enzymatic activity were initially stimulated but, with the progression of infection, they were down-regulated. In contrast, GSK3β expression remained nearly unchanged, but the analysis of its phosphorylation suggests that it was inactivated only at later stages of HSV-1 infection. Thus, our data demonstrate that HSV-1 infection induces early upstream events in the cell that may eventually lead to Aβ deposition and tau hyperphosphorylation and further suggest HSV-1 as a possible risk factor for AD
HERPES SIMPLEX VIRUS TYPE-1 (HSV-1) INDUCES APP PROCESSING FOLLOWED BY C-TERMINAL FRAGMENTS AND AB SECRETION IN HUMAN AND RAT NEURONAL CELLS
No full textHerpes simplex virus type 1 (HSV-1) induces multiple cleavages of Amyloid Precursor Protein (APP) and Abeta accumulation in human and rat neuronal cells
No full textHERPES SIMPLEX VIRUS TYPE 1 (HSV-1) INDUCES ACTIVITY- AND Ca2+-DEPENDENT AMYLOID PRECURSOR PROTEIN PROCESSING AND INTRACELLULAR ACCUMULATION OF AMYLOID-B PEPTIDE (AB) IN RAT NEOCORTICAL NEURONS.
No full textHerpes Simplex Virus type 1 (HSV-1) induces intracellular Ca2+ signal dysregulation triggering amyloid precursor protein (APP) processing in rat neocortical neurons.
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