The occulusion derived virus envelope protein gene (odv e25) of Leucania separata nuclear polyhedrosis virus (LsNPV) was identified by the sequencing the pLsx3 fragment, and compared with other three baculovirus...The occulusion derived virus envelope protein gene (odv e25) of Leucania separata nuclear polyhedrosis virus (LsNPV) was identified by the sequencing the pLsx3 fragment, and compared with other three baculoviruses. The hydrophobility analysis showed that three odv e25 proteins share very high similarity.展开更多
Accumulation of amyloid-β(Aβ) and its neurotoxicity are regarded as a major factor promoting neu-ronal degeneration in Alzheimer's disease (AD). Upon investigation of Aβtoxicity using DNA microarray, we isolate...Accumulation of amyloid-β(Aβ) and its neurotoxicity are regarded as a major factor promoting neu-ronal degeneration in Alzheimer's disease (AD). Upon investigation of Aβtoxicity using DNA microarray, we isolated ubiquitin conjugating enzyme E2-25K/Hip-2 as a mediator of Aβ toxicity. Here we show that expression of E2-25K/Hip-2 was strongly up-regulated in the cultured cortical neurons exposed to Aβ1-42 in vitro and in vulnerable neurons surrounding senile plaques of the brain derived from AD patients and Tg2576 Alzheimer's mice. Aβ1-42-induced neurotoxicity, accumulation of ubiquitin conjugates, and decrease of the proteasome activity were mediated by ubiquitin ligase activity of E2-25K/Hip-2. Aβ-induced展开更多
文摘The occulusion derived virus envelope protein gene (odv e25) of Leucania separata nuclear polyhedrosis virus (LsNPV) was identified by the sequencing the pLsx3 fragment, and compared with other three baculoviruses. The hydrophobility analysis showed that three odv e25 proteins share very high similarity.
文摘Accumulation of amyloid-β(Aβ) and its neurotoxicity are regarded as a major factor promoting neu-ronal degeneration in Alzheimer's disease (AD). Upon investigation of Aβtoxicity using DNA microarray, we isolated ubiquitin conjugating enzyme E2-25K/Hip-2 as a mediator of Aβ toxicity. Here we show that expression of E2-25K/Hip-2 was strongly up-regulated in the cultured cortical neurons exposed to Aβ1-42 in vitro and in vulnerable neurons surrounding senile plaques of the brain derived from AD patients and Tg2576 Alzheimer's mice. Aβ1-42-induced neurotoxicity, accumulation of ubiquitin conjugates, and decrease of the proteasome activity were mediated by ubiquitin ligase activity of E2-25K/Hip-2. Aβ-induced
