A CBP binding transcriptional repressor produced by the PS1/epsilon-cleavage of N-cadherin is inhibited by PS1 FAD mutations
Article Abstract:
Research shows that an epsilon-like cleavage of N-cadherin by presenilin1-dependent gamma-secretase protease produces N-Cad/CTF2 peptide domain, which binds the transcription factor CBP, the CREB binding protein, to promote its degradation by proteasome. Data suggest that the N-Cad/CTF2 functions as a repressor of CBP/CREB-mediated transcription. Furthermore, the familial AD (FAD) mutation-induced transcriptional irregularities may have some implication in FAD-associated dementia.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2003
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Improving synaptic function in a mouse model of AD
Article Abstract:
A study was conducted to show that administration of an enzyme ubiquitin C-terminal hydrolase of the L1 type (UCH-L1) fusion protein to supplement endogenous UCH-L1 has a protective effect on memory loss in a mouse model of Alzheimer's Disease (AD). The findings indicate that enhancing the activity of UCH-L1, an ubiquitin hydrolase, alleviates the synaptic dysfunction and memory loss associated with a mouse mode of AD.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2006
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AIP1/ALIX is a binding partner for HIV-1 p6 and EIAV p9 functioning in virus budding
Article Abstract:
Results indicate that AIP1, also known as ALIX, couples HIV-1 Gag p6 and EIAV p9 to the endosomal sorting complex. Data suggest that AIP1 is a component of the viral budding machinery linking the late assembly L domain of HIV-1 Gag p6 and EIAV P9 to the sorting complex. These processes facilitate retroviruses exit from the infected cells by budding from the plasma membrane.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2003
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