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.

Japan, Influence, Genetic transcription, Transcription (Genetics), Mutation (Biology), Mutation

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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.

Neural transmission, Synaptic transmission, Ubiquitin-proteasome system

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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.

HIV (Viruses), HIV, Retroviruses, Lysogeny, Viral antigens

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