Presenilin 1 is involved in maturation and trafficking of N‐cadherin to the plasma membrane

No abstract is available for this paper.

• Publication year

  2003

• Venue

  Journal of Neuroscience Research

• Publication date

  2003-10-15

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1002/jnr.10753PMID 14515347
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Presenilin-1 Regulates Intracellular Trafficking and Cell Surface Delivery of β-Amyloid Precursor Protein*

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• Presenilin‐1: A Component of Synaptic and Endothelial Adherens Junctions

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• Increasing numbers of synaptic puncta during late-phase LTP: N-cadherin is synthesized, recruited to synaptic sites, and required for potentiation.

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• The Transmembrane Aspartates in Presenilin 1 and 2 Are Obligatory for γ-Secretase Activity and Amyloid β-Protein Generation*

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• Presenilin 1 Controls γ-Secretase Processing of Amyloid Precursor Protein in Pre-Golgi Compartments of Hippocampal Neurons

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• Presenilin-1 forms complexes with the cadherin/catenin cell-cell adhesion system and is recruited to intercellular and synaptic contacts.

  1999influential reference
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• Presenilin 1 deficiency impairs Aβ42-to-Aβ40- and angiotensin-converting activities of ACE

  2023cites this paper
• Flying under the radar: CDH2 (N-cadherin), an important hub molecule in neurodevelopmental and neurodegenerative diseases

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• β2-adrenergic agonists rescue lysosome acidification and function in PSEN1 deficiency by reversing defective ER to lysosome delivery of ClC-7.

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• Aspartic proteases: Potential drug targets for anticancer drug development

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• Presenilins and γ-Secretase in Membrane Proteostasis

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• The Role of Presenilin in Protein Trafficking and Degradation—Implications for Metal Homeostasis

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• Pharmacogenomics in Drug Discovery and Development

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• Presenilin 1/γ-secretase modulates P-cadherin processing and influences cell adhesion in oral squamous cell carcinoma cell lines.

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• Neurodegeneration in Alzheimer Disease: Role of Amyloid Precursor Protein and Presenilin 1 Intracellular Signaling

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• Consequences of Inhibiting Amyloid Precursor Protein Processing Enzymes on Synaptic Function and Plasticity

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• Re-expression of N-cadherin in remyelinating lesions of experimental inflammatory demyelination.

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• A study of the role of presenilin (1) in regulating synaptic function at hippocampal synapses

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• Presenilin: RIP and beyond.

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• N‐cadherin‐based adhesion enhances Aβ release and decreases Aβ42/40 ratio

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• Inhibition of basal activity of c-jun-NH2-terminal kinase (JNK) represses the expression of presenilin-1 by a p53-dependent mechanism.

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• Presenilins Mediate Phosphatidylinositol 3-Kinase/AKT and ERK Activation via Select Signaling Receptors

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