ReviewProgress in neurobiology2012
Cellular mechanisms of γ-secretase substrate selection, processing and toxicity.
Review in Progress in neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Advancements in nose-to-brain drug targeting for Alzheimer's disease: a review of nanocarriers and clinical insights.Inflammopharmacology · 2025Review
- Amyloid-β Pathology Is the Common Nominator Proteinopathy of the Primate Brain Aging.Journal of Alzheimer's disease : JAD · 2024Review
- Preferential Regulation of Γ-Secretase-Mediated Cleavage of APP by Ganglioside GM1 Reveals a Potential Therapeutic Target for Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Notch Signaling Plays a Dual Role in Regulating the Neuron-to-Oligodendrocyte Switch in the Developing Dorsal Forebrain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- APP accumulates with presynaptic proteins around amyloid plaques: A role for presynaptic mechanisms in Alzheimer's disease?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- Evaluation of Virtual Screening Strategies for the Identification of γ-Secretase Inhibitors and Modulators.Molecules (Basel, Switzerland) · 2021Article
- p120 catenin recruits HPV to γ-secretase to promote virus infection.PLoS pathogens · 2020Article
- Role of EGFR in the Nervous System.Cells · 2020Review
- Presenilin1 familial Alzheimer disease mutants inactivate EFNB1- and BDNF-dependent neuroprotection against excitotoxicity by affecting neuroprotective complexes ofBrain communications · 2020Article
- Kainate Receptor Activation Enhances Amyloidogenic Processing of APP in Astrocytes.Molecular neurobiology · 2019Article
- Presenilin-mediated cleavage of APP regulates synaptotagmin-7 and presynaptic plasticity.Nature communications · 2018Article
- The product of the γ-secretase processing of ephrinB2 regulates VE-cadherin complexes and angiogenesis.Cellular and molecular life sciences : CMLS · 2018Article
- Epigenetics in Alzheimer's Disease: Perspective of DNA Methylation.Molecular neurobiology · 2018Review
- Can Co-Activation of Nrf2 and Neurotrophic Signaling Pathway Slow Alzheimer's Disease?International journal of molecular sciences · 2017Review
- Presenilin 1 promotes trypsin-induced neuroprotection via the PAR2/ERK signaling pathway. Effects of presenilin 1 FAD mutations.Neurobiology of aging · 2016Article
- APLP1 as a cerebrospinal fluid biomarker for γ-secretase modulator treatment.Alzheimer's research & therapy · 2015Article
- Presenilin 1 is necessary for neuronal, but not glial, EGFR expression and neuroprotection via γ-secretase-independent transcriptional mechanisms.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Hippocampal Injections of Oligomeric Amyloid β-peptide (1-42) Induce Selective Working Memory Deficits and Long-lasting Alterations of ERK Signaling Pathway.Frontiers in aging neuroscience · 2015Article
- Therapeutic modulation of Notch signalling--are we there yet?Nature reviews. Drug discovery · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Presenilins (PSs) are catalytic components of the γ-secretase proteolytic complexes that produce Aβ and cell signaling peptides. γ-Secretase substrates are mostly membrane-bound peptides derived following proteolytic cleavage of the extracellular domain of type I transmembrane proteins. Recent work reveals that γ-secretase substrate processing is regulated by proteins termed γ-secretase substrate recruiting factors (γSSRFs) that bridge substrates to γ-secretase complexes. These factors constitute novel targets for pharmacological control of specific γ-secretase products, such as Aβ and signaling peptides. PS familial Alzheimer's disease (FAD) mutants cause a loss of γ-secretase cleavage function at epsilon sites of substrates thus inhibiting production of cell signaling peptides while promoting accumulation of uncleaved toxic substrates. Importantly, γ-secretase inhibitors may cause toxicity in vivo by similar mechanisms. Here we review novel mechanisms that control γ-secretase substrate selection and cleavage and examine their relevance to AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.