ReviewFrontiers in aging neuroscience2014
Complex regulation of γ-secretase: from obligatory to modulatory subunits.
Review in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 61 citations in OpenAlex.
- The γ-secretase complex: from discovery to a therapeutic target.RSC chemical biology · 2026Review
- Inhibition of Colorectal Cancer Cell Progression by Picroside II Through Modulation of the Notch1 Signaling Pathway.Journal of biochemical and molecular toxicology · 2026Article
- Prenatal Alcohol Exposure Disrupts γ-Secretase Activity and Impairs Learning and Memory in Wild-Type and 3xTg-AD Mice.bioRxiv : the preprint server for biology · 2026Article
- A new era in neuropharmacology: assessing the efficacy and safety of novel anti-amyloid and non-amyloid drug targets for Alzheimer's disease.Journal of neurology · 2026Review
- Targeting neuroplasticity in old brain: restoring synapse with cognitive strategies.Biogerontology · 2026Review
- Glycogen synthase kinase-3: the master switch driving neurodegeneration in Alzheimer's disease and Parkinson's disease.Archives of toxicology · 2025Review
- Thymosin beta 4 as an Alzheimer disease intervention target identified using human brain organoids.Stem cell reports · 2025Article
- Cerebral perfusion is correlated with cerebral metabolism and amyloid deposition in Alzheimer's disease.Translational psychiatry · 2025Article
- From defense to disease: IFITM3 in immunity and Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Review
- The Azalea Hypothesis of Alzheimer Disease: A Functional Iron Deficiency Promotes Neurodegeneration.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Microbial infection promotes amyloid pathology in a mouse model of Alzheimer's disease via modulating γ-secretase.Molecular psychiatry · 2024Article
- Evolution and Function of the Notch Signaling Pathway: An Invertebrate Perspective.International journal of molecular sciences · 2024Review
- Amyloid β Proteoforms Elucidated by Quantitative LC/MS in the 5xFAD Mouse Model of Alzheimer's Disease.Journal of proteome research · 2023Article
- Structure-activity relationship of BMS906024 derivatives for Cryptosporidium parvum growth inhibition.Bioorganic & medicinal chemistry letters · 2023Article
- Cognitive decline in diabetic mice predisposed to Alzheimer's disease is greater than in wild type.Life science alliance · 2023Article
- Hypoxia Inducible Factor-1α binds and activates γ-secretase for Aβ production under hypoxia and cerebral hypoperfusion.Molecular psychiatry · 2022Article
- Implications of Microorganisms in Alzheimer's Disease.Current issues in molecular biology · 2022Review
- Nanobody-based RFP-dependent Cre recombinase for selective anterograde tracing in RFP-expressing transgenic animals.Communications biology · 2022Article
- The Cause of Alzheimer's Disease: The Theory of Multipathology Convergence to Chronic Neuronal Stress.Aging and disease · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
γ-Secretase is a four subunit, 19-pass transmembrane enzyme that cleaves amyloid precursor protein (APP), catalyzing the formation of amyloid beta (Aβ) peptides that form amyloid plaques, which contribute to Alzheimer's disease (AD) pathogenesis. γ-Secretase also cleaves Notch, among many other type I transmembrane substrates. Despite its seemingly promiscuous enzymatic capacity, γ-secretase activity is tightly regulated. This regulation is a function of many cellular entities, including but not limited to the essential γ-secretase subunits, nonessential (modulatory) subunits, and γ-secretase substrates. Regulation is also accomplished by an array of cellular events, such as presenilin (active subunit of γ-secretase) endoproteolysis and hypoxia. In this review we discuss how γ-secretase is regulated with the hope that an advanced understanding of these mechanisms will aid in the development of effective therapeutics for γ-secretase-associated diseases like AD and Notch-addicted cancer.
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What OpenQuestion holds
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.