ArticlePloS one2010
Intracellular trafficking and synaptic function of APL-1 in Caenorhabditis elegans.
Article in PloS one, 2010. 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.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- Deep transcriptomics reveals cell-specific isoforms of pan-neuronal genes.Nature communications · 2025Article
- Mitochondrial Quality Control in Alzheimer's Disease: Insights fromAntioxidants (Basel, Switzerland) · 2024Review
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
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- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- Structural Studies Providing Insights into Production and Conformational Behavior of Amyloid-β Peptide Associated with Alzheimer's Disease Development.Molecules (Basel, Switzerland) · 2021Review
- Effect of policosanol from insect wax on amyloid β-peptide-induced toxicity in a transgenic Caenorhabditis elegans model of Alzheimer's disease.BMC complementary medicine and therapies · 2021Article
- Deciphering the neuroprotective and neurogenic potential of soluble amyloid precursor protein alpha (sAPPα).Cellular and molecular life sciences : CMLS · 2020Review
- Effects of 5-Aminolevulinic Acid on Gene Expression, Immunity, and ATP Levels in Pacific White Shrimp, Litopenaeus vannamei.Marine biotechnology (New York, N.Y.) · 2018Article
- Alzheimer-related protein APL-1 modulates lifespan through heterochronic gene regulation in Caenorhabditis elegans.Aging cell · 2016Article
- Role of MicroRNA Let-7 in Modulating Multifactorial Aspect of Neurodegenerative Diseases: an Overview.Molecular neurobiology · 2016Review
- The Amyloid Precursor Protein Controls PIKfyve Function.PloS one · 2015Article
- Use of Caenorhabditis elegans as a model to study Alzheimer's disease and other neurodegenerative diseases.Frontiers in genetics · 2014Review
- Advances with RNA interference in Alzheimer's disease research.Drug design, development and therapy · 2013Review
- Article
- The kinesin-3 family motor KLP-4 regulates anterograde trafficking of GLR-1 glutamate receptors in the ventral nerve cord of Caenorhabditis elegans.Molecular biology of the cell · 2012Article
- Pan-neuronal expression of APL-1, an APP-related protein, disrupts olfactory, gustatory, and touch plasticity in Caenorhabditis elegans.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Article
- Caenorhabditis elegans as a model organism to study APP function.Experimental brain research · 2012Review
- Physiological functions of APP family proteins.Cold Spring Harbor perspectives in medicine · 2012Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundAlzheimer's disease (AD) is a neurodegenerative disorder primarily characterized by the deposition of β-amyloid plaques in the brain. Plaques are composed of the amyloid-β peptide derived from cleavage of the amyloid precursor protein (APP). Mutations in APP lead to the development of Familial Alzheimer's Disease (FAD), however, the normal function of this protein has proven elusive. The organism Caenorhabditis elegans is an attractive model as the amyloid precursor-like protein (APL-1) is the single ortholog of APP, and loss of apl-1 leads to a severe molting defect and early larval lethality. METHODOLOGY/PRINCIPAL
findingsWe report here that lethality and molting can be rescued by full length APL-1, C-terminal mutations as well as a C-terminal truncation, suggesting that the extracellular region of the protein is essential for viability. RNAi knock-down of apl-1 followed by drug testing on the acetylcholinesterase inhibitor aldicarb showed that loss of apl-1 leads to aldicarb hypersensitivity, indicating a defect in synaptic function. The aldicarb hypersensitivity can be rescued by full length APL-1 in a dose dependent fashion. At the cellular level, kinesins UNC-104/KIF-1A and UNC-116/kinesin-1 are positive regulators of APL-1 expression in the neurons. Knock-down of the small GTPase rab-5 also leads to a dramatic decrease in the amount of apl-1 expression in neurons, suggesting that trafficking from the plasma membrane to the early endosome is important for apl-1 function. Loss of function of a different small GTPase, UNC-108, on the contrary, leads to the retention of APL-1 in the cell body. CONCLUSIONS/SIGNIFICANCE: Our results reveal novel insights into the intracellular trafficking of APL-1 and we report a functional role for APL-1 in synaptic transmission.
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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.