ArticleThe Journal of biological chemistry2013
MicroRNA-144 is regulated by activator protein-1 (AP-1) and decreases expression of Alzheimer disease-related a disintegrin and metalloprotease 10 (ADAM10).
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
70 citing papers in PubMed, 113 citations in OpenAlex.
- Serum Exosomal miRNA-125b and miRNA-451a are Potential Diagnostic Biomarker for Alzheimer's Diseases.Degenerative neurological and neuromuscular disease · 2024Trial
- Dietary mixed-oxysterols and 27-Hydroxycholesterol induce cognitive impairment by regulating gut microbiota and miR-144-3p in vivo.GeroScience · 2026Article
- Integrated multi-omics analyses of synaptosomes revealed synapse-associated novel targets in Alzheimer's disease.Molecular psychiatry · 2025Article
- Ethanol-induced Nrf2 suppression in the lung is mediated by AP-1-driven expression of miR-144.Alcohol, clinical & experimental research · 2025Article
- miR-32533 Reduces Cognitive Impairment and Amyloid-β Overload by Targeting CREB5-Mediated Signaling Pathways in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- An Update on Neuroaging on Earth and in Spaceflight.International journal of molecular sciences · 2025Review
- Molecular pathogenesis of Alzheimer's disease onset in a mouse model: effects of cannabidiol treatment.Frontiers in neuroscience · 2025Article
- A Valuable Target for Therapy: The Metalloproteinase ADAM10.Current protein & peptide science · 2025Review
- Exercise Alleviates Fluoride-Induced Learning and Memory Impairment in Mice: Role of miR-206-3p and PREG.Biological trace element research · 2024Article
- Unveiling the multifaceted pathogenesis and therapeutic drugs of Alzheimer's disease: A comprehensive review.Heliyon · 2024Review
- The role of ncRNAs in depression.Heliyon · 2024Review
- Exploring small non-coding RNAs as blood-based biomarkers to predict Alzheimer's disease.Cell & bioscience · 2024Article
- miR-3940-5p reduces amyloid β production via selectively targetingFrontiers in aging neuroscience · 2024Article
- RNA mGenes & diseases · 2024Article
- Understanding the multifaceted role of miRNAs in Alzheimer's disease pathology.Metabolic brain disease · 2024Review
- Review
- miR-153-3p suppresses the differentiation and proliferation of neural stem cells via targeting GPR55.Aging · 2023Article
- Review
- Downregulation of miR-144 blocked the proliferation and invasion of nerve cells in Hirschsprung disease by regulating Transcription Factor AP 4 (TFAP4).Pediatric surgery international · 2023Article
- Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroRNA (miR) dysregulation is found in Alzheimer disease (AD). A disintegrin and metalloprotease 10 (ADAM10) prevents generation of amyloid β (Aβ) and decrease AD pathology.
resultsmiR-144 suppresses ADAM10 expression and is up-regulated by activator protein-1.
conclusionmiR-144 is a negative regulator of ADAM10 and may be involved in AD pathogenesis. SIGNIFICANCE: The first work to demonstrate the function of miRNA-144 and its regulation in the pathogenesis of AD. Amyloid β-peptide (Aβ) accumulating in the brain of Alzheimer disease (AD) patients is believed to be the main pathophysiologcal cause of the disease. Proteolytic processing of the amyloid precursor protein by α-secretase ADAM10 (a disintegrin and metalloprotease 10) protects the brain from the production of the Aβ. Meanwhile, dysregulation or aberrant expression of microRNAs (miRNAs) has been widely documented in AD patients. In this study, we demonstrated that overexpression of miR-144, which was previously reported to be increased in elderly primate brains and AD patients, significantly decreased activity of the luciferase reporter containing the ADAM10 3'-untranslated region (3'-UTR) and suppressed the ADAM10 protein level, whereas the miR-144 inhibitor led to an increase of the luciferase activity. The negative regulation caused by miR-144 was strictly dependent on the binding of the miRNA to its recognition element in the ADAM10 3'-UTR. Moreover, we also showed that activator protein-1 regulates the transcription of miR-144 and the up-regulation of miR-144 at least partially induces the suppression of the ADAM10 protein in the presence of Aβ. In addition, we found that miR-451, a miRNA processed from a single gene locus with miR-144, is also involved in the regulation of ADAM10 expression. Taken together, our data therefore demonstrate miR-144/451 is a negative regulator of the ADAM10 protein and suggest a mechanistic role for miR-144/451 in AD pathogenesis.
Indexed as
Identifiers
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.