ReviewJournal of molecular medicine (Berlin, Germany)2014
Amphiphysin 2 (BIN1) in physiology and diseases.
Review in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
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
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.
- Neuropsychological functioning and quality of life in congenital myopathies: a systematic review of children and caregiver outcomes.Frontiers in medicine · 2026Pooled it
- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- Immune cell-specific genetic architecture of Alzheimer's disease revealed by multi-omics analysis for therapeutic target discovery and prioritization.Translational psychiatry · 2026Article
- BIN1 gain-of-function in the presynaptic compartment leads to isoform-specific synaptotoxicity.Alzheimer's research & therapy · 2026Article
- Article
- Evaluating the Impact of Phosphorylation on the Dynamics of the Tau Protein Proline-Rich Region.Journal of chemical theory and computation · 2026Article
- Interactome mapping in human excitatory neurons reveals novel risk genes and pathways in Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- Article
- The association of Alzheimer's disease-related SNPs with mild cognitive impairment susceptibility in the Chinese population.Scientific reports · 2026Article
- Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026Review
- BIN1 gene replacement reverses BIN1-related centronuclear myopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Glial Cells in Alzheimer's Disease: Pathogenic Mechanisms and Therapeutic Frontiers.Journal of molecular neuroscience : MN · 2025Review
- Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025Review
- Synaptic vesicle-omics in mice captures signatures of aging and synucleinopathy.Nature communications · 2025Article
- Uncovering leading compounds for alzheimer's disease treatment: mendelian randomization and virtual screening insights into plasma protein modulation.Biological research · 2025Article
- BIN1 reduction amelioratesProceedings of the National Academy of Sciences of the United States of America · 2025Article
- BIN1 inhibited tumor growth, metastasis and stemness by ALDH1/NOTCH pathway in bladder carcinoma.Hereditas · 2025Article
- Exploring the association betweenFrontiers in neurology · 2025Article
- Article
- Article
47 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
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amphiphysin 2, also named bridging integrator-1 (BIN1) or SH3P9, has been recently implicated in rare and common diseases affecting different tissues and physiological functions. BIN1 downregulation is linked to cancer progression and also correlates with ventricular cardiomyopathy and arrhythmia preceding heart failure. Increased BIN1 expression is linked to increased susceptibility for late-onset Alzheimer's disease. In addition, altered splicing may account for the muscle component of myotonic dystrophies, while recessive germinal mutations cause centronuclear myopathy. Despite undoubtedly underlining the relevance of BIN1 in human diseases, the molecular and cellular bases leading to such different diseases are unclear at present. BIN1 is a key regulator of endocytosis and membrane recycling, cytoskeleton regulation, DNA repair, cell cycle progression, and apoptosis. In light of the recent findings on the molecular, cellular, and physiological roles of BIN1, we discuss potential pathological mechanisms and highlight common disease pathways and also tissue-specific regulation. Next challenges will be to validate BIN1 both as a prognostic marker for the related diseases and as a potential therapeutic target.
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.