Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Modeling Late-Onset Sporadic Alzheimer’s Disease through BMI1 Deficiency

1 May 2018

Abstract excerpt

Late-onset sporadic Alzheimer's disease (AD) is the most prevalent form of dementia, but its origin remains poorly understood. The Bmi1/Ring1 protein complex maintains transcriptional repression of developmental genes through histone H2A mono-ubiquitination, and Bmi1 deficiency in mice results in growth retardation, progeria, and neurodegeneration. Here, we demonstrate that BMI1 is silenced in AD brains, but not...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alzheimer's disease research and treatments
Share to Epigenetics and DNA Methylation
Share to Pluripotent Stem Cells Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 29847796
DOI: 10.1016/j.celrep.2018.04.097

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Modeling Late-Onset Sporadic Alzheimer’s Disease through BMI1 DeficiencyPMID 29847796Read ↗

The Role of BMI1 in Late-Onset Sporadic Alzheimer's Disease.Semantic proximity Read ↗

Pin1: A New Genetic Link between Alzheimers Disease, Cancer and AgingSemantic proximity Read ↗

Pin1 Regulatory miRNAs as Novel Candidates for Alzheimer’s Disease TreatmentSemantic proximity Read ↗

New Insights on Bridging Integrator 1 Protein Isoforms as a Risk Increasing Gene in Alzheimer’s DiseaseSemantic proximity Read ↗

Increased expression of BIN1 mediates Alzheimer genetic risk by modulating tau pathology.Semantic proximity Read ↗

Histone H2A ubiquitination resulting from Brap loss of function connects multiple aging hallmarks and accelerates neurodegenerationSemantic proximity Read ↗

Epigenomic anomalies in induced pluripotent stem cells from Alzheimer’s disease casesSemantic proximity Read ↗

Bridging Integrator 1 (BIN1) Protein Expression Increases in the Alzheimer's Disease Brain and Correlates with Neurofibrillary Tangle PathologySemantic proximity Read ↗

Bridging integrator 1 (BIN1): form, function, and Alzheimer's disease.Semantic proximity Read ↗

Nuclear BIN1 isoforms regulate c-Myc-mediated cell cycle control in oligodendrocytesSemantic proximity Read ↗

BIN1 deficiency leads to DNA damage and neuronal insulin resistance through ATM dysregulationSemantic proximity Read ↗

Proteomic characterization of the Alzheimer’s disease risk factor BIN1 interactomeSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.