Becn1 Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
:: infobox .infobox-gene
Symbol: BECN1
Full Name: Beclin 1
Chromosomal Location: 17q21.31
NCBI Gene ID: 9277
OMIM: 604378
Ensembl ID: ENSG00000126581
UniProt: Q14457
Proteins: Beclin-1
Associated Diseases: Alzheimer's Disease, Parkinson's Disease, Breast Cancer, Neurodegeneration
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BECN1 is a gene/protein encoding a key neuronal protein involved in synaptic function, signal transduction, and cellular homeostasis. Dysfunction of BECN1 is associated with neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and related disorders.
BECN1 encodes Beclin-1, a key regulator of autophagy and apoptosis. Beclin-1 is part of the PI3K complex that initiates autophagosome formation. It plays a dual role in cell survival (via autophagy) and cell death (via apoptosis). In neurodegenerative diseases, impaired autophagy leads to accumulation of protein aggregates, and Beclin-1 expression is often reduced.
Beclin-1 is widely expressed in:
- Brain (neurons and glia)
- Heart, liver, kidney
- Moderate expression in hippocampus, cortex, cerebellum
- Higher expression during development
Ubiquitous expression reflects its essential role in basic cellular processes.
- Liang XH, et al. (1999). "Induction of autophagy and inhibition of tumorigenesis by beclin 1." Nature. PMID:10521303
- Pickford F, et al. (2008). "The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice." J Clin Invest. PMID:18425089
- Wang RC, et al. (2012). "Beclin 1 in the context of macroautophagy and apoptosis." Cell Mol Life Sci. PMID:22382918
The study of Becn1 Gene has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
- Xu Y, Wan W. "Acetylation in the regulation of autophagy." Autophagy (2023). DOI: 10.1080/15548627.2022.2062112 PubMed: 35435793
- Hegdekar N et al.. "Inhibition of autophagy in microglia and macrophages exacerbates innate immune responses and worsens brain injury outcomes." Autophagy (2023). DOI: 10.1080/15548627.2023.2167689 PubMed: 36652438
- Yao RQ et al.. "Organelle-specific autophagy in inflammatory diseases: a potential therapeutic target underlying the quality control of multiple organelles." Autophagy (2021). DOI: 10.1080/15548627.2020.1725377 PubMed: 32048886
- Rusmini P et al.. "Trehalose induces autophagy via lysosomal-mediated TFEB activation in models of motoneuron degeneration." Autophagy (2019). DOI: 10.1080/15548627.2018.1535292 PubMed: 30335591
- Chen ML et al.. "Inhibition of miR-331-3p and miR-9-5p ameliorates Alzheimer's disease by enhancing autophagy." Theranostics (2021). DOI: 10.7150/thno.47408 PubMed: 33500732
- Yi J et al.. "Spautin-1 promotes PINK1-PRKN-dependent mitophagy and improves associative learning capability in an alzheimer disease animal model." Autophagy (2024). DOI: 10.1080/15548627.2024.2383145 PubMed: 39051473
- Luo R et al.. "Activation of PPARA-mediated autophagy reduces Alzheimer disease-like pathology and cognitive decline in a murine model." Autophagy (2020). DOI: 10.1080/15548627.2019.1596488 PubMed: 30898012
- Beccari S et al.. "Microglial phagocytosis dysfunction in stroke is driven by energy depletion and induction of autophagy." Autophagy (2023). DOI: 10.1080/15548627.2023.2165313 PubMed: 36622892