Dbn1 — Drebrin is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
This page provides comprehensive information about this gene. See the content below for detailed information.
| DBN1 — Drebrin | |
|---|---|
| Symbol | DBN1 |
| Full Name | Drebrin |
| Chromosome | 5q33.3 |
| NCBI Gene | 1627 |
| Ensembl | ENSG00000113758 |
| OMIM | 124060 |
| UniProt | Q16643 |
| Diseases | Alzheimer's Disease, Epilepsy, Intellectual Disability |
| Expression | Hippocampus, Cerebral cortex, Dendritic spines, Postsynaptic densities |
Drebrin is an actin-binding protein that plays a critical role in synaptic plasticity, dendritic spine morphology, and neuronal migration. It is abundant in the brain and localizes to dendritic spines, where it regulates the organization of actin filaments and synaptic proteins.
The DBN1 gene encodes Drebrin, an actin-binding protein that modulates the cytoskeletal structure of dendritic spines. Drebrin promotes the formation and maintenance of dendritic spines, which are the primary sites of excitatory synaptic transmission in the brain. It interacts with actin filaments and various synaptic proteins to regulate synaptic plasticity, learning, and memory.
Alzheimer's Disease, Epilepsy, Intellectual Disability — Drebrin expression is significantly reduced in Alzheimer's disease brain, particularly in areas affected by amyloid pathology. Loss of drebrin contributes to synaptic dysfunction and cognitive decline. Mutations in DBN1 have been linked to epileptic disorders and intellectual disability.
Drebrin is highly expressed in the hippocampus and cerebral cortex, with particular enrichment in dendritic spines and postsynaptic densities. Its expression is developmentally regulated, with highest levels in the adult brain.
The study of Dbn1 — Drebrin 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.