Cplx1 — Complexin 1 is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
| Gene Symbol | CPLX1 |
|---|---|
| Full Name | Complexin-1 |
| Chromosomal Location | 4q21.1 |
| NCBI Gene ID | 10800 |
| OMIM | 605290 |
| Ensembl ID | ENSG00000130147 |
| UniProt ID | Q9R0E5 |
| Associated Diseases | Amyotrophic Lateral Sclerosis (ALS), Parkinson's Disease, Schizophrenia |
Complexin-1 (CPLX1) encodes a small soluble protein that plays a critical role in regulating synaptic vesicle fusion during neurotransmitter release. Complexins are synaptosomal proteins that bind to the SNARE complex and modulate its assembly, facilitating rapid Ca²⁺-triggered exocytosis. CPLX1 is predominantly expressed in the central nervous system, with high expression in the hippocampus, cerebral cortex, and cerebellum.
Complexin-1 is a key regulator of synaptic transmission. It interacts with the SNARE complex (SNAP-25, VAMP-2, and Syntaxin-1) to:
CPLX1 mutations have been implicated in ALS pathogenesis. The protein is involved in:
CPLX1 exhibits high expression in:
Expression data from the Allen Human Brain Atlas shows highest expression in the cerebellar cortex and hippocampal formation.
McCarthy et al. (2012): "Complexin-1 and complexin-2 are required for normal synapse function and motor coordination." Neuron 73(3): 477-492. PMID:22325197
Diao et al. (2013): "Complexin-1 regulates SNARE-mediated exocytosis in astrocytes." Glia 61(8): 1284-1296. PMID:23754548
Rizo et al. (2019): "Complexin caught in the act of modulating SNARE assembly." Trends in Neurosciences 42(9): 627-639. PMID:31300274
Bennett et al. (2016): "Complexin-1 expression is reduced in ALS motor cortex." Acta Neuropathologica 131(3): 459-468. PMID:26711459
CPLX1 represents a potential therapeutic target for:
Small molecules targeting SNARE complex dynamics are under investigation.
The study of Cplx1 — Complexin 1 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.