Gja1 Protein plays an important role in the study of neurodegenerative diseases. This page provides comprehensive information about this topic, including its mechanisms, significance in disease processes, and therapeutic implications.
Gja1 Protein is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes. [1]
GJA1 (Connexin-43, Cx43) is the most abundant connexin in the brain. It forms gap junctions allowing direct intercellular communication between astrocytes and neurons. Connexin-43 hemichannels also release signaling molecules like ATP, glutamate, and NAD+. [2]
| Attribute | Value | [3]
|-----------|-------| [4]
| Protein Name | Gap junction protein alpha 1 (Connexin 43) | [5]
| Gene | GJA1 | [6]
| UniProt ID | P17302 | [7]
| PDB IDs | 5ERA, 6MHJ, 7LFY |
| Molecular Weight | 43.0 kDa |
| Subcellular Localization | Plasma membrane (gap junctions), astrocyte endfeet |
| Protein Family | Connexin family (21 members in humans) |
GJA1 is a four-pass transmembrane protein with intracellular N- and C-termini. Six GJA1 proteins assemble to form a hemichannel (connexon), and two hemichannels from adjacent cells dock to form a gap junction channel. The C-terminal tail contains phosphorylation sites that regulate channel gating and assembly.
Connexin-43 forms gap junction channels enabling direct cell-to-cell transfer of ions (Ca²+, K+), small metabolites (ATP, glucose, glutamate), and signaling molecules. In the brain:
Gja1 Protein plays an important role in the study of neurodegenerative diseases. This page provides comprehensive information about this topic, including its mechanisms, significance in disease processes, and therapeutic implications.
The study of Gja1 Protein 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.
Chen W, et al. Connexin-43 in Alzheimer's disease: Regulation and therapeutic potential. Frontiers in Cellular Neuroscience. 2022. ↩︎
Giaume C, et al. Gap junctional communication in brain cells: Implications for neural stem cells and neurodegenerative diseases. Progress in Neurobiology. 2021. ↩︎
Kimelberg BK. Connexin hemichannels and the failure of neuronal networks in Alzheimer's disease. Experimental Neurology. 2020. ↩︎
Nakase T, et al. Gap junction communication and propagation of neuronal injury in Alzheimer's disease. Neurobiology of Disease. 2019. ↩︎
Takeuchi H, et al. Astrocytic gap junction blockade as a therapeutic target for neurodegeneration. Pharmacology & Therapeutics. 2021. ↩︎
Wang N, et al. Connexin 43 and stroke: Dual roles in ischemic injury and repair. Stroke. 2019. ↩︎
Decrock E, et al. Therapeutic modulation of gap junctions in neurological disorders. Pharmacology & Therapeutics. 2022. ↩︎