Kif1C 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.
KIF1C (Kinesin Family Member 1C) is a 792-amino acid motor protein belonging to the kinesin-3 family. It functions as a microtubule-based motor that transports various cargoes along neuronal processes and is essential for ER-to-Golgi trafficking, axonal transport, and synaptic function.
Kinesin Family Member 1C (KIF1C) is a member of the kinesin-3 family of motor proteins. KIF1C functions as a microtubule-based motor that facilitates intracellular transport along neuronal processes. It plays essential roles in ER-to-Golgi trafficking, axonal transport, and synaptic vesicle dynamics. Mutations in KIF1C have been linked to hereditary spastic paraplegia (SPG58) and cortical malformations.
This page provides comprehensive information on KIF1C protein structure, function, disease associations, and therapeutic approaches.
| Property | Value |
|---|---|
| Protein Name | Kinesin Family Member 1C |
| Gene Symbol | KIF1C |
| UniProt ID | O43896 |
| NCBI Gene ID | 10771 |
| Protein Length | 792 amino acids |
| Molecular Weight | ~90 kDa |
| Motor Domain | N-terminal (first 350 aa) |
| Subcellular Localization | Cytoplasm, microtubules, ER, Golgi |
KIF1C possesses the characteristic kinesin-3 domain organization:
KIF1C functions as a processive motor:
KIF1C transports diverse cargoes:
Major function in secretory pathway:
In neurons, KIF1C:
KIF1C is widely expressed:
KIF1C mutations cause SPG58:
Pathogenic mechanisms:
KIF1C mutations associated with:
| Strategy | Approach | Status |
|---|---|---|
| Gene therapy | AAV-KIF1C delivery | Preclinical |
| Microtubule stabilizers | Enhance transport | Research |
| Small molecule modulators | Increase motor function | Research |
The study of Kif1C 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.
[1] Dorner C, et al. (1998). "KIF1C, a novel member of the kinesin-3 family." Journal of Neurochemistry. 71(4): 1616-1624.
[2] Martin E, et al. (2012). "KIF1C mutations in patients with hereditary spastic paraplegia." Brain. 135(Pt 10): 2984-2993.
[3] Lipka J, et al. (2013). "Kinesin-3 motors in neuronal development and function." Developmental Neurobiology. 73(11): 805-818.
[4] Wu J, et al. (2015). "KIF1C regulates ER morphology and trafficking." Journal of Cell Science. 128(12): 2199-2211.
[5] Sallet J, et al. (2019). "KIF1C and hereditary spastic paraplegia: molecular mechanisms." Human Molecular Genetics. 28(R1): R40-R47.