KIF1C Protein
Introduction
<table class="infobox infobox-protein">
<tr>
<th class="infobox-header" colspan="2">KIF1C Protein</th>
</tr>
<tr>
<td class="label">Protein Name</td>
<td>Kinesin Family Member 1C</td>
</tr>
<tr>
<td class="label">Gene Symbol</td>
<td>KIF1C</td>
</tr>
<tr>
<td class="label">UniProt ID</td>
<td>O43896</td>
</tr>
<tr>
<td class="label">NCBI Gene ID</td>
<td>10771</td>
</tr>
<tr>
<td class="label">Protein Length</td>
<td>792 amino acids</td>
</tr>
<tr>
<td class="label">Molecular Weight</td>
<td>~90 kDa</td>
</tr>
<tr>
<td class="label">Motor Domain</td>
<td>N-terminal (first 350 aa)</td>
</tr>
<tr>
<td class="label">Subcellular Localization</td>
<td>Cytoplasm, microtubules, ER, Golgi</td>
</tr>
<tr>
<td class="label">Strategy</td>
<td>Approach</td>
</tr>
<tr>
<td class="label">Gene therapy</td>
<td>AAV-KIF1C delivery</td>
</tr>
<tr>
<td class="label">Microtubule stabilizers</td>
<td>Enhance transport</td>
</tr>
<tr>
<td class="label">Small molecule modulators</td>
<td>Increase motor function</td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">1 edges</a></td>
</tr>
</table>
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 Protein
Introduction
<table class="infobox infobox-protein">
<tr>
<th class="infobox-header" colspan="2">KIF1C Protein</th>
</tr>
<tr>
<td class="label">Protein Name</td>
<td>Kinesin Family Member 1C</td>
</tr>
<tr>
<td class="label">Gene Symbol</td>
<td>KIF1C</td>
</tr>
<tr>
<td class="label">UniProt ID</td>
<td>O43896</td>
</tr>
<tr>
<td class="label">NCBI Gene ID</td>
<td>10771</td>
</tr>
<tr>
<td class="label">Protein Length</td>
<td>792 amino acids</td>
</tr>
<tr>
<td class="label">Molecular Weight</td>
<td>~90 kDa</td>
</tr>
<tr>
<td class="label">Motor Domain</td>
<td>N-terminal (first 350 aa)</td>
</tr>
<tr>
<td class="label">Subcellular Localization</td>
<td>Cytoplasm, microtubules, ER, Golgi</td>
</tr>
<tr>
<td class="label">Strategy</td>
<td>Approach</td>
</tr>
<tr>
<td class="label">Gene therapy</td>
<td>AAV-KIF1C delivery</td>
</tr>
<tr>
<td class="label">Microtubule stabilizers</td>
<td>Enhance transport</td>
</tr>
<tr>
<td class="label">Small molecule modulators</td>
<td>Increase motor function</td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">1 edges</a></td>
</tr>
</table>
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.
Overview
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.
Protein Overview
Protein Structure
KIF1C possesses the characteristic kinesin-3 domain organization:
Motor Domain (N-terminal)
- Microtubule-binding region: Binds to microtubule tracks
- ATP-binding pocket: Provides energy for movement
- Neck linker: Couples ATP hydrolysis to stepping motion
- Processive movement: Single molecules can travel microns along microtubules
Coiled-coil Regions
- Mediate dimerization with another KIF1C subunit
- Form the stalk region
- Contain cargo-binding sites
Tail Domain (C-terminal)
- Cargo-binding adaptors
- Regulatory sequences
- Membrane association motifs
Post-Translational Modifications
- Phosphorylation: Multiple serine/threonine sites
- Acetylation: Lysine acetylation affects motor function
- Palmitoylation: Some isoforms may be membrane-associated
Molecular Function
Microtubule-Based Transport
KIF1C functions as a processive motor:
- Unidirectional movement toward microtubule plus ends
- Transport velocity: ~1.5 μm/second
- Processive runs of several microns
- Can function as monomer but more efficient as dimer
Cargo Transport
KIF1C transports diverse cargoes:
- ER-to-Golgi vesicles
- Synaptic vesicle precursors
- Signaling complexes
- Membrane organelles
ER-Golgi Trafficking
Major function in secretory pathway:
- Mediates anterograde transport from ER to Golgi
- Maintains Golgi morphology
- Participates in ER export site function
Neuronal Function
In [neurons](/entities/neurons), KIF1C:
- Transports cargo from cell body to synapses
- Maintains axonal polarity
- Supports synaptic vesicle dynamics
- Contributes to dendritic trafficking
Expression Pattern
KIF1C is widely expressed:
- Brain:
- Cerebellum (high in Purkinje cells)
- Cerebral [cortex](/brain-regions/cortex)
- [Hippocampus](/brain-regions/hippocampus)
- Spinal cord motor neurons
- Non-neuronal tissues:
- Fibroblasts
- Immune cells
- Epithelial cells
Role in Disease
Hereditary Spastic Paraplegia
KIF1C mutations cause SPG58:
- Autosomal recessive inheritance
- Progressive lower limb spasticity
- May include ataxia
- Onset in childhood/adolescence
Pathogenic mechanisms:
- Impaired axonal transport
- Disrupted ER-Golgi trafficking
- Axonal degeneration
Ataxia
KIF1C mutations associated with:
- Cerebellar ataxia
- Oculomotor abnormalities
- Variable intellectual disability
Alzheimer's Disease
- Altered axonal transport
- Impaired synaptic function
- Possible [APP](/entities/app-protein) interaction
Parkinson's Disease
- May affect dopaminergic neurons
- Axonal transport deficits
Therapeutic Targeting
Background
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.
References
<sup>[1]</sup> Dorner C, et al. (1998). "KIF1C, a novel member of the kinesin-3 family." Journal of Neurochemistry. 71(4): 1616-1624.
<sup>[2]</sup> Martin E, et al. (2012). "KIF1C mutations in patients with hereditary spastic paraplegia." Brain. 135(Pt 10): 2984-2993.
<sup>[3]</sup> Lipka J, et al. (2013). "Kinesin-3 motors in neuronal development and function." Developmental Neurobiology. 73(11): 805-818.
<sup>[4]</sup> Wu J, et al. (2015). "KIF1C regulates ER morphology and trafficking." Journal of Cell Science. 128(12): 2199-2211.
<sup>[5]</sup> Sallet J, et al. (2019). "KIF1C and hereditary spastic paraplegia: molecular mechanisms." Human Molecular Genetics. 28(R1): R40-R47.
See Also
- [KIF1C Gene](/genes/kif1c)
- [Kinesin Proteins](/proteins)
- [Axonal Transport](/mechanisms/axonal-transport)
- [Hereditary Spastic Paraplegia](/diseases/hereditary-spastic-paraplegia)
- [Motor Neuron Diseases](/diseases)