KIF17 — Kinesin Family Member 17

KIF17 — Kinesin Family Member 17

KIF17 (Kinesin Family Member 17) is a neuronal-specific [kinesin](/proteins/kinesin-family) motor protein that mediates intracellular transport along [microtubules](/entities/microtubules). It plays critical roles in [synaptic plasticity](/mechanisms/synaptic-plasticity), [memory formation](/mechanisms/memory-consolidation), and neuronal signaling.

<div class="infobox infobox-gene">
<table>
<tr><th colspan="2" style="background:#f0f0f0;">KIF17</th></tr>
<tr><td><b>Full Name</b></td><td>Kinesin Family Member 17</td></tr>
<tr><td><b>Chromosome</b></td><td>1p34.2</td></tr>
<tr><td><b>NCBI Gene ID</b></td><td>[57576](https://www.ncbi.nlm.nih.gov/gene/57576)</td></tr>
<tr><td><b>Ensembl ID</b></td><td>ENSG00000125485</td></tr>
<tr><td><b>OMIM ID</b></td><td>608341</td></tr>
<tr><td><b>UniProt ID</b></td><td>[Q9P2E5](https://www.uniprot.org/uniprot/Q9P2E5)</td></tr>
<tr><td><b>Protein Class</b></td><td>Kinesin motor protein</td></tr>
<tr><td><b>Transport Direction</b></td><td>Anterograde (dendrite → soma)</td></tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">1 edges</a></td>
</tr>
</table>
</div>

Overview

KIF17 — Kinesin Family Member 17

KIF17 (Kinesin Family Member 17) is a neuronal-specific [kinesin](/proteins/kinesin-family) motor protein that mediates intracellular transport along [microtubules](/entities/microtubules). It plays critical roles in [synaptic plasticity](/mechanisms/synaptic-plasticity), [memory formation](/mechanisms/memory-consolidation), and neuronal signaling.

<div class="infobox infobox-gene">
<table>
<tr><th colspan="2" style="background:#f0f0f0;">KIF17</th></tr>
<tr><td><b>Full Name</b></td><td>Kinesin Family Member 17</td></tr>
<tr><td><b>Chromosome</b></td><td>1p34.2</td></tr>
<tr><td><b>NCBI Gene ID</b></td><td>[57576](https://www.ncbi.nlm.nih.gov/gene/57576)</td></tr>
<tr><td><b>Ensembl ID</b></td><td>ENSG00000125485</td></tr>
<tr><td><b>OMIM ID</b></td><td>608341</td></tr>
<tr><td><b>UniProt ID</b></td><td>[Q9P2E5](https://www.uniprot.org/uniprot/Q9P2E5)</td></tr>
<tr><td><b>Protein Class</b></td><td>Kinesin motor protein</td></tr>
<tr><td><b>Transport Direction</b></td><td>Anterograde (dendrite → soma)</td></tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">1 edges</a></td>
</tr>
</table>
</div>

Overview

KIF17 is a member of the kinesin-3 family, characterized by its Neuronal-specific expression and unique cargo-binding properties. Unlike other kinesins that transport cargo toward the plus end of microtubules (anterograde), KIF17 transports specific synaptic proteins in the opposite direction—toward the minus end (retrograde) within dendrites.

The protein consists of:

• Motor domain: At the N-terminus, binds microtubules and hydrolyzes ATP for movement
• Coiled-coil region: Mediates dimerization
• Cargo-binding domain: At the C-terminus, binds specific synaptic proteins

Function

Synaptic Protein Transport

KIF17 transports several critical synaptic proteins:

| Cargo | Function |
|-------|----------|
| NR2B (GRIN2B) | NMDA receptor subunit |
| Synaptic vesicle proteins | Neurotransmitter release machinery |
| mRNA particles | Local protein synthesis |
| RhoGEF | Synaptic signaling |

Synaptic Plasticity

KIF17 is crucial for activity-dependent synaptic plasticity:

• Mediates activity-dependent trafficking of NMDA receptors
• Regulates synaptic strength
• Critical for long-term potentiation (LTP)
• Required for memory consolidation

Neuronal Function

• Dendritic trafficking: Moves cargo within dendrites toward the soma
• Synapse formation: Participates in synaptogenesis
• Activity-dependent regulation: Translocates in response to neuronal activity

Disease Associations

Memory Impairment

KIF17 dysfunction contributes to memory deficits through:

• Impaired NMDA receptor trafficking
• Disrupted synaptic plasticity
• Altered synaptic strength

Intellectual Disability

| Aspect | Details |
|--------|---------|
| Link | KIF17 mutations identified in ID patients |
| Mechanism | Impaired synaptic protein transport |
| Phenotype | Cognitive impairment, sometimes with other neurological features |

Alzheimer's Disease

While not directly causal, KIF17 may be relevant to:

• Amyloid-induced transport deficits
• Synaptic dysfunction in AD
• NMDA receptor dysregulation

Parkinson's Disease

KIF17-mediated transport may be affected in:

• Synaptic vesicle trafficking deficits
• Axonal transport impairment

Expression Pattern

KIF17 is primarily expressed in:

• Brain ([hippocampus](/brain-regions/hippocampus), [cortex](/brain-regions/cortex))
• [Neurons](/entities/neurons) — specifically in dendrites
• Retina

• Dendritic shafts
• Synaptic regions
• Growth cones during development

Therapeutic Implications

Target for Cognitive Disorders

• Enhancing KIF17 function may improve memory
• Small molecules that enhance motor activity

Biomarker Potential

• KIF17 expression may serve as a marker of synaptic health

Key Publications

See Also

• [Axonal Transport](/mechanisms/axonal-transport)
• [Kinesin Proteins](/proteins/kinesin-family)
• [Alzheimer's Disease](/diseases/alzheimers-disease)
• [Parkinson's Disease](/diseases/parkinsons-disease)
• [Synaptic Plasticity](/mechanisms/synaptic-plasticity)
• [NMDA Receptor Signaling](/mechanisms/nmda-receptor-signaling)
• [Memory Consolidation](/mechanisms/memory-consolidation)

External Links

• [NCBI Gene: KIF17](https://www.ncbi.nlm.nih.gov/gene/57576)
• [UniProt: KIF17](https://www.uniprot.org/uniprot/Q9P2E5)
• [Ensembl: ENSG00000125485](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000125485)

References

<references>

• Setou M, et al. (2000). KIF17 mediates NMDA receptor subunit transport. Nature 408(6809):322-328.
• Gu W, et al. (2004). KIF17 regulates synaptic plasticity and memory. Cell 117(5):649-662.
• Wakana Y, et al. (2012). KIF17 mutation in patients with intellectual disability. J Med Genet 49(6):400-402.