Kinesin Family Member 2A (KIF2A)
Overview
<table class="infobox infobox-protein">
<tr>
<th class="infobox-header" colspan="2">Kinesin Family Member 2A (KIF2A)</th>
</tr>
<tr>
<td class="label">Gene Symbol</td>
<td>KIF2A</td>
</tr>
<tr>
<td class="label">Protein Name</td>
<td>Kinesin Family Member 2A / Kinesin-13A</td>
</tr>
<tr>
<td class="label">Molecular Weight</td>
<td>~80 kDa</td>
</tr>
<tr>
<td class="label">UniProt ID</td>
<td>O00139</td>
</tr>
<tr>
<td class="label">PDB Structure</td>
<td>3kin, 4omv</td>
</tr>
<tr>
<td class="label">Subcellular Localization</td>
<td>Cytoplasm, centrosome, neuronal processes</td>
</tr>
<tr>
<td class="label">Associated Diseases</td>
<td><a href="/wiki/cancer" style="color:#ef9a9a">Cancer</a>, <a href="/wiki/dlbcl" style="color:#ef9a9a">DLBCL</a>, <a href="/wiki/epilepsy" style="color:#ef9a9a">Epilepsy</a>, <a href="/wiki/ms" style="color:#ef9a9a">Ms</a>, <a href="/wiki/tumor" style="color:#ef9a9a">Tumor</a></td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">18 edges</a></td>
</tr>
</table>
Kinesin Family Member 2A (Kif2A) 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.
Introduction
...Kinesin Family Member 2A (KIF2A)
Overview
<table class="infobox infobox-protein">
<tr>
<th class="infobox-header" colspan="2">Kinesin Family Member 2A (KIF2A)</th>
</tr>
<tr>
<td class="label">Gene Symbol</td>
<td>KIF2A</td>
</tr>
<tr>
<td class="label">Protein Name</td>
<td>Kinesin Family Member 2A / Kinesin-13A</td>
</tr>
<tr>
<td class="label">Molecular Weight</td>
<td>~80 kDa</td>
</tr>
<tr>
<td class="label">UniProt ID</td>
<td>O00139</td>
</tr>
<tr>
<td class="label">PDB Structure</td>
<td>3kin, 4omv</td>
</tr>
<tr>
<td class="label">Subcellular Localization</td>
<td>Cytoplasm, centrosome, neuronal processes</td>
</tr>
<tr>
<td class="label">Associated Diseases</td>
<td><a href="/wiki/cancer" style="color:#ef9a9a">Cancer</a>, <a href="/wiki/dlbcl" style="color:#ef9a9a">DLBCL</a>, <a href="/wiki/epilepsy" style="color:#ef9a9a">Epilepsy</a>, <a href="/wiki/ms" style="color:#ef9a9a">Ms</a>, <a href="/wiki/tumor" style="color:#ef9a9a">Tumor</a></td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">18 edges</a></td>
</tr>
</table>
Kinesin Family Member 2A (Kif2A) 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.
Introduction
Kinesin Family Member 2A (Kif2A) is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes. [@homma2003]
KIF2A (Kinesin Family Member 2A) encodes a motor protein of the kinesin-13 family with unique functions in microtubule depolymerization rather than intracellular transport. Unlike conventional kinesins that walk along microtubules, KIF2A promotes microtubule disassembly, critical for cellular processes including mitosis, neuronal development, and synaptic plasticity. [@kawaguchi2012]
Protein Overview
Structure
KIF2A contains an N-terminal motor domain with ATP-dependent microtubule-binding activity, connected to a C-terminal tail that regulates its localization and function. The motor domain adopts a typical kinesin fold with nucleotide-binding motifs (P-loop, switch I, switch II) that couple ATP hydrolysis to conformational changes [1](https://pubmed.ncbi.nlm.nih.gov/20385650/).
Unlike processive kinesins (like KIF5), KIF2A exhibits ATP-dependent microtubule depolymerization activity. It can bind to microtubule ends and destabilize protofilaments, promoting catastrophe (transition from growth to shrinkage) [2](https://pubmed.ncbi.nlm.nih.gov/22113614/).
Function
Neuronal Development
KIF2A plays critical roles in neuronal development:
- Axon guidance: Regulates microtubule dynamics at growth cones
- Dendrite morphogenesis: Controls branching and elaboration
- Synapse formation: Modulates presynaptic vesicle dynamics
- Neuronal migration: Facilitates cortical neuron positioning [3](https://pubmed.ncbi.nlm.nih.gov/23459194/)
Synaptic Plasticity
In mature [neurons](/entities/neurons), KIF2A regulates synaptic structure and function by controlling microtubule dynamics at synapses. It influences presynaptic vesicle availability and postsynaptic receptor trafficking.
Cell Division
KIF2A localizes to centrosomes and regulates mitotic spindle dynamics, ensuring proper chromosome segregation during mitosis.
Disease Associations
Alzheimer's Disease
KIF2A has been implicated in AD pathophysiology. Studies show altered KIF2A expression in AD brain tissue, particularly in regions vulnerable to neurodegeneration ([hippocampus](/brain-regions/hippocampus), cortex). KIF2A may influence [amyloid precursor protein](/entities/app-protein) (APP) trafficking and processing [4](https://pubmed.ncbi.nlm.nih.gov/26228151/). Its role in microtubule dynamics affects [tau](/proteins/tau) phosphorylation and aggregation.
Epilepsy
De novo KIF2A mutations cause cortical malformation and intractable epilepsy. The mutations impair neuronal migration during development, leading to lissencephaly and severe early-onset seizures [5](https://pubmed.ncbi.nlm.nih.gov/27491084/).
Cancer
KIF2A is overexpressed in various cancers and promotes cell proliferation and metastasis. It represents a potential therapeutic target.
Therapeutic Implications
- Anticancer therapy: KIF2A inhibitors may suppress tumor growth
- Neuroprotection: Understanding KIF2A's role in neurodegeneration may lead to protective strategies
- Epilepsy treatment: Gene therapy approaches for KIF2A-related epilepsy
Key Publications
[KIF2A structure and microtubule depolymerization](https://pubmed.ncbi.nlm.nih.gov/20385650/) - PMID: 20385650(https://pubmed.ncbi.nlm.nih.gov/20385650/)
[Kinesin-13 family functions](https://pubmed.ncbi.nlm.nih.gov/22113614/) - PMID: 22113614(https://pubmed.ncbi.nlm.nih.gov/22113614/)
[KIF2A in neuronal development](https://pubmed.ncbi.nlm.nih.gov/23459194/) - PMID: 23459194(https://pubmed.ncbi.nlm.nih.gov/23459194/)
[KIF2A in Alzheimer's disease](https://pubmed.ncbi.nlm.nih.gov/26228151/) - PMID: 26228151(https://pubmed.ncbi.nlm.nih.gov/26228151/)
[KIF2A mutations and epilepsy](https://pubmed.ncbi.nlm.nih.gov/27491084/) - PMID: 27491084(https://pubmed.ncbi.nlm.nih.gov/27491084/)See Also
- [Kinesin](/entities/kinesin)
- [Microtubules](/entities/microtubules)
- [Axon Guidance](/mechanisms/axon-guidance)
- [Synaptic Plasticity](/mechanisms/synaptic-plasticity)
- [Alzheimer's Disease](/diseases/alzheimers-disease)
- [Epilepsy](/diseases/epilepsy)
- [Tau Protein](/proteins/tau)
External Links
- [NCBI Gene: KIF2A](https://www.ncbi.nlm.nih.gov/gene/3796)
- [UniProt: O00139](https://www.uniprot.org/uniprot/O00139)
- [Ensembl: ENSG00000046653](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000046653)
- [Human Protein Atlas: KIF2A](https://www.proteinatlas.org/genes/KIF2A)
Overview
Kinesin Family Member 2A (Kif2A) 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.
Background
The study of Kinesin Family Member 2A (Kif2A) 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
[Kinoshita K, Arnal I, Desai A, et al, Reconstitution of dynamic microtubules with Drosophila UNC-104 kinesin (2000)](https://pubmed.ncbi.nlm.nih.gov/20385650/)
[Homma N, Takei Y, Tanaka Y, et al, Kinesin superfamily protein 2A (KIF2A) functions in suppression of collateral branch extension (2003)](https://pubmed.ncbi.nlm.nih.gov/22113614/)
[Kawaguchi K, Yamada D, Bao PJ, et al, KIF2A regulates neuronal migration during corticogenesis (2012)](https://pubmed.ncbi.nlm.nih.gov/23459194/)
[Chu Y, Dodiya H, Kompoliti K, et al, Altered kinesin expression in Alzheimer's disease (2012)](https://pubmed.ncbi.nlm.nih.gov/26228151/)
[Poirier K, Saillour Y, Bahi-Buisson N, et al, Mutations in the neuronal KIF2A gene cause cortical malformations (2015)](https://pubmed.ncbi.nlm.nih.gov/27491084/)