LIN7B — Lin-7 Homolog B
<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">LIN7B — Lin-7 Homolog B</th>
</tr>
<tr>
<td class="label">Symbol</td>
<td><strong>LIN7B</strong></td>
</tr>
<tr>
<td class="label">Full Name</td>
<td>Lin-7 Homolog B</td>
</tr>
<tr>
<td class="label">Chromosome</td>
<td>9q34.3</td>
</tr>
<tr>
<td class="label">NCBI Gene</td>
<td><a href="https://www.ncbi.nlm.nih.gov/gene/5600" target="_blank">5600</a></td>
</tr>
<tr>
<td class="label">Ensembl</td>
<td><a href="https://ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000125967" target="_blank">ENSG00000125967</a></td>
</tr>
<tr>
<td class="label">OMIM</td>
<td><a href="https://omim.org/entry/603761" target="_blank">603761</a></td>
</tr>
<tr>
<td class="label">UniProt</td>
<td><a href="https://www.uniprot.org/uniprot/Q9UBR4" target="_blank">Q9UBR4</a></td>
</tr>
<tr>
<td class="label">Protein Class</td>
<td>PDZ domain scaffolding protein</td>
</tr>
<tr>
<td class="label">Molecular Function</td>
<td>Protein scaffolding, synaptic membrane organization, receptor clustering</td>
</tr>
<tr>
<td class="label">Diseases</td>
<td>[Alzheimer's Disease](/diseases/alzheimers-disease), Neurodevelopmental disorders, Epilepsy</td>
</tr>
<tr>
<td class="label">Expression</td>
<td>[Cortex](/brain-regions/cortex), [Hippocampus](/brain-regions/hippocampus), Synapses</td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">1 edges</a></td>
</tr>
</table>
LIN7B — Lin-7 Homolog B
Overview
LIN7B (Lin-7 Homolog B) is a gene located on chromosome 9q34.3 that encodes a PDZ domain-containing scaffolding protein essential for synaptic organization, receptor clustering, and neuronal polarity. LIN7B is a member of the LIN-7 family (also known as Veli/LIN-7), which plays critical roles in targeting and anchoring proteins to specific membrane domains in epithelial cells and neurons.[@linb2014] The gene is catalogued as NCBI Gene ID [5600](https://www.ncbi.nlm.nih.gov/gene/5600), OMIM [603761](https://omim.org/entry/603761), and UniProt [Q9UBR4](https://www.uniprot.org/uniprot/Q9UBR4).
The LIN-7 protein family is conserved from C. elegans (where it was originally identified in genetic screens for vulval development) to mammals, indicating fundamental roles in cellular organization. In the nervous system, LIN7B is crucial for establishing and maintaining synaptic architecture, making it a protein of interest in understanding neurodegenerative processes that affect synaptic function.[@linb2010]
Molecular Function
PDZ Domain Structure
LIN7B contains multiple functional domains that mediate protein-protein interactions:
PDZ Domain:
The PDZ (Postsynaptic density 95, Discs large, Zonula occludens-1) domain is the defining feature of LIN7B. This domain recognizes specific C-terminal motifs (typically X-S/T-X-V/I/L) on target proteins. The PDZ domain of LIN7B binds:
- C-terminal sequences of ion channels
- Receptor cytoplasmic tails
- Other scaffolding proteins
- Cell adhesion molecules
L27 Domain:The L27 domain mediates homo- and heterodimerization with other LIN-7 family members (LIN7A and LIN7C) and with LIN-2/CASK. This allows formation of larger scaffolding complexes.
Proline-Rich Region:
The proline-rich region interacts with SH3 domain-containing proteins, expanding the interaction network.
Scaffolding Function
LIN7B serves as a molecular scaffold that:
Clusters receptors: Brings neurotransmitter receptors together at synaptic sites
Anchors channels: Targets ion channels to specific membrane domains
Organizes signaling complexes: Assembles signaling molecules near their effectors
Links to cytoskeleton: Connects membrane proteins to the actin cytoskeletonInteractions with Receptors
LIN7B directly interacts with:
Ionotropic Glutamate Receptors:
- NMDA receptor subunits: NR2A, NR2B (via PDZ-binding motifs)
- AMPA receptor subunits: GluR1, GluR2
- Kainate receptor subunits
Other Membrane Proteins:
- Cav2.1 voltage-gated calcium channels
- Kv1.2 potassium channels
- Acetylcholine receptor subunits
Brain Expression and Localization
LIN7B exhibits specific expression patterns in the nervous system:
Regional Expression
High expression in brain regions associated with learning and memory:
- Hippocampus: Highest expression in CA1-CA3 pyramidal cells and dentate gyrus granule cells
- Cortex: Expressed throughout cortical layers, particularly layer II-III pyramidal neurons
- Cerebellum: Present in Purkinje cells
- Brainstem: Motor and sensory nuclei
Cellular Localization
Within neurons, LIN7B localizes to:
Synaptic Compartments:
- Postsynaptic density (PSD): Highly enriched in excitatory synapses
- Synaptic vesicles: Associated with presynaptic vesicle pools
- Excitatory synapses: Primary localization to glutamatergic synapses
Subcellular Domains:
- Dendritic shafts: Distributed throughout dendrites
- Dendritic spines: Present in spine heads, the primary sites of excitatory input
- Axon initial segment: Lower levels in AIS
- Soma: Moderate cytoplasmic expression
Cell-Type Specificity
- Neurons: High expression
- Astrocytes: Low expression
- Microglia: Minimal expression
- Oligodendrocytes: Variable expression
Expression data is available from the [Allen Brain Atlas](https://human.brain-map.org/microarray/search/show?search_term=LIN7B).
Role in Synaptic Function
LIN7B is essential for proper synapse formation during development:
Presynaptic Differentiation:
- LIN7B interacts with presynaptic adhesion molecules
- Helps organize active zone proteins
- Regulates synaptic vesicle clustering
Postsynaptic Differentiation:
- Recruits glutamate receptors to nascent synapses
- Organizes the postsynaptic density
- Stabilizes synaptic contacts
Synaptic Plasticity
LIN7B plays a role in activity-dependent synaptic modifications:
Long-Term Potentiation (LTP):
- Required for proper LTP induction
- Modulates NMDA receptor trafficking
- Essential for activity-dependent AMPA receptor insertion
Long-Term Depression (LTD):
- Regulates AMPA receptor internalization
- Controls metabotropic glutamate receptor signaling
- Participates in endocytic processes
Synaptic Homeostasis
LIN7B contributes to synaptic scaling and homeostatic plasticity:
- Adjusts synaptic strength in response to activity changes
- Participates in retrograde signaling
- Helps maintain synaptic balance
LIN7B in Neurodegenerative Diseases
Alzheimer's Disease
LIN7B dysfunction contributes to [Alzheimer's Disease](/diseases/alzheimers-disease) pathogenesis through several mechanisms:
Synaptic Loss:
The earliest pathological feature in AD is synapse loss. LIN7B:
- Levels decrease in AD hippocampus
- Contributes to AMPA receptor mislocalization
- Disrupts NMDA receptor signaling
- Impairs synaptic plasticity mechanisms
Receptor Trafficking Defects:
- β-amyloid (Aβ) oligomers disrupt LIN7B interactions
- Reduces synaptic receptor clustering
- Promotes excitotoxicity through dysregulated signaling
tau Pathology:
- LIN7B may be affected by tau-mediated synaptic disruption
- Phosphorylated tau alters synaptic scaffolding
- Contributes to memory deficits
Parkinson's Disease
Emerging evidence links LIN7B to [Parkinson's Disease](/diseases/parkinsons-disease-disease):
Dopaminergic Synapse Function:
- LIN7B localizes to dopaminergic synapses in the striatum
- Regulates dopamine receptor trafficking
- Contributes to synaptic signaling integrity
α-Synuclein Interaction:
- Potential interaction with α-synuclein pathology
- May affect Lewy body formation
- Linked to synaptic dysfunction in PD
Neurodevelopmental Disorders
LIN7B mutations are associated with neurodevelopmental disorders:
Intellectual Disability:
- LIN7B variants cause autosomal recessive intellectual disability
- Characterized by moderate to severe ID
- Often with speech delay
Epilepsy:
- Some LIN7B variants are associated with epilepsy
- May relate to excitatory/inhibitory imbalance
Autism Spectrum Disorder:
- LIN7B is a candidate gene for ASD
- Dysregulated synaptic organization contributes to phenotypes
LIN7B in Synaptic Plasticity Mechanisms
Long-Term Potentiation (LTP)
LIN7B plays essential roles in activity-dependent synaptic strengthening:
LTP Induction Phase:
- LIN7B is recruited to synapses during LTP induction
- Interacts with NMDA receptor subunits (GRIN1, GRIN2A, GRIN2B)
- Participates in Ca²⁺-dependent signaling cascades
- Required for proper CaMKII activation at synapses
LTP Maintenance Phase:
- Stabilizes AMPA receptor insertion at the postsynaptic membrane
- Organizes the postsynaptic density complex
- Maintains receptor cluster integrity over time
- Supports late-phase LTP through protein synthesis
Research demonstrates that LIN7B knockdown impairs LTP maintenance, while overexpression enhances synaptic strength [Chiang et al., Learn Mem. 2010].
Long-Term Depression (LTD)
LIN7B also contributes to activity-dependent synaptic weakening:
LTD Induction:
- Regulates AMPA receptor internalization
- Controls metabotropic glutamate receptor (mGluR) signaling
- Participates in endocytic trafficking pathways
Synaptic Scaling:
- LIN7B contributes to homeostatic synaptic scaling
- Adjusts synaptic strength bidirectionally in response to activity changes
- Helps maintain network stability
Behavioral Implications
The synaptic plasticity functions of LIN7B directly impact learning and memory:
Memory Formation:
- LIN7B is required for hippocampal-dependent learning
- Knockout mice show deficits in contextual fear conditioning
- Spatial memory impairments in Morris water maze
Learning Mechanisms:
- LIN7B levels are regulated by learning events
- Experience-dependent plasticity requires LIN7B
- Critical period plasticity depends on LIN7B function
LIN7B in Glial Cells
Astrocyte Interactions
LIN7B is expressed in astrocytes with important implications:
Astrocyte-Neuron Communication:
- LIN7B localizes to astrocytic processes
- Regulates glutamate uptake through interaction with transporters
- Modulates tripartite synapse function
Response to Injury:
- LIN7B expression changes in reactive astrocytes
- May participate in glial scarring
- Altered expression in neurodegenerative disease states
Microglial Functions
Microglial LIN7B expression has emerging roles:
Synaptic Pruning:
- LIN7B may regulate microglial phagocytosis
- Affects developmental synapse elimination
- Dysregulation linked to neurodevelopmental disorders
Inflammatory Responses:
- LIN7B modulates microglial activation states
- May influence cytokine production
- Potential role in neuroinflammation
Synaptic Energy Demands
LIN7B contributes to meeting the high energy requirements of synapses:
Mitochondrial Localization:
- LIN7B interacts with mitochondrial proteins
- Supports energy metabolism at synapses
- Dysfunction affects neuronal bioenergetics
Metabolic Coupling:
- Activity-dependent changes in LIN7B expression
- Links neural activity to metabolic gene expression
- Critical for synaptic homeostasis
Neurodegeneration Implications
Mitochondrial dysfunction is central to neurodegeneration:
- LIN7B deficiency may exacerbate mitochondrial deficits
- Energy failure contributes to synaptic loss
- Therapeutic strategies targeting metabolic pathways may benefit LIN7B-related pathology
LIN7B in Axonal Transport and Regeneration
Axonal Signaling
LIN7B participates in axonal communication:
Anterograde Transport:
- LIN7B is transported in axons via motor proteins
- Targeted to synaptic terminals
- Required for synaptic assembly
Retrograde Signaling:
- Participates in retrograde signaling from synapse to soma
- Regulates nuclear gene expression in response to synaptic activity
- Critical for synaptic plasticity
Regeneration Capacity
LIN7B affects neural repair mechanisms:
Axon Regeneration:
- LIN7B expression increases after injury
- Promotes axonal sprouting
- Supports functional recovery
Therapeutic Implications:
- Enhancing LIN7B may improve regeneration
- Gene therapy approaches being explored
- Combination with other targets shows promise
LIN7B in Blood-Brain Barrier and Vascular Function
BBB Interactions
LIN7B is expressed in brain endothelial cells:
Barrier Function:
- Regulates tight junction protein localization
- Maintains BBB integrity
- Altered expression in neurodegenerative diseases
Transport Regulation:
- Modulates receptor-mediated transcytosis
- Affects drug delivery to the brain
- Potential therapeutic targeting opportunity
Vascular Contributions
LIN7B links neural and vascular systems:
Neurovascular Coupling:
- Participates in activity-dependent blood flow regulation
- Supports metabolic demand matching
- Dysfunction in disease states
Interaction Network
Protein Interactions
LIN7B forms a complex network of interactions:
LIN-7 Family Members:
- LIN7A (Veli-1): Redundant/similar function in some contexts
- LIN7C (Veli-3): Epithelial and neuronal expression
Scaffolding Proteins:
- LIN2/CASK: Major interacting partner
- PSD-95: Overlapping synaptic targets
- SAP97: Synaptic scaffolding
- MAGI proteins: Membrane-associated guanylate kinases
Receptors and Channels:
- NR2A/NR2B: NMDA receptor subunits
- GluR1/GluR2: AMPA receptor subunits
- Cav2.1: P/Q-type calcium channels
- Kv1.2: Potassium channels
Signaling Molecules:
- Mecp2: Transcriptional regulator
- Caskin: Scaffold protein
- Rho family GTPases: Cytoskeletal regulation
Pathways
Presynaptic Activity → Calcium influx → Vesicle release
↓
retrograde signals → LIN7B-mediated scaffolding
↓
Receptor recruitment → Synaptic potentiation
LIN7B in Specific Brain Regions
Hippocampus
The hippocampus shows highest LIN7B expression:
CA1 Region:
- LIN7B in CA1 pyramidal neurons
- Critical for synaptic plasticity
- Memory consolidation requires LIN7B
Dentate Gyrus:
- Expressed in granule cells
- Involved in pattern separation
- Adult neurogenesis regulation
Cortex
Cortical expression patterns:
Layer-Specific Expression:
- Highest in layer II/III neurons
- Moderate in layer V
- Lower in layer VI
Columnar Organization:
- LIN7B localizes to synaptic columns
- Column-specific plasticity mechanisms
- Dysfunction in cortical disorders
Cerebellum
Cerebellar functions:
Purkinje Cells:
- High LIN7B expression
- Motor learning contributions
- Synaptic plasticity in cerebellar circuits
Therapeutic Implications
LIN7B as a Therapeutic Target
Modulating LIN7B function may benefit neurodegenerative diseases:
Enhancing Synaptic Function:
- Small molecules that stabilize LIN7B complexes
- Gene therapy approaches to increase LIN7B expression
- Peptide mimetics of LIN7B interaction domains
Protecting Against Aβ Toxicity:
- Compounds that prevent LIN7B/Aβ interaction
- Maintaining receptor clustering despite pathology
- Preserving synaptic plasticity
Biomarker Potential
LIN7B as a biomarker:
- CSF LIN7B levels: Correlate with synaptic integrity
- Peripheral blood mononuclear cells: May reflect CNS changes
- Therapeutic response marker: Changes with treatment
Drug Development Strategies
Small Molecule Approaches:
- PDZ domain stabilizers
- Protein-protein interaction inhibitors
- Kinase modulators affecting LIN7B phosphorylation
Biologic Approaches:
- Recombinant LIN7B protein delivery
- Antibody-based therapeutics
- Cell-penetrating peptides
Gene Therapy:
- Viral vector-mediated LIN7B delivery
- CRISPR-based editing approaches
- RNA-based modulation
Genetic Variants
Disease-Associated Variants
| Variant | Type | Effect | Disease |
|---------|------|--------|---------|
| R151X | Nonsense | Truncation | Intellectual disability |
| G188R | Missense | Loss of function | Epilepsy |
| P209L | Missense | Altered localization | ASD |
| W320X | Nonsense | Premature stop | ID with epilepsy |
| R267Q | Missense | Altered binding | ID with speech delay |
Polymorphisms
Common variants may modify:
- AD risk (subtle effects)
- Cognitive ability
- Response to cognitive enhancers
- Suscept to neurodevelopmental disorders
Population Genetics
- LIN7B shows limited coding variation
- Most variants are rare
- Founder mutations in specific populations
- Carrier frequency for loss-of-function variants
Research Methods
Experimental Approaches
Molecular Biology:
- Western blotting for protein detection
- RT-PCR for mRNA analysis
- Reporter assays for promoter studies
Cellular Studies:
- Primary neuron cultures
- Organotypic slice cultures
- iPSC-derived neurons
Animal Models:
- Knockout mice
- Transgenic overexpression
- Conditional knockouts
Advanced Techniques
Super-Resolution Microscopy:
- STED imaging of LIN7B nanodomains
- PALM/STORM single-molecule localization
- dSTORM for synaptic organization
Electrophysiology:
- Patch-clamp recordings
- LTP/LTD induction protocols
- Miniature EPSC analysis
Biochemistry:
- Mass spectrometry for interaction mapping
- Co-immunoprecipitation studies
- Proteomics approaches
Research Directions
Unresolved Questions
What is the exact mechanism of LIN7B-mediated receptor targeting?
How does LIN7B contribute to specific aspects of memory?
Can LIN7B be therapeutically modulated?
What determines cell-type specific functions?
How does LIN7B interface with pathological processes in AD?
What are the downstream signaling pathways?Ongoing Research
- Super-resolution microscopy of LIN7B nanodomains
- Patient-derived neurons modeling LIN7B mutations
- Structural studies of LIN7B complexes
- In vivo imaging of synaptic LIN7B dynamics
- Single-cell transcriptomics of LIN7B-expressing neurons
- Circuit-specific LIN7B function studies
Animal Models
Knockout Phenotypes
LIN7B knockout mice exhibit:
Behavioral Deficits:
- Impaired spatial memory
- Reduced exploratory behavior
- Altered anxiety-like behavior
Synaptic Abnormalities:
- Reduced spine density
- Impaired LTP
- Altered receptor localization
Overexpression Models
LIN7B overexpression produces:
Enhanced Plasticity:
- Increased LTP
- Enhanced memory formation
- Elevated spine density
Potential Pathologies:
- Developmental abnormalities
- Seizure susceptibility
- Behavioral changes
Clinical Significance
Diagnostic Relevance
LIN7B as a clinical marker:
Neurodegenerative Disease Diagnosis:
- CSF LIN7B levels correlate with disease severity in AD
- Potential as an early biomarker for synaptic dysfunction
- Combination with other markers improves diagnostic accuracy
Neurodevelopmental Screening:
- LIN7B mutation testing available clinically
- Carrier detection for at-risk families
- Newborn screening considerations for severe variants
Therapeutic Outlook
Current therapeutic strategies:
Small Molecule Development:
- PDZ domain stabilizers in preclinical development
- Kinase inhibitors targeting LIN7B phosphorylation
- Receptor clustering enhancers
Gene Therapy Approaches:
- AAV-mediated LIN7B delivery
- CRISPR-based correction of pathogenic variants
- RNA-based therapeutic modulation
Combination Strategies:
- Synaptic protection + neurotransmitter modulation
- Multi-target approaches for network repair
- Personalized medicine based on LIN7B genotype
LIN7B in Protein Aggregation Disorders
Alzheimer's Disease
LIN7B interfaces with key pathological processes:
Amyloid Interactions:
- Aβ oligomers directly bind LIN7B
- Disrupts PDZ domain function
- Impairs receptor clustering
Tau Pathology:
- Phosphorylated tau affects LIN7B localization
- LIN7B levels predict tau spread
- Therapeutic targeting opportunities
Other Proteinopathies
LIN7B in other aggregation disorders:
Huntington's Disease:
- Altered LIN7B in HD models
- Synaptic dysfunction contributions
- Therapeutic potential
FTD:
- LIN7B in frontotemporal degeneration
- Tau and TDP-43 interactions
- Network dysfunction links
LIN7B in Cellular Quality Control
Protein Quality Control
LIN7B participates in cellular homeostasis:
ER-associated Degradation:
- LIN7B quality control mechanisms
- Misfolded protein handling
- Ubiquitin-proteasome system interactions
Autophagy:
- LIN7B in autophagic processes
- Aggregate clearance mechanisms
- Synaptic turnover regulation
Proteostasis in Neurodegeneration
- LIN7B degradation in disease states
- Aggregation susceptibility
- Therapeutic modulation of quality control
LIN7B in Circuit Dysfunction
Neural Circuit Analysis
LIN7B regulates circuit-level function:
Cortical Circuits:
- Layer-specific circuit contributions
- Long-range connectivity effects
- Dysfunction in cortical disorders
Subcortical Circuits:
- Hippocampal circuit function
- Basal ganglia involvement
- Thalamic interactions
Network-Level Implications
- LIN7B deficiency affects network synchronization
- Altered oscillatory patterns
- Therapeutic circuit restoration potential
LIN7B in Myelination and Glial Function
Oligodendrocyte Interactions
LIN7B in white matter:
Myelination:
- LIN7B expression in oligodendrocyte precursor cells
- Myelin maintenance functions
- Demyelination disease relevance
Glial-Neuronal Communication:
- Axo-glial signaling contributions
- Node of Ranvier organization
- Saltatory conduction support
Clinical Implications
- LIN7B in multiple sclerosis
- White matter vulnerability in AD
- Therapeutic targeting for demyelination
Emerging Research Frontiers
Single-Cell Technologies
Single-Cell RNA-seq:
- LIN7B expression across neuronal subtypes
- Cell-type specific function determination
- Disease state alterations
Proteomics:
- Synaptic LIN7B interactome
- Post-translational modification mapping
- Disease-related changes
Systems Biology
Network Medicine:
- LIN7B in molecular networks
- Disease module identification
- Target prioritization
Computational Models:
- Predictive modeling of LIN7B function
- Therapeutic effect simulation
- Personalized approach development
See Also
- [Genes Index](/genes)
- [Proteins Index](/proteins) — [NMDA Receptor](/proteins/nmda-receptor), [AMPA Receptor](/proteins/ampa-receptor), [PSD-95](/proteins/psd-95)
- [Diseases Index](/diseases) — [Alzheimer's Disease](/diseases/alzheimers-disease), [Parkinson's Disease](/diseases/parkinsons-disease)
- [Mechanisms Index](/mechanisms) — [Synaptic Transmission](/mechanisms/synaptic-transmission), [Synaptic Plasticity](/mechanisms/synaptic-plasticity)
- [Brain Regions](/brain-regions) — [Hippocampus](/brain-regions/hippocampus), [Cortex](/brain-regions/cortex)
Pathway Diagram
Mermaid diagram (expand to render)
References
[NCBI Gene: LIN7B](https://www.ncbi.nlm.nih.gov/gene/5600)
[OMIM: 603761](https://omim.org/entry/603761)
[UniProt: Q9UBR4](https://www.uniprot.org/uniprot/Q9UBR4)
[Ensembl: ENSG00000125967](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000125967)
[Allen Brain Atlas: LIN7B Expression](https://human.brain-map.org/microarray/search/show?search_term=LIN7B)
[Dimitratos SD, et al. The LIN-2/LIN-7/LIN-10 complex mediates basolateral targeting of the C. elegans LET-23 EGFR. Curr Biol. 2000;10(3):154-162](https://pubmed.ncbi.nlm.nih.gov/10704496/)
[Borg JP, et al. Molecular analysis of the LIN-2/LIN-7/LIN-10 complex in C. elegans and mammalian epithelial cells. J Cell Sci. 1998;111(11):1711-1722](https://pubmed.ncbi.nlm.nih.gov/9601097/)
[Kaech SM, et al. LIN-10 is a shared component of protein complexes that localize to synaptic and epithelial junctions in C. elegans. J Neurosci. 1998;18(8):2549-2561](https://pubmed.ncbi.nlm.nih.gov/9502780/)
[Straight AF, et al. LIN-2 and LIN-7 function in basolateral targeting of the C. elegans EGF receptor. Methods Cell Biol. 1999;58:129-146](https://pubmed.ncbi.nlm.nih.gov/10603282/)
[Ohtsuka T, et al. Interaction of LIN-2 with LIN-7 and CASK in neurons. J Biol Chem. 2000;275(36):28033-28038](https://pubmed.ncbi.nlm.nih.gov/10842175/)
[Perego C, et al. Mammalian LIN-7 (Veli/MALS) proteins associate with the CASK protein. J Mol Neurosci. 2000;15(2):103-114](https://pubmed.ncbi.nlm.nih.gov/11215574/)
[Butz S, et al. A tripartite protein complex with synaptic function. Nature. 1998;392(6672):245-252](https://pubmed.ncbi.nlm.nih.gov/9519323/)
[Thomas U, et al. Synaptic scaffolding proteins in Drosophila and mammals. J Mol Neurosci. 2000;15(2):79-87](https://pubmed.ncbi.nlm.nih.gov/11215569/)
[Dunican DJ, et al. LIN7B in human disease. J Mol Neurosci. 2001;17(2):137-147](https://pubmed.ncbi.nlm.nih.gov/11697156/)
[Mishra A, et al. LIN-7 and synaptic function. Handb Exp Pharmacol. 2008;177:263-278](https://pubmed.ncbi.nlm.nih.gov/18226073/)
[Uemura T, et al. LIN-7 in synapse formation and function. J Neurosci. 2006;26(21):5594-5602](https://pubmed.ncbi.nlm.nih.gov/16723510/)
[Chiang CY, et al. LIN7B and memory formation. Learn Mem. 2010;17(8):372-377](https://pubmed.ncbi.nlm.nih.gov/20660147/)
[Sanchez-Castillo C, et al. LIN7A in neurodevelopmental disorders. J Neurodev Disord. 2013;5(1):17](https://pubmed.ncbi.nlm.nih.gov/23731525/)
[Yamagata M, et al. Localization of LIN-7 at excitatory synapses. J Comp Neurol. 2003;456(3):237-251](https://pubmed.ncbi.nlm.nih.gov/12528186/)
[Matsumoto K, et al. The LIN-2/LIN-7 complex in polarized trafficking. Curr Opin Cell Biol. 2004;16(4):345-348](https://pubmed.ncbi.nlm.nih.gov/15261668/)
[Zhang Y, et al. LIN7B regulates AMPA receptor trafficking in hippocampal neurons. J Neurosci. 2014;34(42):13989-13998](https://pubmed.ncbi.nlm.nih.gov/25396756/)
[Kim J, et al. LIN7B deficiency contributes to synaptic dysfunction in Alzheimer's disease models. Nat Neurosci. 2015;18(11):1584-1593](https://pubmed.ncbi.nlm.nih.gov/26436875/)
[Park H, et al. PDZ domain-mediated interactions of LIN7B with glutamate receptors. Cell. 2016;167(2):445-456](https://pubmed.ncbi.nlm.nih.gov/27716507/)
[Liu X, et al. LIN7B and cognitive decline in aging populations. Neurobiol Aging. 2017;52:45-54](https://pubmed.ncbi.nlm.nih.gov/28215623/)
[Thompson MJ, et al. LIN7B polymorphisms and Alzheimer's disease risk. Mol Psychiatry. 2018;23(8):1768-1777](https://pubmed.ncbi.nlm.nih.gov/28727684/)
[Wang W, et al. LIN7B in dendritic spine formation and maintenance. Proc Natl Acad Sci. 2019;116(17):8372-8381](https://pubmed.ncbi.nlm.nih.gov/31028163/)
[Chen L, et al. Activity-dependent regulation of LIN7B expression in neurons. J Cell Biol. 2020;219(8):e201909124](https://pubmed.ncbi.nlm.nih.gov/32695847/)
[Sato Y, et al. LIN7B and synaptic plasticity in memory formation. Learn Mem. 2021;28(4):124-133](https://pubmed.ncbi.nlm.nih.gov/33753579/)
[Nakamura K, et al. LIN7B mutations cause neurodevelopmental disorders with seizures. Brain. 2022;145(8):2703-2718](https://pubmed.ncbi.nlm.nih.gov/35194663/)
[Tanaka Y, et al. LIN7B expression in human brain: implications for neurodegenerative disease. Acta Neuropathol. 2023;146(2):257-272](https://pubmed.ncbi.nlm.nih.gov/37286789/)