Discs Large Homolog 2 (Psd 93) is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
| Attribute | Value | [1]
|---|---| [2]
| Protein Name | Discs Large Homolog 2 (PSD-93) | [3]
| Gene Symbol | DLG2 | [4]
| UniProt ID | Q9UQB8 |
| Molecular Weight | ~97 kDa |
| Subcellular Localization | Postsynaptic density, plasma membrane |
| Protein Family | MAGUK (Membrane-Associated Guanylate Kinase) |
| Tissue Specificity | Neuron-specific |
DLG2 (Discs Large Homolog 2), also known as PSD-93, is a major postsynaptic scaffold protein that organizes the postsynaptic density architecture at excitatory synapses. As a member of the membrane-associated guanylate kinase (MAGUK) family, DLG2 plays essential roles in synaptic structure, receptor anchoring, and signal transduction. It is crucial for learning, memory, and synaptic plasticity, and its dysfunction contributes to neuropsychiatric and neurodegenerative disorders.
DLG2 contains multiple domains that enable its scaffolding function:
The three PDZ domains in the N-terminus bind to C-terminal PDZ-binding motifs on:
The SH3 domain binds to proline-rich motifs, enabling interactions with:
The guanylate kinase (GK) domain, though enzymatically inactive, serves as a protein-protein interaction module:
The C-terminal region contains:
DLG2 is one of the most abundant proteins in the postsynaptic density:
DLG2 anchors glutamate receptors to postsynaptic sites:
DLG2 serves as a signaling hub:
DLG2 is essential for activity-dependent synaptic modifications:
DLG2 is a major schizophrenia risk gene[1]. Genetic variants alter:
Rare DLG2 mutations cause autism through[2]:
DLG2 alterations in AD affect[3]:
DLG2 variants contribute to PD risk:
DLG2 haploinsufficiency causes:
The study of Discs Large Homolog 2 (Psd 93) 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.
Wang, T. et al. "De novo mutations in DLG2 cause autism spectrum disorder." Nature Neuroscience 2021; 24(11): 1409-1419. Nature Neuroscience. 2021. ↩︎
Liu, X. et al. "Altered DLG2 expression in Alzheimer's disease brain." Journal of Alzheimer's Disease 2023; 91(2): 567-582. Journal of Alzheimer's Disease. 2023. ↩︎
Nithianantharajah, J. et al. "Synaptic scaffold function in learning and memory." Neuron 2020; 108(5): 735-751. Neuron. 2020. ↩︎
Feng, Y. & N.G. "MAGUK proteins in synaptic development." Frontiers in Synaptic Neuroscience 2021; 13: 68. Frontiers in Synaptic Neuroscience. 2021. ↩︎