SRR — Serine Racemase
Introduction
Srr — Serine Racemase is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
<div class="infobox infobox-gene">
<table>
<tr><th colspan="2" style="background:#f0f0f0; text-align:center;">Gene Information</th></tr>
<tr><td><strong>Symbol</strong></td><td>SRR</td></tr>
<tr><td><strong>Full Name</strong></td><td>Serine Racemase</td></tr>
<tr><td><strong>Chromosome</strong></td><td>17</td></tr>
<tr><td><strong>NCBI Gene ID</strong></td><td><a href="https://www.ncbi.nlm.nih.gov/gene/57328" target="_blank">57328</a></td></tr>
<tr><td><strong>OMIM</strong></td><td><a href="https://www.omim.org/entry/607521" target="_blank">607521</a></td></tr>
<tr><td><strong>UniProt ID</strong></td><td><a href="https://www.uniprot.org/uniprot/Q9GZN8" target="_blank">Q9GZN8</a></td></tr>
<tr><td><strong>Ensembl ID</strong></td><td><a href="https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000167751" target="_blank">ENSG00000167751</a></td></tr>
<tr>
<td class="label">Associated Diseases</td>
<td><a href="/wiki/diabetic-retinopathy" style="color:#ef9a9a">diabetic retinopathy</a></td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">2 edges</a></td>
</tr>
</table>
</div>
Overview
SRR (Serine Racemase) is the enzyme responsible for converting L-serine to D-serine, a neuromodulator that acts as an endogenous co-agonist at [NMDA](/entities/nmda-receptor) receptors. D-serine plays crucial roles in synaptic plasticity, memory, and neurodegeneration. SRR is implicated in Alzheimer's disease, schizophrenia, and ischemic brain injury.
Normal Function
SRR catalyzes the racemization of L-serine to D-serine using pyridoxal 5'-phosphate (PLP) as a cofactor. D-serine is the primary endogenous co-agonist for NMDA receptors, modulating synaptic transmission and plasticity. SRR activity is regulated by phosphorylation, protein interactions, and cellular energy status.
Expression Pattern
Brain-enriched, particularly in [cortex](/brain-regions/cortex), [hippocampus](/brain-regions/hippocampus), and glia.
Disease Associations
| Disease | Role in Disease |
|---------|-----------------
| [Alzheimer's Disease](/diseases/alzheimers-disease) | D-serine dysregulation, NMDA receptor hypofunction, excitotoxicity |
| [Schizophrenia](/diseases/schizophrenia) | D-serine deficiency, NMDA receptor signaling |
| [Stroke](/diseases/stroke) | Excitotoxicity, ischemic neuronal damage |
| [Parkinson's Disease](/diseases/parkinsons-disease) | Dopaminergic neuron survival, NMDA modulation |
Key Publications
[^1] [^2] [^3] [^4] [^5]
Overview
SRR (Serine Racemase) is an enzyme that catalyzes the conversion of L-serine to D-serine, an endogenous NMDA receptor co-agonist. D-serine plays critical roles in NMDA receptor-mediated synaptic transmission, plasticity, and excitotoxicity.
Gene Characteristics
- Gene Symbol: SRR
- Location: Chromosome 17p13
- NCBI Gene ID: 5657
- Expression: Brain ([neurons](/entities/neurons), astrocytes)
Enzyme Function
SRR catalyzes:
- L-serine → D-serine (racemization)
- Requires pyridoxal phosphate (PLP) as cofactor
- D-serine is endogenous NMDAR co-agonist
Role in Neurodegeneration
Alzheimer's Disease
- Altered D-serine levels in AD brain
- Dysregulated NMDAR signaling
- Contributes to excitotoxicity
Parkinson's Disease
- SRR expression in dopaminergic regions
- NMDAR hyperactivity in PD
- Therapeutic target potential
Schizophrenia
- D-serine as potential biomarker
- SRR gene variants associated with risk
Therapeutic Targeting
| Approach | Strategy | Status |
|----------|----------|--------|
| SRR inhibitors | Reduce D-serine | Research |
| D-serine supplementation | NMDAR modulation | Clinical trials |
See Also
- [NMDA Receptors](/therapeutics/nmda-receptor-antagonists)
- [D-Serine Signaling](/mechanisms/d-serine-signaling)
- [Alzheimer's Disease](/diseases/alzheimers-disease)
- [Parkinson's Disease](/diseases/parkinsons-disease)
External Links
- [UniProt: Q9GZT4](https://www.uniprot.org/uniprot/Q9GZT4)
- [NCBI Gene: 5657](https://www.ncbi.nlm.nih.gov/gene/5657)
Expression Pattern
SRR is expressed in brain (highest in hippocampus and cortex), spinal cord, and peripheral tissues. Expression is activity-dependent.
Molecular Mechanisms
D-Serine Synthesis
SRR catalyzes the racemization of L-serine to D-serine, the endogenous co-agonist of NMDA receptors.
Brain Function
D-serine released from [astrocytes](/entities/astrocytes) and neurons modulates NMDA receptor activity, synaptic plasticity, and learning and memory.
Role in Neurodegeneration
Alzheimer's Disease
D-serine levels are altered in AD brains. NMDA receptor dysregulation contributes to excitotoxicity (PubMed: 10077666).
Schizophrenia
SRR polymorphisms are associated with schizophrenia. D-serine is a potential therapeutic agent (PubMed: 14572456).
Stroke
Excessive D-serine release contributes to excitotoxic cell death after stroke (PubMed: 21458745).
Therapeutic Implications
D-serine supplementation trials in schizophrenia, SRR inhibitors for stroke treatment, and modulators of D-serine metabolism are under investigation.
Background
The study of Srr — Serine Racemase 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> De Camilli P, Cameron R, Greengard P. Synapsin I: a synaptic vesicle-associated neuronal phosphoprotein. J Cell Biol. 1983;96(5):1355-1373. PMID: 6682992(https://pubmed.ncbi.nlm.nih.gov/6682992/)
<sup>[2]</sup> Hsia AY, Masliah E, McConlogue L, et al. Plaque-independent disruption of neural circuits in Alzheimer's disease. Proc Natl Acad Sci U S A. 1999;96(6):3228-3233. PMID: 10077666(https://pubmed.ncbi.nlm.nih.gov/10077666/)
<sup>[3]</sup> Chesselet MF, Richter F, Zhu C, et al. Alpha-synuclein and synaptic function. J Mol Neurosci. 2012;47(3):461-470. PMID: 22328567(https://pubmed.ncbi.nlm.nih.gov/22328567/)
<sup>[4]</sup> Fassio A, Patry L, Congia S, et al. De novo mutations of the gene encoding synapsin I (SYN1) in patients with epilepsy. Brain. 2011;134(Pt 10):2864-2878. PMID: 28628578(https://pubmed.ncbi.nlm.nih.gov/28628578/)
[^1]: [Reference missing - citation needed]
[^2]: [Reference missing - citation needed]
[^3]: [Reference missing - citation needed]
[^4]: [Reference missing - citation needed]
[^5]: [Reference missing - citation needed]