SLC6A8

Chr XXLR

solute carrier family 6 member 8

Also known as: CCDS1, CRT, CRT-1, CRT1, CRTR, CT1, CTR5

The encoded protein is a creatine transporter that mediates cellular uptake of creatine and supplies creatine to the brain via the blood-brain barrier. Mutations cause X-linked cerebral creatine deficiency syndrome 1, characterized by intellectual disability, speech delay, and seizures. This gene follows X-linked recessive inheritance and is highly constrained against loss-of-function variants.

OMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismXLRLOEUF 0.211 OMIM phenotype
VCEP Guidelines: Cerebral Creatine DeficiencyPilot
View SpecificationsClinGen Panel
Clinical SummarySLC6A8
🧬
Gene-Disease Validity (ClinGen)
creatine transporter deficiency · XLDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
📋
ClinVar Variants
112 unique Pathogenic / Likely Pathogenic· 147 VUS of 400 total submissions
💊
Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.21LOEUF
pLI 0.998
Z-score 4.18
OE 0.04 (0.010.21)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
3.05Z-score
OE missense 0.46 (0.400.54)
118 obs / 255.0 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.04 (0.010.21)
00.351.4
Missense OE0.46 (0.400.54)
00.61.4
Synonymous OE1.14
01.21.6
LoF obs/exp: 1 / 22.3Missense obs/exp: 118 / 255.0Syn Z: -1.17
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveSLC6A8-related creatine deficiency syndromeLOFXLR
DN
0.4785th %ile
GOF
0.74top 25%
LOF
0.51top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOF54% of P/LP variants are LoF · LOEUF 0.21
GOFprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

400 submitted variants in ClinVar

Classification Summary

Pathogenic68
Likely Pathogenic44
VUS147
Likely Benign97
Benign5
68
Pathogenic
44
Likely Pathogenic
147
VUS
97
Likely Benign
5
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
35
2
31
0
68
Likely Pathogenic
25
15
4
0
44
VUS
3
116
20
8
147
Likely Benign
0
5
49
43
97
Benign
0
1
4
0
5
Total6313910851361

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

SLC6A8 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →