MXRA8

Chr 1

matrix remodeling associated 8

Also known as: ASP3

The protein is a transmembrane molecule that modulates integrin signaling pathways, inhibits angiogenesis by suppressing endothelial cell migration and promoting apoptosis, and plays a role in blood-brain barrier maturation and maintenance. Mutations cause autosomal recessive developmental and epileptic encephalopathy with microcephaly, typically presenting in early infancy with severe intellectual disability, seizures, and brain malformations. The gene is not highly constrained against loss-of-function variants, consistent with recessive inheritance where heterozygous carriers are typically unaffected.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
12
Pubs (1 yr)
136
P/LP submissions
1%
P/LP missense
1.13
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryMXRA8
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
129 unique Pathogenic / Likely Pathogenic· 97 VUS of 254 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.13LOEUF
pLI 0.000
Z-score 1.15
OE 0.71 (0.461.13)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
1.05Z-score
OE missense 0.81 (0.730.91)
208 obs / 255.3 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.71 (0.461.13)
00.351.4
Missense OE0.81 (0.730.91)
00.61.4
Synonymous OE1.17
01.21.6
LoF obs/exp: 13 / 18.3Missense obs/exp: 208 / 255.3Syn Z: -1.51
DN
0.6743th %ile
GOF
0.76top 25%
LOF
0.3647th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). Both the Badonyi & Marsh prediction and the broader genomic evidence point to gain-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median
DNprediction 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.

ClinVar Variant Classifications

254 submitted variants in ClinVar

Classification Summary

Pathogenic122
Likely Pathogenic7
VUS97
Likely Benign13
Benign3
122
Pathogenic
7
Likely Pathogenic
97
VUS
13
Likely Benign
3
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
122
0
122
Likely Pathogenic
0
1
6
0
7
VUS
0
78
19
0
97
Likely Benign
0
5
2
6
13
Benign
0
2
0
1
3
Total0861497242

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

View in ClinVar →

Protein Context — Lollipop Plot

MXRA8 · protein map & ClinVar variants

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

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

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Clinical Literature
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